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Results: Three patients were managed with this technique. The procedure was successful in all the patients. Two patients had recurrent stenotic stoma from Crohn’s disease, while the third patient had colostomy following colon cancer resection and developed recurrent stricture even after surgical revision and multiple balloon dilations. All patients had great response following stent placement with marked decrease abdominal girth within 24 hours. One patient had severe pain and could tolerate the stent for only 4 days. The other 2 patients’ stents were left in situ for 6 weeks. All 3 patients had symptomatic improvement following stent placement. The patient who could not tolerate the stent developed recurrent stenosis in 4 weeks. Conclusion: Fully covered metal stents appear to be a safe, effective, and less invasive option in the management of stomal stenosis. Larger studies are needed to validate the results of our pilot study.

766 Basaloid Squamous Cell Carcinoma of the Ascending Colon: An Unusual but Aggressive Malignancy Rasha Issa, MD, Omar Majdobeh, MD, Hareth Raddawi, MD, FACG. Christ Advocate Medical Center, Oak Lawn, IL. Introduction: Basaloid squamous cell carcinoma of the ascending colon is the first case of its kind by location. Other documented cases have demonstrated this aggressive high-grade tumor in the anal canal, descending colon, splenic flexure, rectosigmoid, and sigmoid colon, respectively. It is an important differential diagnosis to consider given its very aggressive nature and relative obscurity. We describe a patient who presents with weakness associated with incidental A-fib. A 74-year-old male with a past history of osteoarthritis requiring hip replacement presented with weakness of 3-months’ duration followed by a syncopal episode and loose stools for 3 weeks. Blood was detected on rectal exam. His initial hemoglobin was 6.5 g, MCV 99.5, and platelet count 193. Following transfusion, the hemoglobin rose to 7.8 g. Alkaline phosphatase was 280 initially. Abdominal CT demonstrated multiple masses compatible with metastasis and focal mural thickening of the ascending colon near the hepatic flexure with infiltrative changes in the adjacent mesenteric fat and multiple lymph nodes measuring 1 cm. Esophagoduodenoscopy and biopsy demonstrated a gastric ulcer. Colonoscopy revealed a large ulcerated irregular mass lesion measuring 5 x 6 cm in the ascending colon. Extensive colonic diverticulosis were also noted. Immediate surgical removal of the bleeding and obstructing colonic mass was performed. Biopsy showed infiltrating solid nests of poorly differentiated carcinoma without glandular formation atypical of adenocarcinoma. Pathology further demonstrated a 3.8 x 3 x 0.7 cm ulcerated mass located above the peritoneal reflection, extending through the colonic wall, reaching the peritoneal serosal surface, with extensive angiolymphatic invasion and vascular invasion. The tumor forms many small nodules in the mesenteric pericolic adipose tissue with metastasis in 12 of 17 pericolic lymph nodes. Treatment is ongoing. Basaloid colorectal tumors are extremely rare, with only a handfull of documented cases worldwide. They are very aggressive and have a propensity for metastasis. Their histopathology, however, makes them easy to distinguish from other common forms of colorectal cancers. The present literature suggests a link between basaloid colorectal cancer in combination with anal sex, HPV, and smoking as possible risk factors. It is helpful for clinicians to keep this rather aggressive but rare form of colorectal malignancy in mind especially given the known risk factors and suggestive histopathological findings. Basaloid SCC remains a difficult and challenging diagnosis. Their rarity and subsequent delayed diagnosis are major factors that ultimately lead to a poor prognosis and inevitable failed treatment.

[767A] Figure 1. CT abdomen/pelvis with marked splenomegaly with the spleen measuring 23 cm longitudinally.

768 An Unusual Case of Obstruction Due to Colonic Intussusception in a Patient With Scleroderma Kristina Katz, MD,1 Kevin Skole, MD,2 Jean Fede, DO2. 1. Rutgers Robert Wood Johnson Medical School, New Brunswick, NJ; 2. University Medical Center of Princeton at Plainsboro, Plainsboro, NJ.

Kristina Katz, MD, Muhammad Shafqet, MD, S. Devi Rampertab, MD, Nakechand Pooran, MD. Rutgers Robert Wood Johnson Medical School, New Brunswick, NJ.

Introduction: Scleroderma is a rheumatologic disease that affects many organs including the gastrointestinal (GI) tract. Intussusception has been associated with scleroderma, however, the only reported cases of this have involved the small bowel. We present a case of colonic intussusception secondary to scleroderma. A 44-year-old female with systemic scleroderma presented with abdominal pain and constipation. CT abdomen/pelvis showed significant large bowel distention and sigmoid intussusception with secondary colonic obstruction. Sigmoidoscopy revealed erythema, ulceration and necrotic bowel. She underwent a laparotomy with sigmoid resection and diverting colostomy. Pathologic findings included ulcerated colonic mucosa with granulation, fibropurulent exudate and inflammation. Scleroderma has many systemic manifestations due to collagen infiltration of the mucosa and submucosa, with atrophy of the muscularis externa. Intussusception occurs when a bowel segment with its associated mesentery invaginates into the lumen of adjacent bowel. It is believed that any lesion or irritant within the bowel lumen can alter peristaltic activity and initiate invagination. In most cases there is an organic lesion, with others attributed to functional disturbances, including scleroderma, lymphoid hyperplasia and celiac disease. In the latter cases, it is likely due to abnormal contraction and peristaltic forces, causing rotation of the abnormal segment inward, leading to a kink. Colonic intussusception is uncommon, and reported causes are almost exclusively secondary to neoplasm. Loss of haustration is seen in sclerodermatous large bowel, but is unknown if it could be partly responsible in causing intussusception. Abnormal peristalsis, colonic atony and decreased contractility could explain the intussusception in our patient. In addition, scleroderma is associated with inflammation, collagen deposition and fibrosis, all of which create mural abnormalities, leading to intussusception. It is proposed that the development of the sigmoid intussusception resulting in bowel obstruction in our patient with scleroderma was multifactorial and mostly attributed to the gastrointestinal manifestations of her rheumatologic disease.

Introduction: Osteopetrosis (OP) is a rare genetic disorder of abnormal bony architecture that obliterates the marrow cavity, resulting in bone marrow failure. Extramedullary hematopoiesis occurs in the spleen and can lead to left-sided portal hypertension. We present a rare case of OP induced portal hypertension manifesting as an upper GI bleed. Case Report: A 52-year-old woman with OP complicated by recurrent fractures and transfusion dependent pancytopenia was admitted for coffee ground emesis. She had no history of PUD, NSAID or alcohol use. Her exam revealed hypotension, tachycardia and a palpable spleen tip in the left lower quadrant with a normal liver span. Hemoglobin was 5.0 g/dL and platelet count was 39,000/uL. Liver enzymes and INR were normal. EGD revealed grade 3 non-bleeding esophageal varices and severe portal gastropathy. Workup was negative for chronic hepatitis, iron overload and portal system thrombi. CT abdomen revealed marked splenomegaly measuring 23cm longitudinally extending into left iliac fossa, abdominal ascites and normal sized liver. The GI bleed resolved with octreotide and pantoprazole. A diuretic was started for ascites along with nadolol for esophageal varices. Discussion: Our case highlights the rare occurrence of left-sided portal hypertension in a patient with OP. Left sided portal hypertension occurs when splenic venous outflow increases to a level greater than hepatic capacity. Elevated pressures in the splenic vasculature causes dilatation of collateral vessels leading to variceal formation. We hypothesize that our patient had left-sided portal hypertension from extramedullary hematopoiesis in the spleen. Her spleen was the major reservoir for erythropoiesis due to bone marrow failure from OP, but the excessive blood flow through the spleen overwhelmed the liver’s capacity, resulting in varices and eventual rupture. To our knowledge, there has only been one case report of OP manifesting as portal hypertension in 1971. Our case is the second reported case of portal hypertension from OP and the first presenting as GI bleeding.

[768A] Figure 1.

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CLINICAL VIGNETTES/CASE REPORTS - ESOPHAGUS

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[769A] Figure 1. Endoscopic visualization of tumor in the esophagus (left), tumor plunged into the stomach (right).

769 A Case of Plunging GIST Presenting as Intermittent Dysphagia Rahman Nakshabendi, MD,1 Matthew Clark, MD,1 Juan Munoz, MD, FACG,1 Imad Nakshabendi, MD, PHD, FACG2. 1. University of Florida COM, Jacksonville, FL; 2. Tampa General Hospital, Tampa, FL. Introduction: The patient is a 71-year-old woman with a past medical history of melenoma, who presented to the hospital with progressively worsening intermittent dysphagia, mainly for solid foods over the past year. Associated symptoms included reflux without significant weight loss. She typically had to chase solid food down with liquids in order to prevent any type of impaction. She has never had any food impaction that has required a food bolus removal. EGD 6 months prior was unremarkable. Endoscopy revealed a large 4-5-cm subepithelial lesion in the mid-esophagus at around 30 cm. The lesion appeared smooth with normal overlying smooth tissue. There were no obvious ulcerations. Biopsies were not taken at that time. CT scan of the chest confirmed the presence of a large submucosal mass in the distal esophagus. Repeat biopsy was performed with EUS and biopsy. No extra-esophageal masses were identified, and biopsy was proven for gastrointestinal stromal tumor. The patient was started on neoadjuvant chemotherapy with Gleevec®, with future plans for surgical resection. Discussion: Gist tumors’ presentation is generally vague, and varies depending on which part of the GI tract is affected. As they are a mass-occupying lesion, they may present as an obstruction.In the esophagus, it may present as dysphagia; it may even mimic symptoms of GERD. In this case, when the tumor was in the esophagus, it presented as dysphagia. When it plunged into the stomach, patient was asymptomatic. When EGD was first performed 6 month prior to diagnosis, the mass was missed, as it was most likely plunged into the stomach. Gist tumors may often present simply as abdominal discomfort with weight loss, as 75% of these tumors arise from the stomach. Some of the GIST tumors are found incidentally, and in about 2/3 of the cases, the size of the tumor is less than 4 cm at diagnosis. As it is evident that GIST has a wide array of symptoms, the differential is vast and modalities for diagnosis would be dependent on which part of the gut is affected. Generally, these tumors may be visualized on imaging such as barium swallow, CT, MRI, and may also be visualized and biopsied via EGD in the upper GI, or colonoscopy in the lower GI tract. Treatment for GIST is surgical resection when possible. Pharmaceutical therapies such as imatinib, Sunitib, and regorafebib all acting as a tyrosince kinase receptor blocker.

65% early mortality.2 Given the severity of potential short-term complications, patients with suspected injury should undergo urgent endoscopy within 24 hours and be closely followed thereafter. Long-term complications of esophageal caustic injuries include esophageal strictures and a 1000-times increased risk of esophageal squamous cell cancer.

771 Pure Primary Signet Ring Cell Adenocarcinoma of Non-Barrett’s Esophagus: Case Report of A Rare Tumor Simranjit Singh, MD, Sahibzada Latif, MD, FACG, Patricia Henry, DO, FACG, Manav Sharma, MD, Fnu Sanna, MD, Hafiz Khalid, MD, Ike Uzoaru, MD, FACG. Carle Foundation Hospital, University of Illinois at Urbana-Champaign, Urbana, IL. Introduction: Primary signet ring cell adenocarcinoma (SRCA) is an extremely rare histologic variant of esophageal adenocarcinoma, with very few case reports in published literature [1,2]. In addition, most of

770 A Burning Sensation: Caustic Esophageal Injury Following Suicide Attempt Ajayi Tokunbo, MD, Joshua Namias, MD, Navya Nambudiri, MD. Salem Hospital, Salem, MA. Introduction: Caustic esophageal injuries are caused by corrosive damage to the gastrointestinal mucosa following ingestion of a toxic substance, usually either a strong acid or alkali. We present the case of a man who attempted suicide using ingestion of a powerful drain cleaner, leading to severe esophageal injury and reviewing the importance of early diagnosis, complication, and supportive management in the acute setting. Case Report: A 51-year-old male with history of depression and 3 suicide attempts was found obtunded in his car. Naloxone was administered in the ambulance with no effect. One half of a bottle of industrial strength drain cleaner (Draino) was found in the car. His vitals were: temp. 99.9F, blood pressure 139/93 mmHg, pulse 100/min, and respiratory rate 21. His exam was notable for a Glasgow coma score of 3. He was noted to be in respiratory distress and was successfully intubated in the ER. Laboratory data showed potassium of 5.6 meq/L, lactate of 2.5 mmol/L, total bilirubin of 3.5mg/dL, WBC count of 13.1k/uL, and hematocrit of 58%. Toxicology screening was positive for urine benzodiazepines and oxycodone. Abdominal x-ray demonstrated gastric wall thickening and extensive small bowel gas without evidence of free air. In the ICU, he had an NG tube place and a surgical consult. An urgent upper endoscopy was performed, which showed severe ulceration, necrotic appearing mucosa in the esophagus, and ulcerated friable gastric mucosa with blood in the stomach without evidence of perforation, which were consistent with a grade-3 esophageal caustic injury from alkali intake. He was started on an I.V proton pump inhibitor infusion, TPN, and supportive care. He developed septic shock, anemia, pleural and pericardial effusion during his hospitalization. Discussion: Ingestion of strong caustic agents presents a significant risk for esophageal injury, while strongly acidic agents are more likely to injure the gastric mucosa. Caustic injuries represent direct trauma to the mucosal tissue causing liquefaction necrosis, which may ultimately lead to perforation, rupture, or death if severe. The clinical presentations vary based on the severity of the ingestion. The extent of caustic injury can be accessed via endoscopy and is graded from grade 0 (normal, no injury) to grade 3 (3A, focal necrosis; 3B extensive necrosis).1 Grade 3B injuries are associated with

© 2014 by the American College of Gastroenterology

[771A] Figure 1. The American Journal of GASTROENTEROLOGY

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cell population. We report a case of primary SRCA in non-barett’s esophagus and without co-occurrence of other cell types. Case Report: A 49-year-old man presented with 6 month of dysphagia and 20 lbs weight loss in 2 months. EGD showed about 5 cm circumferential friable mass in lower esophagus. There was no Barrett’s esophagus. There was no evidence of tumor in stomach and duodenum, also confirmed on CT scan. PET scan did not show any evidence of metastases. EUS revealed circumferential hypoechoic mass extending through muscularis mucosa with pseudopodia and peritumoral LAP, consistent with T3N2. Microscopically, tumor showed pure signet-ring cell adenocarcinoma histology with normal squamous epithelial lining, without any evidence of Barrett’s esophagus. Discussion: Primary SRCA in esophagus is a very rare tumor to begin with. Occurrence of primary SRCA without concurrent Barrett’s esophagus is an extremely rare presentation. The pathogenesis of SRCA in present case remains unclear. We speculate the origin of carcinoma in this case from esophageal glands, as there was no abnormal squamous epithelium or Barrett’s esophagus. Also, majority of the cases reported had mixed type of cell population with only one case reported so far was of primary pure SRCA type (i.e tumor composed only of SRCA cells) [1]. SRCAs are very aggressive neoplasms and have poor prognosis. References: [1] Tadashi Terada. Signet-Ring Cell Carcinoma of the Esophagus in Dermatomyositis: a Case Report with Immunohistochemical Study. J Gastrointest Cancer. 2013 Dec. [2] Maezato K, Nishimaki T, Oshiro M, Yamashiro T, Sasaki H, Sashida Y. Signet-ring cell carcinoma of the esophagus associated with Barrett’s epithelium: Report of a case. Surg Today. 2007;37:1096-101. e-pub 26 November 2007.

772 “Black Esophagus” Presenting 3 Weeks After an Episode of Urosepsis Joseph Yarze, MD, FACG. Gastroenterology Associates of Northern New York, Glens Falls, NY. Introduction: To present a case of acute esophageal necrosis in a patient who presented 3 weeks after an episode of urosepsis. Case Report: A 76-year-old female with a history of hypertension, hyperlipidemia, and cerebral palsy presented with a solitary episode of hematemesis in the absence of hemodynamic instability or other symptoms. She was discharged from the hospital 1 week previously, after being hospitalized for 2 weeks for treatment of urosepsis due to ureteral obstruction from an impacted ureterolith. During that hospitalization, she presented with septic shock, acute renal failure, and associated mild ischemic hepatopathy. She responded to broad-spectrum antibiotic therapy with ureteral stenting and was discharged uneventfully (to complete a 10-day course of levofloxacin) 1 week prior to her most recent presentation. She then presented after being at home and experiencing a 300-ml episode of bright red colored hematemesis. She remained hemodynamically stable and had no other symptoms. Physical exam was unremarkable and laboratory testing was normal, aside from revealing a peripheral WBC=21.6 (N=4.0-10.5). After informed consent was obtained, EGD revealed a diffusely abnormal esophagus with confluent black-colored mucosal ulceration and necrosis. The changes involved the tubular esophagus from 25 cm from the incisors to the EGJ (Figure 1). Biopsies of the esophagus were performed and the upper endoscopic exam was otherwise normal to the second portion of the duodenum. The biopsies revealed changes consistent with acute necrotizing esophagitis, with no evidence of fungal or viral infection. The patient was treated conservatively with intravenous PPI therapy and a liquid diet. She had no further bleeding and was discharged on a soft diet and oral PPI therapy. She was not interested in pursuing a follow-up examination. Conclusion: Although acute necrotizing esophagitis (“black esophagus”) has been associated with a variety of acute precipitating disease processes, this patient presented in an atypical fashion from home 3 weeks after an episode of urosepsis. Recovery was uneventful with conservative therapy.

recognized in the small bowel and colon but rarely appreciated in the esophagus. We report the first case of circumferential esophagitis and symptomatic esophageal stricture from MMF. Case Report: A 46-year-old male with end-stage renal disease underwent deceased donor kidney transplant followed by immunosuppression with MMF, tacrolimus, and prednisone. Shortly after transplantation, he noted new solid food intermittent dysphagia with slow progression over 6 months. He was later hospitalized with progressive worsening of nausea, vomiting, and dysphagia. EGD showed LA Class D esophagitis about 10 cm above the GE junction with a stenosis at 30 cm. Biopsies showed acute and chronic inflammation without increased eosinophils or evidence of Barrett’s mucosa. Stains for fungi, CMV, and HSV were negative. He was treated with esomeprazole 40 mg twice a day, but was re-hospitalized 1 month later with persistent symptoms. A repeat EGD demonstrated LA Class D esophagitis with worsening stricture in the proximal part of the lower third of the esophagus along with candida plaques. The stricture was dilated up to 44 F using Maloney dilators and fluconazole and nystatin were added to his PPI. Symptoms recurred despite compliance with therapy and EGD 2 months later showed persistent LA class D esophagitis without histologic evidence of opportunistic infection. A barium swallow showed a 3 cm long, 4 mm diameter stricture in the same location. Given the unusually refractory nature and location of his circumferential esophagitis and stricture, and no histologic evidence of Barrett’s, opportunists, or neoplasia, MMF was suspected to be the culprit. His MMF was discontinued and azathioprine was substituted. He was redilated to 12 mm using a TTS balloon and he has had no recurrence of dysphagia at 3 months’ follow-up. Barium swallow at 3 month follow-up showed no evidence of esophagitis or stricture and PPI therapy is being withdrawn gradually. MMF has well-known gastrointestinal adverseeffects including abdominal pain, nausea, vomiting, anorexia, ileus, diarrhea, and, less commonly, has been shown to cause gastrointestinal mucosal injury usually appreciated as segmental SB or colonic inflammatory disease. Similar to GVHD, histologic evidence of lamina propria edema/inflammation, and crypt architectural disarray with prominent epithelial apoptosis have been characteristic. This case highlights that MMF-related esophageal mucosal injury may be an underappreciated cause of symptomatic esophageal disease following solid organ transplantation.

774 A Rare Finding Among Common Conditions: Esophageal Intramural Pseudodiverticulosis Audrey Menezes, MBBS,1 Aparna Goel, MD, FACG,2 Gina Sam, MD,MPH2. 1. University of Sydney Medical School, Sydney, NSW, Australia; 2. Mount Sinai Hospital, New York, NY. Introduction: Esophageal intramural pseudodiverticulosis (EIPD) is characterized by multiple small, epithelium-lined cystic foci or diverticula within the esophageal wall. The disease presents anywhere along the esophagus, but strictures commonly form distally. EIPD was first described in 1960 and only 200 cases have since been reported. Although its etiology is unknown, it is associated with inflammatory and motility conditions such as GERD, diabetes, candidiasis, and alcoholism. Chronic inflammation or increased intraluminal pressure results in dilated submucosal duct openings, producing the characteristic appearance of EIPD. Endoscopy shows clusters or tracks of tiny outpouchings in the esophageal mucosa. The most common symptom is dysphagia. We present a 53-year-old male with HIV-HCV coinfection who presented with a 3-day history of odynophagia. Medical history included several episodes of azoleresistant esophageal candidiasis, pneumocystis pneumonia, and substance abuse. He reported chest and mid-epigastric abdominal pain associated with a sensation of solid food getting stuck in his chest. He was admitted 1 month prior with similar symptoms and treated for presumed esophageal candidiasis with caspofungin. On this admission, caspofungin was started empirically and he was subsequently referred for endoscopy. EGD revealed several 2-5-cm linear strips of diverticula in the mid and lower esophagus, consistent with EIPD (Figure 1). Biopsies of the diverticula showed acute nonspecific esophagitis with ulceration and no viral inclusions or microorganisms. As the endoscopy was performed 4 days after initiating caspfungin, the decision was made to complete a 14-day course of therapy for esophageal candidiasis. Management of EIPD is largely symptomatic, targeting reflux, infections, and strictures. The causal relationship between candida esophagitis and EIPD is unknown; EIPD may predispose to secondary candida infections or vice versa. Although prognosis is generally good, few cases have reported symptom progression requiring surgical management and complications including esophagopleural and esophagopulmonary fistulas, mediastinitis, and pseudodiverticular perforation.

[772A] Figure 1. EGD revealing black- colored esophageal mucosal ulceration and necrosis.

773 Refractory Esophagitis and Mid-esophageal Stricture due to Mycophenolate Mofetil Yan Zhao, MD, Jatinder Goyal, MD, Frederick Weber, MD. University of Alabama-Birmingham, Birmingham, AL. Introduction: Mycophenolate mofetil (MMF) is a commonly used immunosuppressive agent in solid organ-transplant recipients. GI tract injury from MMF histologically similar to graft vs host disease is


[774A] Figure 1.EGD demonstrating mid-esophageal diverticula. VOLUME 109 | SUPPLEMENT 2

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Abstracts 775 Black Esophagus: Acute Esophageal Necrosis Hiren Patel, MD,1 Deepshikha Nag Chowdhury, MD,2 Nihar Shah, MD,2 Arya Karki, MD,2 Robert Spira, MD, FACG2. 1. St. Joseph’s Regional Medical Center, Paterson, NJ; 2. Seton Hall University School of Health and Medical Sciences, South Orange, NJ. Introduction: Acute esophageal necrosis (AEN) is an uncommon clinical entity. It is usually due to ischemia secondary to various etiologies. AEN presents as upper gastrointestinal bleeding and is an endoscopic diagnosis where a circumferential, well-demarcated area of black, necrotic esophageal mucosa is seen in the distal one-third of the esophagus. The associated mortality rates remain high while management is mostly supportive. We report a case of a male with alcohol abuse who presented with hematemesis and was noted to have AEN. Case Report: A 50-year-old male presented to the emergency department with several episodes of hematemesis and epigastric pain following an alcohol binge. He had no significant past medical history other than alcohol abuse. He denied ingestion of caustic liquids, use of NSAIDs or anticoagulants, and had no prior endoscopy. Vital signs in the emergency department included a temperature of 98.6 F, blood pressure of 150/84 mmHg, heart rate of 114 beats/minute and a pulse oximetry of 95% on room air. Physical examination was unremarkable other than severe epigastric tenderness. Laboratory examination showed a white cell count of 12,100/μl, hemoglobin of 12 g/dl, platelet count of 600,000/ μl. Blood urea nitrogen was elevated at 26. 4 mg/dl and creatinine was 1.64 mg/dl. The patient was aggressively resuscitated with intravenous fluids and was taken emergently to endoscopy, which showed black, necrotic and friable mucosa in the distal esophagus from 25 cm to the gastroesophageal junction at 35 cm. No esophageal or gastric varices were noted. The gastric and duodenal mucosa were completely normal in appearance. Due to the severity of necrosis, biopsies were not obtained. The patient was transferred to the intensive care unit, kept nil-per-os and treated with high-dose proton pump inhibitor infusion and sucralfate suspensions. There were no further episodes of hematemesis. The patient was discharged home in a stable condition after 3 days of hospitalization. Repeat endoscopy several months later showed complete resolution of AEN. Conclusion: AEN results from tissue ischemia and damaged protective barrier of the esophagus and has been reported in the setting of multiorgan dysfunction, hypoperfusion, vasculopathy, sepsis, alcohol intoxication, gastric volvulus, traumatic transection of the thoracic aorta, variceal bleeding, and malignancy. Treatment of AEN is conservative. Complications include esophageal perforation and strictures.

[776B] Figure 2. Distal esophageal exudate and stricture.

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Endoscopic Evolution of Acute Necrotizing Esophagitis

Chronic Gasoline Ingestion As a Predisposing Factor of Severe Cytomegalovirus Esophagitis in an Immunocompetent Patient

Joseph Yarze, MD, FACG. Gastroenterology Associates of Northern New York, Glens Falls, NY. Introduction: To describe the endoscopic evolution noted in a case of acute necrotizing esophagitis. Case Report: A 76-year-old female with a history of hypertension, hyperlipidemia, and cerebral palsy presented with acute necrotizing esophagitis after an episode of urosepsis. The presenting symptom was a solitary episode of low-volume hematemesis in the presence of hemodynamic stability. After intravenous fluid resuscitation and attainment of informed consent, EGD revealed a diffusely abnormal esophagus with confluent black-colored mucosal ulceration and necrosis. The changes involved the tubular esophagus from 25 cm from the incisors to the EGJ (see Figure 1). Biopsies were taken and the exam was otherwise normal to the second portion of the duodenum. The biopsies revealed changes consistent with acute necrotizing esophagitis. The patient was treated conservatively with intravenous PPI therapy and a liquid diet. She had no further bleeding and was discharged on a soft diet and oral PPI therapy. She was initially not interested in pursuing a follow-up EGD examination. Six weeks after discharge, she was referred for evaluation of dysphagia to solids and liquids, and repeat EGD revealed confluent, circumferential exudate over the distal esophagus with a smooth, high-grade benign-appearing stricture at the EGJ (Figure 2). Biopsies of the esophagus showed nonspecific change and 8- and 9-mm TTS balloon dilations were performed. Dysphagia improved but persisted, and she required 2 further esophageal dilation sessions, after which she remained asymptomatic. Conclusion: This patient’s episode of acute necrotizing esophagitis evolved through an exudative healing phase with a high-grade esophageal stricture, which required multiple dilations.

Parit Mekaroonkamol, MD,1 Michael Flood, MD,2 Robert Cohen, MD, FACG1. 1. Emory University School of Medicine, Atlanta, GA; 2. Morehouse School of Medicine, Atlanta, GA. Introduction: Cytomegalovirus (CMV) esophagitis is a debilitating disease in immunocompromised patients. To date, there have been only five cases reported in immunocompetent hosts. Here, we report a case of severe CMV esophagitis in an immunocompetent adult who had a history of chronic gasoline ingestion as a predisposing factor. A 79-year-old Hispanic male presented with a 4-week history of progressive dysphagia and odynophagia. He had no significant past medical history except for chronic gasoline ingestion for 8 months while he was repairing his car. He orally sucked gasoline from the engine through a siphon tube and accidentally swallowed it several times. One week prior to admission, he had an esophagogastroduodenoscopy performed at a local hospital, which showed oral thrush, severe distal esophagitis with white plaques, and mild gastritis. Fluconazole was empirically started without any clinical improvement. Brush cytology was negative for candidiasis. A repeat esophagogastroduodenoscopy revealed severe erosive esophagitis with large circumferential ulcers at the distal esophagus and severe esophageal stricture. A barium swallow showed a ten-centimeter-long stricture from mid-esophagus to gastroesophageal junction. A savory dilation under fluoroscopic guidance and mucosal biopsy were successfully performed. The pathology revealed necro-inflammatory tissue with endothelial intranuclear inclusions and a positive CMV immunohistochemical stain, diagnostic for CMV esophagitis. Serum CMV antibody was negative, suggesting an acute infection rather than a reactivation. This case demonstrates the rare diagnosis of acute CMV esophagitis in an immunocompetent patient. CMV infection in healthy individuals is usually asymptomatic and severe morbidity from an organ specific manifestation is extremely rare. The predisposing factors of CMV esophagitis in immunocompetent patients remain unknown. However, hydrocarbon ingestion can induce nuclear anomalies and histological changes of gastrointestinal epithelium in animal models, both of which have been proposed to play an important role in the pathogenesis of CMV infection. Moreover, elderly patients have shown to have a poorer outcome from causatic ingestion, together with the lack of other risk factors led us to believe that his erosive esophagitis and stricture were results of chronic gasoline ingestion that was complicated by acute CMV infection. In patients with esophagitis of unclear etiology, a mucosal biopsy to rule out infectious etiology should be performed despite patients’ immunocompetency.

778 A Calcific Mass in The Distal Esophagus Rupal Patel, MD, Steven Clayton, MD, Prasad Kulkarni, MD. University of South Florida, Tampa, FL.

[776A] Figure 1. Initial EGD revealing changes of acute necrotizing esophagitis.


Introduction: A 76-year-old male presented to our medical center complaining of indigestion, epigastric pain, and regurgitation, which started after consuming venison the day prior. The patient had dysphagia to solids, but tolerated liquids. Evaluation in the emergency room revealed a distal esophageal calcific mass measuring 3 cm in diameter on plain films and CT (Figures 1 and 2). With endoscopy, a large food bolus impaction coated with bismuth subsalicylate was visualized in the distal esophagus. This correlated with the radiographic finding of a distal esophageal calcific mass, since bismuth is a known radio-dense substance. Also found during endoscopy were a hiatal hernia and a partially occluding distal esophageal stricture. Interestingly, in the past, bismuth was widely utilized as a gastrointestinal radiographic contrast agent, although now barium sulfate has taken its place. After the procedure the patient tolerated clear


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liquids and soft foods. He was discharged on protonix, carafate, and a course of levofloxacin. Follow-up upper endoscopy one week after discharge showed improvement of mucosal injury and confirmed resolution of the food bolus. This case presents a unique example of food bolus impaction with radiographic images not previously reported in the literature.

the contralateral side (Figure 2). The patient became progressively tachycardic (heart rate of 160) hypoxic (oxygen saturation of 85% on 100% FiO2), hypotensive (blood pressure of 90/60), hypercarbic (paCO2 of 50) and acidotic (pH 7.29) , as he was having an evolving tension colothorax causing cardiac tamponade. Following perioperative optimization, he was taken for surgery to decompress his tension colothorax. Laparoscopic hiatal hernia repair was performed. An immediate and dramatic improvement in hemodynamic parameters was observed following reduction of the herniated bowel. Postoperative chest radiograph confirmed complete expansion of the left lung. His subsequent post-op course was uneventful.

[779A] Figure 1. Chest x-ray shows bowel loops in the left hemithorax along with mediastinal shift to the contralateral side. [778A] Figure 1. Abdominal plain film with a peripherally enhancing 3.0-cm mass at the level of the distal esophagus. This mass was not present on a prior film taken 9 months earlier.

[778B] Figure 2. Abdominal CT image showing a 3.0 x 2.9 cm peripherally calcified mass at the gastroesophageal junction. [779B] Figure 2. CT chest shows large hiatal hernia with distended stomach in right chest, with the colon and small bowel occupying the left hemithorax, displacing the surrounding organs to the contralateral side.

779 A Rare Case of Tension Colothorax Following Esophageal Dilation Syed Amer, MBBS, Cuong Nguyen, MD. Mayo Clinic, Phoenix, AZ.

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Introduction: A 80-year-old male with history of esophageal adenocarcinoma, status post minimally invasive esophagectomy in 2011, complicated by multiple dilations of the anastomosis, was seen for repeat dilation and botox injection of the pylorus. Since the surgery, he also had interval development of diaphragmatic hernia. He tolerated the procedure well and was sent home. Within hours, he presented to the ED, with worsening abdominal pain. CXR showed presence of bowel loops in the left hemithorax (Figure 1). CT of the chest, abdomen and pelvis revealed a large hiatal hernia with colon and small bowel occupying most of the left hemithorax with notable displacement of surrounding intrathoracic organs to

Esophageal Leukoplakia: A Rare Cause of White Patches in Esophagus with Malignant Potential


Komal Thind, MBBS,1 Shiva Ratuapli, MD,1 Amy Foxx-Orenstein, MD,1 David Fleischer, MD,1 Shiff Arthur, MD,1 Dora Lam-Himlin, MD2. 1. Gastroenterology, Mayo Clinic Arizona, Scottsdale, AZ; 2. Laboratory Medicine and Pathology, Mayo Clinic Arizona, Scottsdale, AZ. Introduction: A white patch or patches within the oral cavity, termed as oral leukoplakia, is a premalignant condition typically seen in men with a history of alcohol and tobacco intake, and has a well-documented risk for progression to squamous cell carcinoma. An analogous condition found in the esophagus


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[780A] Figure 1. (A and B) EGD showing white plaques at the lower third of the esophagus. (C) Biopsies of the plaque show squamous mucosa with a prominent granular layer and hyperorthokeratosis (Hematoxylin and eosin; original magnification 200x.)

is esophageal leukoplakia. Due to its infrequency, the malignant potential of esophageal leukoplakia is not well established, despite a reported association with adjacent severe squamous dysplasia or squamous cell carcinoma in the few reported cases. On endoscopy, these esophageal lesions are highly characteristic and appear similar to those in the oral cavity, featuring well-demarcated white patches or plaques. Case Report: We report a 75-year-old male presenting with persistent cough and migratory pulmonary infiltrates, who was referred for evaluation of gastroesophageal reflux. He smoked half a pack of cigarettes a day for 10 years and drank 2 cocktails per day. Testing for infectious and autoimmune causes was unrevealing. A 24-hour laryngopharyngeal pH study off acid suppression showed high acid exposure during supine and upright periods. Esophagogastroduodenoscopy showed LA-grade D esophagitis, along with a single well demarcated white plaque in the lower third of esophagus (Figure 1A and 1B). Biopsies showed changes of epithelial hyperplasia, a prominent granular cell layer, and superficial hyperorthokeratosis, features diagnostic for epidermoid metaplasia that is the histologic correlate to esophageal leukoplakia (Figure 1C). Discussion: The etiology of esophageal leukoplakia is unknown but is thought to be due to chronic irritation from acid reflux in the setting of alcohol and tobacco use, as was seen in this case. The highly characteristic endoscopic appearance should alert the endoscopist to the diagnosis. Despite the unclear premalignant status of esophageal leukoplakia, its association with squamous dysplasia and invasive squamous carcinoma in some patients in our practice warrants endoscopic surveillance.

agitis with deep ulcer formation followed by granulation tissue overgrowth. Our case demonstrates a rare finding of esophageal tissue remodeling in the setting of reflux esophagitis and goblet cell metaplasia.

781 Acquired Double Barrel Esophagus in the Setting of Barrett’s Kimberly Kolkhorst, DO,1 Prasad Kulkarni, MD,2 Gitanjali Vidyarthi, MD, FACG2. 1. University of South Florida, Tampa, FL; 2. James A Haley VA, Tampa, FL. Introduction: Acquired double barrel esophagus, or esophagogastric fistula, is a rare endoscopic finding that has been reported in association with esophagogastric surgery, esophageal ulcer, epidermolysis bullosa dystrophica, and esophageal carcinoma. We report a case of esophageal remodeling with formation of 2 esophageal lumens in a patient with chronic reflux esophagitis and Barrett’s metaplasia. A 65-yearold male with a history of GERD (on BID Omeprazole) presented with progressively worsening dysphagia to solids, daily heartburn, and an unintentional 10-lb weight loss x 18 months. Barium esophagram revealed a longitudinal filling defect with mucosal abnormalities in the distal esophagus (Figure 1). EGD revealed a 6-cm segment of BE (C4M6), a 3-cm hiatal hernia, and extensive scarring in the distal esophagus with mucosal bridging and formation of 2 lumens in the distal 3 cm of the BE (Figure 2). Esophageal biopsies were consistent with reflux esophagitis, extensive goblet cell intestinal metaplasia, and negative for dysplasia or malignancy. Esophageal dilation was performed with improvement in symptoms. Repeat EGD with needle-knife resection of the mucosal bridge is planned in the future if dysphagia persists. In this case, the formation of an acquired esophagogastric fistula was likely due to chronic, ulcerative esoph-

[781A] Figure 1. Barium esophagram with mucosal abnormalities in distal esophagus. © 2014 by the American College of Gastroenterology


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783 Acute Respiratory Failure Caused by a Dilated Esophagus Pavel Teslya, MD, Natalya Teslya, MD, Tro Kalayjian, DO, Charles Seelig, MD. Greenwich Hospital, Greenwich, CT.

[781B] Figure 2. Endoscopic view of distal esophagus with scarring and mucosal bridging with formation of 2 lumens.

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Introduction: We report a case of a 91-year-old woman with a history of esophageal dysmotility, who presented with acute respiratory distress triggered by tracheal compression from severe dilation of the esophagus and exacerbated by the use of NIPPV. A review of the literature demonstrated several cases of respiratory distress in patients using NIPPV with a history of achalasia, but our patient had only a history of esophageal dysmotility. It is important to recognize esophageal dysmotility as a risk factor for complications prior to using NIPPV. The recognition of this risk factor may modify a treatment approach and prevent respiratory failure and possible death from tracheal compression. Case Report: We report a 91-year-old woman with a history of poliomyelitis, kyphosis, CHF, and osteoporosis who was brought to the emergency room of a community hospital secondary to acuteonset shortness of breath. The patient had no prior symptoms except for mild dysphagia. There was no improvement of the patient’s oxygen saturation despite supplemental oxygen. An initial arterial blood gas was significant for severe respiratory acidosis. The initial chest x-ray and the EKG were unremarkable. A CT Chest with IV contrast demonstrated a markedly dilated esophagus with abundant debris in the distal esophagus. Given the severe respiratory acidosis with impending respiratory failure, the decision was made to use NIPPV. The patient’s clinical status worsened on NIPPV. At that point, we believed that the primary etiology of the patient’s respiratory failure was from tracheal compression due to the dilated esophagus, which was exacerbated by the NIPPV. The team secured the airway with endotracheal intubation and then proceeded with decompression of the esophagus with a naso-esophageal tube. Immediately, the patient’s clinical status improved so much that she was successfully extubated only 8 hours later and tolerated room air. Discussion: We believe that the patient’s esophageal dysmotility and the resulting esophageal dilation lead to the initial event, and the use of NIPPV created worsening dilation and compression of the trachea. This case highlights the importance to recognize esophageal dysmotility as a risk factor for tracheal compression when using NIPPV.

Primary Malignant Melanoma of Esophagus: A Rare Entity Brijesh Patel, MD,1 Adnan Muhammad, MD,2 Joel Richter, MD,2 Anne Champeaux, MD2. 1. Internal Medicine, University of South Florida, Tampa, FL; 2. University of South Florida, Tampa, FL. Introduction: Primary malignant melanoma of the esophagus (PMME) is a rare malignancy of the esophagus with estimated incidence of 0.1-0.2% of all malignant esophageal tumors. There are approximately 337 cases reported worldwide. In most cases, endoscopy shows a polypoid mass in the distal esophagus. Biopsy is the gold standard with definitive diagnosis achieved via immunohistochemistry. A 69-year-old female who had undergone trans-hiatal esophagectomy in 2003 for biopsy-proven invasive PMME presented to us for surveillance endoscopy. EGDs in 2007 and 2010 did not show any recurrent disease. The patient did not have any complaints of dysphagia or odynophagia. EGD showed dark pigmentation with bluish discoloration at the anastomosis site (25 cm) without any mass-like features (Figure 1). The pathology was interpreted as melanoma in site. IHC was positive for S-100, HMB-45, and Melan-A, confirming the diagnosis of primary melanoma. PMME is a rare esophageal malignancy with dismal prognosis, as it has aggressive behavior. It generally presents as a polypoid mass-like lesions and it is highly metastatic at the time of diagnosis. Survival was reported to be only 4.2% in the 1980s, although it has improved to 37% more recently, likely due to early detection. The origin of melanocytes in esophagus leading to PMME is uncertain. The proposed mechanism is migration of melanoblasts from the neural crest and pluripotent immature cells migrating to the esophagus and then differentiating into melanocytes. One interesting feature about our case is the recurrence of the disease after patient had been disease free for approximately 10 years after initial surgery without any chemotherapy. Our patient presented with discoloration of esophagus without any mass-like features compared to most reported cases that described polypoid lesions. We present this rare case of PMME to increase awareness about the subtle findings on endoscopy, where it can present as a discoloration instead of a mass-like lesion. It also demonstrates the “difficulty” of early detection and close monitoring in PMME, as it is an aggressive cancer with poor prognosis.

[783A] Figure 1.

784 That’s Pretty Hard to Swallow: A Rare Case of Dysphagia Due to Myasthenia Gravis Kumkum Patel, MD, MPH, Jacqueline Forman, MD, Bhawna Halwan, MD, James Grendell, MD. Winthrop-University Hospital, Mineola, NY.

[782A] Figure 1. Endoscopy demonstrating discoloration of esophagus. The American Journal of GASTROENTEROLOGY

Introduction: An 89-year-old woman with GERD and hypothyroidism presented with a 7-month history of dysphagia and odynophagia to both solids and liquids. She was admitted 1 month prior to this admission for similar symptoms and underwent an EGD, which revealed a hiatal hernia. Despite compliance with omeprazole 40 mg daily, she returned to the emergency room with worsening symptoms. She denied abdominal pain, nausea, vomiting, diarrhea, constipation, dark stools, blood per rectum, or jaundice. Physical exam revealed an elongated face with bitemporal wasting, bilateral partial ptosis, and dysarthria. Motor strength was 4/5 in both upper and lower extremities. The abdominal exam was benign. Evaluation for gastrointestinal causes of dysphagia included a video esophagram showing decreased peristalsis and a repeat EGD revealing no resistance to a balloon dilator nor evidence of stricture, rings, or masses. Due to negative GI imaging, evaluation for neurological causes of dysphagia was completed. This included MRI brain and MRA of the head & neck which were negative for infarction or stenosis of vessels. CT scan of the neck was negative for right recurrent laryngeal nerve paralysis. By hospital admission day 4, she was intubated for inability to swallow her secretions and given an NG tube for feeds. Labs revealed elevated aldolase level of 7.9. Due to suspicion for neuromuscular causes of dysphagia, electromyography was completed, revealing a neuromuscular junction abnormality. Voltage-gated Ca-channel antigen and anti-MuSK antibody were negative while acetylcholine receptor-binding antibody level was 5.63 (high), acetylcholine receptor-modulating antibody level was 30 (high), and acetylcholine receptor-blocking antibody was 83 (high), thus confirming the diagnosis of myasthenia gravis as the cause of dysphagia. Repetitive nerve stimulation showed a decremental response further solidifying the diagnosis. CT scan of the chest did not reveal presence of a thymoma. She was started on IV immunoglobulins for 5 days, prednisone 50 mg daily, and pyridostigmine 60 mg three times a day with improvement in her muscle weakness, ptosis, and dysphagia. Dysphagia as the primary presenting symptom of myasthenia gravis is very rare and has only been reported in 6-15% of cases of myasthenia


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Abstracts gravis. Myasthenia gravis is more commonly reported as a paraneoplastic phenomenon associated with a thymoma/thymic tumor, which was absent in our case. Late-onset myasthenia gravis is more common in men and is often acetylcholine-receptor antibody negative. The age of onset along with the gender and antibody profile of our patient makes this case very unique. Our case truly increases awareness of nongastrointestinal causes of dysphagia. Disclosure – 1. Dr. Kumkum Patel--no financial relationships. 2. Dr. Jacqueline Forman--no financial relationships. 3. Dr. Bhawna Halwan--no financial relationships. 3. Dr. James Grendell-Consultant: NPS Pharmaceuticals Advisory Board.

785 “Wheezing from the Gut!” GERD: A Forgotten Diagnosis Jean Abed, MD, Hani Judeh, MD, Pavan Mankal, MD, Elie Abed, MD, Rajan Gurunathan, MD, Donald Kotler, MD. Mount Sinai St Luke’s and Mount Sinai Roosevelt Hospitals, Icahn School of Medicine, Mount Sinai Health System, New York, NY.

cin and inhalers without improvement. Patient denied any fever, chills, chest pain, nausea, vomiting or abdominal pain. In ED, patient was in mild respiratory distress, given nebulizers and was admitted to medicine. Physical exam was remarkable for diffuse wheezing and mild epigastric tenderness. CBC and BMP were unremarkable. CXR was negative for focal consolidation or vascular congestion. Patient was treated for COPD/asthma exacerbation with antibiotics, IV steroids, nebulizers and O2 for few days. Since patient’s cough, hoarseness and wheezing did not improve with aggressive therapy, an esophagram done showed significant esophageal dysmotility with marked retention and delayed clearance of barium from the esophagus with component of esophageal reflux and a positive water-siphon test. Patient was started on PPI with rapid improvement of her respiratory status. Patient was discharged with PPI and GI appointment. Wheezing is a common manifestation of respiratory illness in adults. While wheezing typically is secondary to airway obstruction due to asthma or COPD, wheezing is also caused by a spectrum of other processes that can be present on their own or coexist with asthma or COPD, contributing to difficult to control symptoms. GERD is known to cause wheezing by bronchoconstriction, increased vagal tone and microaspiration of gastric contents into the upper airway. If GERD is suspected, patient will benefit from a trial of PPI for 3 months rather than diagnosis testing. If the empiric therapy is unsuccessful, diagnostic tests such as 24-hour esophageal pH test or barium swallow can be performed.

Introduction: A 58-year-old woman with PMH of asthma, COPD, OSA presented with productive cough, wheezing, sore throat, hoarseness and progressively worsening SOB. Patient tried azithromy-

786 When Diagnosing HIV Is a Good Thing: Cytomegalovirus Presenting as Gastroesophageal Junction Mass in a Young Patient With Weight Loss Jessica Davis, MD,1 Ramsey Daher, MD,2 Katherine Bull-Henry, MD2. 1. Internal Medicine, George Washington University, Washington, DC; 2. Georgetown University, Washington, DC.

[785A] Figure 1. Esophagram.

Introduction: Dysphagia with weight loss is concerning for a malignant process involving the gastroesophageal (GE) junction. In patients without obvious risk factors for malignancy, however, alternative etiologies of GE junction obstruction must be considered. We present a case of Cytomegalovirus (CMV) infection presenting as weight loss and dysphagia in a young patient. A 33-year-old female with no significant medical history presented, complaining of 4 months of vomiting and weight loss. Her vomiting was accompanied by dysphagia and odynophagia. At presentation, her symptoms had progressed so that she was vomiting 6 times daily. She reported an 80-pound weight loss. Her family history was notable for esophageal cancer in her grandfather. She had a 3.5 pack-year history of smoking and drank alcohol less than once weekly. She denied illicit drug use and was not currently sexually active. On physical exam, her vitals were normal and her BMI was 33.5. She had some tenderness over her epigastrium. Her abdomen was soft with normal bowel sounds, and the remainder of her physical exam was unremarkable. Admission laboratory evaluation was notable for an AST of 49, ALT of 52, and alkaline phosphatase of 62. Bilirubin and lipase were normal, and her albumin was 3.2. Her electrolytes and creatinine were normal. Her complete blood count showed microcytic anemia. Rapid HIV test was negative. Contrast CT showed circumferential thickening of the distal esophagus, concerning for esophagitis, but was otherwise normal. Esophagogastroduodenoscopy was performed and showed white esophageal plaques as well as a nodular GE junction mass with a nearby ulceration. Brushings were taken of the plaques, as well as biopsy of both the ulceration and mass. Cytology from the brushings showed Candida. Repeat HIV testing was positive and the patient was found to have a CD4 count of 55. Histology from the mass and ulcer biopsies revealed inflammation and inclusion bodies consistent with CMV infection. There was no evidence of malignancy. She was started on fluconazole, ganciclovir, and antiretrovirals, and her oral intake gradually improved. She was discharged with follow-up with infectious diseases and gastroenterology. Our patient presented with symptoms concerning for malignancy, including a family history of esophageal cancer; however, her young age and minimal tobacco and alcohol use made malignancy less likely. Although her initial HIV testing was negative, given our concern and the Candida seen on her endoscopy, her testing was repeated and she was diagnosed with HIV. A high index of suspicion must be maintained for diagnosis of non-malignant etiologies of GE-junction obstruction.

787 Desiccant-Induced Esophageal Obstruction: An Emerging Patient Safety Issue Jodie Barkin, MD, Jamie Barkin, MD, MACG, FACG. University of Miami, Leonard M. Miller School of Medicine, Dept of Medicine, Division of Gastroenterology, Miami, FL.

[785B] Figure 2. Water siphon test. © 2014 by the American College of Gastroenterology

Introduction: With an aging and increasingly health-conscious American population, there has been increased usage of medications, vitamins, and supplements. In an effort to preserve products from being lost to the effects of moisture over time, many commercially packaged pill and vitamin bottles contain a desiccant. A desiccant is a hygroscopic substance that absorbs water, with the most common being silica gel. Desiccant packages vary in shapes and sizes, and are commonly in small packets or cylindrical canisters. The aim of this case report and review of the literature is to present an esophageal foreign body obstruction caused by unintentional ingestion of a desiccant. Case Report: A 75-year-old man with past medical history of GERD complicated by esophageal stricture requiring dilation was on chronic PPI therapy. He presented with 24 hours of solid-phase dysphagia, described as different from his prior dysphagia, with ability to swallow his saliva. Symptoms began after taking vitamins, but he denied any unusual ingestion. Upper endoscopy with monitored anesthesia care revealed a cylindrically shaped foreign body in the distal-esophagus, approximately 2.0 x 1.0 x 1.0 cm in size, which was removed with a Roth basket and identified to be a pill bottle desiccant. An underlying distal esophageal stricture was discovered, subsequently biopsied, and dilated with resolution of symptoms. Discussion: This is the first reported case of esophageal obstruction due to accidental desiccant ingestion. Two reports of 3 total cases of pill bottle desiccants causing gastrointestinal obstruction exist in the literature. Desiccants were responsible for 2 partial mechanical obstructions in the pylorus due to an underlying organic stricture 1 and a small bowel obstruction as a de novo presentation of structuring Crohn’s Disease 2. The rarity of our report lies in the unique combination of a partial structural narrowing of the esophagus and an ingested foreign body. An underlying esophageal motility disorder might produce a similar clinical picture without a structural abnormality. The potential for unintentional ingestion of a desiccant contained in a medication or vitamin bottle is likely to rise. This effect is multifactorial due to increased overall medication and vitamin consumption, an aging population predisposed to higher rates of accidental medication errors, and a rising prevalence of GERD and its sequelae in the general


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population. Proactive interventions such as a change by bottle manufacturers to anchor desiccants to the bottle to prevent accidental ingestion are warranted to overcome this patient safety issue. References: [1] JAMA. 1980;243:1921-2. [2] Am J Gastroenterol. 1998;93:2595-7.

789 Early Detection and Non-surgical Treatment of Squamous Cell Carcinoma of the Esophagus Anthony Flaim, DO,1 Steven Lichtenstein, DO2. 1. Mainline Health, Philadelphia, PA; 2. Mercy Fitzgerald Hospital, Darby, PA.

788 Metachronous Primary Distal Esophageal Small Cell Carcinoma and Adenocarcinoma Arising From the Same Site Inside a Barrett’s Segment Mustapha El-Halabi, MD, Michael Green, MD, Patrick Seitz, MD, William Salyers, MD. Internal Medicine, University of Kansas School of Medicine, Wichita, KS. Introduction: Small cell carcinoma of the esophagus is rare and represents around 1% of esophageal cancer cases. Synchronous primary small cell carcinoma and adenocarcinoma of the esophagus in the same lesion are extremely rare, with metachronous presentations of these tumors within a Barrett’s segment not previously reported. We herein describe a case of a metachronous presentation of an adenocarcinoma arising 14 months later from the same site of a distal esophageal primary small cell carcinoma in remission within a Barrett’s segment. Case Report: A 55-year-old white male presented with dysphagia and unintentional weight loss. Esophagogastroduodenoscopy (EGD) showed an ulcerated friable mass in the distal esophagus at 35 cm from the incisors and extended to the level of the gastroesophageal (GE) junction at 40 cm within a C11M14 Barrett’s segment that extended from 26-40 cm from the incisors. Biopsies from the mass showed highgrade neuroendocrine carcinoma, small cell type. There were no lung masses or any distant metastases on PET/CT. On endoscopic ultrasound (EUS), the lesion measured 3.08 x 3.12 cm in maximum width and depth with breakthrough to the adventitia. Four malignant-appearing para-esophageal lymph nodes were identified. TNM staging was T3N2M0. The patient received radiotherapy and chemotherapy with VP16 and cisplatin. He improved clinically and repeat PET/CT showed a drop in SUV values with no distal metastasis. Repeat EGD with EUS at 6 and 9 months after diagnosis were showing the same Barrett’s segment in addition to thickening of the mucosa from 36 to 39 cm from the incisors within the area of the previously identified tumor, with significant improvement in the appearance of the lesion. Biopsies from the Barrett’s segment including the site of the previously described lesion were showing intestinal metaplasia without dysplasia. However,14 months after diagnosis, biopsies came back positive for adenocarcinoma within the ulcerating lesion at 38-39 cm in addition to high-grade dysplasia at multiple locations within the Barrett’s segment. The patient subsequently underwent Ivor Lewis esophagectomy. The surgical specimen had negative margins with focal residual adenocarcinoma at the GE junction, invading only the muscularis mucosa, with greatest dimension of 0.1 cm. Pathologic staging was pT1aN0. Twenty months after diagnosis with small cell carcinoma, and then with adenocarcinoma at the same site, the patient is alive and recovering from post-operative complications. Conclusion: This case provides important additional evidence to the presence of totipotent cells within Barrett’s metaplasia that are capable of multidirectional differentiation causing multiple types of carcinoma.

Introduction: Squamous cell carcinoma of the esophagus, despite decreasing in incidence in the U.S. in relation to adenocarcinoma, is still a very devastating diagnosis. Due to symptoms such as dysphagia and odynophagia not occurring until greater than 60% of the esophageal circumference is infiltrated, these are often diagnosed late in their course. The presentations of the lesions on endoscopy are often very minute, stressing the value of vigilance and a low threshold for biopsy. The patient was a 76-year-old Caucasian male with a history of hypertension, coronary artery disease, COPD, and PUD with anemia and heme-positive brown stool. He also had an extensive history of tobacco and alcohol abuse, as well as a family history of various GI malignancies. On EGD, he was found to have a 2-mm gastric polyp that came back as adenomatous with focal intestinal metaplasia. On repeat EGD 2 years later, the polypectomy site was unremarkable, but there was a small area of erythema in the mid-esophagus that was biopsied. This biopsy showed squamous cell carcinoma. After the initial finding of squamous cell carcinoma was confirmed by 2 pathologists, the patient was sent for CT scan to evaluate for distal metastasis and for EUS to complete staging. The CT was negative for distant metastases. The EUS showed extension into the submucosa, but not the adventitia with no lymphadenopathy. Throughout this work-up, he remained asymptomatic from a GI standpoint. Despite the recommendations of a cardiothoracic surgeon, the patient chose to forgo resection and trial chemotherapy and radiation. He was treated with 5FU, leucovorin, and radiation therapy. The patient had good response to treatment and was cancer-free for 3 years when he was found to have thickening of the esophagus with biopsy showing squamous carcinoma. He was treated with Taxotere and carboplatin, and remained cancer-free until his death of an MI 7 years later. Throughout this patient’s course, he remained free of GI symptomatology.

790 Congenital Bronchoesophageal Fistula Diagnosed in Late Adulthood Anna Christina Dela Cruz, MD,1 Joseph Valentino, MD,4 Jeremiah Martin, MB BCh,2 Ashish Maskey, MD,3 Luis Pena, MD, FACG1. 1. Division of Digestive Diseases and Nutrition, University of Kentucky, Lexington, KY; 2. Division of Cardiothoracic Surgery, University of Kentucky, Lexington, KY; 3. Division of Pulmonary, Critical Care and Sleep Medicine, University of Kentucky, Lexington, KY; 4. Division of General Surgery, University of Kentucky, Lexington, KY. Introduction: A 69-year-old man with a history of right thoracotomy with decortication and drainage of empyema 34 years ago, presented with a 25-year history of dysphagia and coughing up of food and liquids and recurrent respiratory infections. EGD 8 years ago showed possible achalasia and mid-esopha-

[789A] Figure 1. (A) Erythematous esophageal lesion at 30 cm from the incisors (arrow), visualized by EGD on July 12, 1999, with biopsy results of in situ squamous cell carcinoma. (B) Repeat EGD 1year following treatment showing a small non-bleeding possible vascular ectasia (arrow), 30 cm from the incisors.

[790A] Figure 1. (A) EGD of esophageal side of fistula. (B) Bronchoscopy showing methylene blue leaked through bronchial side of fistula when methylene blue was instilled into the fistula during EGD. The American Journal of GASTROENTEROLOGY


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Abstracts geal diverticulum. Recent evaluation for pneumonia included barium esophagram showing a fistula from the lower esophagus to the right lower lobe bronchi. CT showed right lower lobe bronchiectasis, infiltrate and dilated esophagus but did not visualize a fistula. EGD revealed a 3mm fistula in the middle third of the esophagus and no other lesions in the esophagus. Bronchoscopy showed no endobronchial lesions but could not initially identify the fistula site. EGD was performed simultaneously with bronchoscopy and saline with methylene blue was injected through the esophageal side of the fistula using an ERCP cannula. Bronchoscopy revealed passage of air bubbles and methylene blue through a bronchus [posterior subsegment of the superior basal segment of right lower lobe (B8a)], localizing the exact fistula site. He had surgical repair involving division of the fistula tract with intercostal muscle-flap interposition. There was no persistent fistula on EGD and esophagram. Congenital bronchoesophageal fistula (BEF) is rare in adults but can be unrecognized for years, with symptom duration varying from 5-50 years before diagnosis. Age at diagnosis ranges from 9-83 years. Symptoms include cough, frequent respiratory infections, hemoptysis and bouts of cough when swallowing liquids (Ohno’s sign). Barium esophagram is the most sensitive test compared to endoscopy and bronchoscopy. Complications include recurrent pneumonia, abscess and bronchiectasis. Definitive treatment involves surgical closure of the fistula tract, with interposition of viable tissue such as intercostal muscle to prevent refistulization. The insidious course of congenital BEF, the absence of surrounding inflammation and adherent lymph nodes, and our patient’s history support a congenital nature of the fistula. In summary, we illustrated a case of congenital bronchoesophageal fistula diagnosed in late adulthood by barium esophagram, confirmed by simultaneous EGD and bronchoscopy and managed by surgical repair.

791 A Case Report on a Rare Cause of Upper Gastrointestinal Bleed Silpa Mandava, MBBS, Akriti Dewanwala, MBBS, Katie Agnello, MD, Abha Rani, MD, FACG. Internal Medicine, University at Buffalo, Buffalo, NY. Introduction: Proximal esophageal varices, or “downhill varices”, are a rare cause of upper GI hemorrhage, reported only in a handful of cases. A 48-year-old female with history of HTN, ESRD on HD, presented with abdominal pain and hematemesis. Her medications included valsartan, Plavix, omeprazole. Though hemodynamically stable, hemoglobin dropped from 9.9 to 8.8g/dL. NG lavage revealed 300cc coffee ground material. Pantoprazole IV was started; EGD showed grade III esophageal varices extending from upper esophageal sphincter till mid esophagus and a Mallory-Weiss tear with stable clot. There was no active bleeding and the varices lacked stigmata of recent bleed. No endoscopic intervention was performed. Liver ultrasound was normal. CT venogram showed complete occlusion of SVC and bilateral brachiocephalic, with extensive collaterals. Detailed history revealed multiple prior upper extremity dialysis catheters and failed forearm grafts. Vascular surgery advised conservative management as risks from recanalization or anticoagulation outweighed benefits. Esophageal varices are not always indicative of portal hypertension [2]. SVC obstruction is common in malignancy, but other rare causes such as infection, venous thrombosis from catheters are also reported [1]. Patients can be asymptomatic or present with arm/facial swelling, dyspnea, syncope, ataxia, or convulsions [1]. Treatment of bleeding varices includes endoscopic band ligation and sclerotherapy. Although rare, physicians should have a high index of suspicion for downhill varices in hemodialysis patients with upper GI bleed as its etiology and management differs from portal hypertensive varices.

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the various interventions and treatments arose. In this report, we discuss the literature regarding the incidence, risk factors, and potential complications of an esophageal perforation; bleeding, spread of infection into the mediastinum and the surrounding structures. Given the reported 20% mortality associated with esophageal perforation, the management discussed centers around prompt treatment and adequate monitoring. Gastroenterology was consulted and the patient underwent successful deployment of an esophageal stent overlying an esophageal wall defect located in the middle third of the esophagus overlying the left atrium. A multidisciplinary approach focusing on evaluation and management by several subspecialists is recommended and helps to assist the primary provider in the decision making process. The patient was able to be safely discharged to a rehabilitation facility following ICU monitoring and treatment for mediastinitus. He returned 6 weeks later for removal of esophageal stent with resolution of his pericardial-esophageal fistula.

793 Acute Chemical Esophagitis After Chromoendoscopy in a Patient With Squamous Cell Dysplasia of Esophagus Gokul Samudrala, MD, Kaartik Soota, MD, Mohammad Telfah, MD, Karthik Ramakrishna, MD, Andrej Strapko, MD, Deerajnath Lingutla, MD. Internal Medicine, Unity Health System of Rochester, Rochester, NY. Introduction: Lugol’s iodine is used for chromoendoscopy to identify abnormal areas in patients with squamous cell dysplasia and early squamous cell carcinoma of esophagus. We report a rare case of acute chemical esophagitis following Lugol’s iodine solution during chromoendoscopy. A 39-year-old white male with family history of Barrett’s esophagus and esophageal adenocarcinoma was found to have squamous cell dysplasia of the esophagus during his screening esophagogastroduodenoscopy. Lugol’s chromoendoscopy was performed to identify dysplastic areas for radio frequency ablation. During the procedure esophagus was sprayed with 5% Lugol’s iodine but the patient regurgitated it and developed laryngeal spasm. Nasal suctioning was unsuccessful. Sodium thiosulfate was instilled through spray catheter but the patient developed severe throat pain, inability to swallow his own secretions and hoarse voice. Rest of the examination including vital signs were normal but because of this complication, he was admitted to hospital for further monitoring. Fiberoptic laryngoscopy exam was performed by an otorhinolaryngologist which showed severe edema and secretions in the hypopharynx of the patient. He was started on steroids and pantoprazole which improved his symptoms over a period of 4 days. Lugol’s iodine solution is potassium iodide in iodine solution. It has been increasingly used to detect early mucosal abnormalities to target biopsies from unstained areas due to its high affinity for glycogen in non-keratinized squamous epithelium. It can cause severe allergic reactions including laryngeal spasm, bronchospasm or even anaphylaxis in severe cases. Acute gastric mucosal injury after application of Lugol’s iodine has been reported in the past. However, chemical esophagitis after its application is very rare. Previous studies in the murine model have shown that gastric columnar epithelium is more susceptible to the toxic effect of Lugol’s iodine than the squamous esophageal mucosa. These studies also demonstrated that mucosal damage worsens with higher concentrations of iodine. Therefore, lower concentration of 1.2- 2% which may be less toxic to esophageal or gastric mucosa should be used. Previous studies have shown that sodium thiosulfate solution spray can decrease the mucosal irritation caused by Lugol’s iodine, but this needs to be further evaluated in prospective trials. Gastroenterologists need to be aware of adverse reactions of Lugol’s iodine solution, before utilizing it in their clinical practice. Using lower concentrations may be less toxic to the esophageal or gastric mucosa.

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Iatrogenic Pericardial-Esophageal Fistula Following Atrial Ablation Eric Hilgenfeldt, MD, Alex Schlachterman, MD. Internal Medicine, University of Florida, Gainesville, FL. Introduction: Over half of all esophageal perforations are reported as iatrogenic. In patients who undergo transesophageal echocardiography, the percent chance of perforation is estimated at 0.01-0.05%. In the case reviewed, a 56-year-old male with sick-sinus syndrome and atrial fibrillation presents 2 weeks after undergoing an atrial ablation with complaints of chest pain, fevers and cough. When computed tomography of the chest revealed pneumomediastinum and pneumopericardium, questions regarding

[792A] Figure 1. CT scan of the chest showing pneumopericardium best visualized anterior to the heart. © 2014 by the American College of Gastroenterology

A Case of a Giant Esophageal Papilloma Geoffrey You, MD,1 Melissa Reynon, MD,2 Amy Tilara, MD2. 1. Department of Medicine, Rutgers Robert Wood Johnson Medical School, New Brunswick, NJ; 2. Division of Gastroenterology and Hepatology, Department of Medicine, Rutgers Robert Wood Johnson Medical School, New Brunswick, NJ. Introduction: Only several dozen cases of esophageal verrucous squamous cell cancer (VSCC) have been reported in the literature, and management of this disease remains undefined. We present a case illustrating the diagnostic dilemma of a locally invasive VSCC of the esophagus presenting as a giant papilloma in a patient who benefited from endoscopic tumor debulking with placement of an esophageal stent. Case Report: A 56-year-old female with HIV presented with rapidly progressive dysphagia to solids and liquids with weight loss over the course of 4 months. An esophagram showed a large circumferential mass of the distal esophagus. Multiple incomplete EGDs, due to inability to traverse the mass, with superficial biopsies were performed, but only revealed squamous mucosa with hyperkeratosis. The patient then presented to our hospital for evaluation. A CT scan confirmed the finding of the mass with perigastric lymphadenopathy. On EGD, an exophytic, friable, circumferential mass concerning for a giant papilloma was noted at 24 cm from the incisors extending to the GE junction at 40 cm. Snare polypectomy of the mass and EUS with FNA of perigastric lymph nodes was then performed. The mass involved the muscularis propria and adventitia on EUS. The aspirate of the lymph nodes was deemed to be reactive. The specimen was initially diagnostic of a squamous papilloma. Subsequent exploratory laparotomy was performed. At the time of surgery, esophagectomy was not feasible, given the complex anatomy of the mass with involvement of adjacent organs. Ultimately, the decision was made for endoscopic tumor debulking with placement of an esophageal stent given the patient’s worsening dysphagia. Nearly 10 cm of tumor was removed, and a 12-cm fully covered esophageal stent was placed under fluoroscopic guidance. The final pathology of the tumor debulking was ultimately diagnostic of VSCC of the esophagus. The patient noted drastic improvement after the procedure. She was then referred for follow-up with oncology and repeat endoscopic palliative treatment with cryotherapy of the tumor. Unfortunately, she was lost to follow-up and passed away 4 months later from unknown causes. Discussion: This is a unique case that demonstrated the diagnostic challenge of VSCC of the esophagus presenting as a giant esophageal papilloma. The case presented a unique approach to the diagnosis and management in those patients whose disease is not amenable to surgical intervention. While previous case reports have documented the use of chemo-radiation with intermittent esophageal dilation in nonsurgical patients, our method of using endoscopic tumor debulking with placement of an esophageal stent may provide an alternative palliative approach.


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795 A Rare Presentation of Colon Cancer Diagnosed on an Upper Endoscopy Ashutosh Gupta, MD, Bashar Attar, MD, PhD, FACG, Bikram Padda, MD, William Riles, MD. John H Stroger Hospital of Cook County, Chicago, IL. Introduction: Colonic interposition is now the second line treatment after esophagectomy for both benign and malignant conditions if a gastric pull up is technically not feasible. One of the unusual delayed complications of the procedure is the occurrence of an adenocarcinoma of the colonic conduit. Case Report: A 65-year-old woman with past medical history of diabetes, hypertension, stroke and dementia presented with complaints of nausea, vomiting, abdominal pain and weight loss. She had a history of lye ingestion with subsequent esophagectomy and colonic interposition performed 35 years ago. She smoked for 50 years, and had a past history of heavy alcohol use, however denied any illicits. Vitals were stable and physical exam was unremarkable. Labs revealed normocytic anemia and elevated CA 19-9 and CEA levels. CT abdomen was performed which showed numerous hypo-attenuating lesions throughout the enlarged liver suggestive of likely metastases. A colonoscopy was done which was unremarkable except for an ileocolonic anastomoses seen at 70 cm from the site of insertion. An upper endoscopy was then performed which showed an anastomoses at 20 cm from incisors related to previous surgery and a large, circumferential, necrotic appearing, friable mass protruding into the lumen at 35 cm from the incisors from what appeared to be the colonic mucosa (Fig 1). Multiple biopsies were obtained which showed invasive, moderately differentiated adenocarcinoma. Given the presence of multiple metastases she was deemed not to be a surgical candidate and was started on chemotherapy with FOLFOX and Bevacizumab. The development of any new symptoms in a patient with colonic interposition like dysphagia, melena, and weight loss must be taken seriously. There have been less than 12 reported cases of cancer in the interposed segment described so far occurring mostly in men and were diagnosed anywhere from 2-37 years post operatively. It is important to perform surveillance endoscopies in patients with history of colonic interposition; however the frequency at which such surveillance needs to be done remains unknown.

This allowed the patient to eat normally, and take all her po medications. Only complication was recurrent candida esophagitis, which was treated with fluconazole. Since then patient has been dilated every 6-9 months and the stricture has remained stable. Chronic GI tract GVH is less frequent with advances in hematopoetic transplantation but remains disabling. Submucosal corticosteroid injections combined with oral immunotherapy have been used to treat oral GVH, but we could not find a case of similar case of combined endoscopic therapy for esophageal GVH. This approach had minimal morbidity and resulted in a marked symptomatic and endoscopic response.

797 A Rare Cause of Abdominal Pain, Nausea, and Vomiting: “Black” Esophagus Jason Rubinov, MD, Craig Gluckman, MD, Seth Homer, MD, Gil Ascunce, MD, FACG, Veevek Agrawal, DO. Mount Sinai Beth Israel, New York, NY. Introduction: A 30-year-old male with a past medical history of HIV on HAART, type 1 diabetes mellitus, end stage renal disease on chronic hemodialysis and blindness presented with two days of epigastric abdominal pain, nausea and non-bloody, non-bilious vomiting. He also endorsed odynophagia to solids. The patient was admitted to the hospital two other times within the last three months for similar complaints of abdominal pain associated with vomiting and anorexia. His symptoms were always thought to be secondary to underlying diabetic ketoacidosis and they would largely resolve with aggressive intravenous fluids and insulin. On this admission, physical examination was significant for mild epigastric tenderness. CT scan of his abdomen revealed circumferential wall thickening of the distal esophagus compatible with esophagitis. The patient underwent an EGD which showed circumferential, blackening of the distal esophagus consistent with acute esophageal necrosis. Biopsies were obtained, which revealed necro-inflammatory mucosa with multiple fungal forms consistent with Candida species. The patient was treated with intravenous esomeprazole and an oral sucralfate suspension, along with fluconazole given the findings of fungal infection on mucosal biopsy. The patient’s symptoms markedly improved. The patient was discharged home with complete resolution of his presenting symptoms to have close endoscopic follow-up at a later date. Acute esophageal necrosis, or the so-called “black esophagus,” is a rare finding first described in 1990 by Goldenberg et al, with an estimated prevalence reported in one autopsy study to be 0.2%. The exact pathogenesis remains unknown but ischemia is believed to be the main inciting event. Low-flow states such as diabetic ketoacidosis, as seen in our patient, result in hypo-perfusion of the distal esophagus, a region that is more “watershed” and less vascularized than the proximal portions of the esophagus. Treatment is largely supportive with correction of the predisposing event and better control of the underlying medical condition. Complications include esophageal perforation, mediastinitis, stricture formation and death.

[795A] Figure 1.

796 Successful Combined Intralesional Corticosteroid Therapy and Wire-Guided Dilation of Severe Esophageal Graft-Versus-Host Disease V. Alin Botoman, MD, FACG,1 Eleonor Botoman, HS2. 1. Gastroenterology, University of Miami, Fort Lauderdale, FL; 2. Pine Crest School/GI Research Institute of Ft Lauderdale, Fort Lauderdale, FL. Introduction: This 63-year-old woman first presented in 2009 with a 4 year history of severe dysphagia following allogenic hematopoetic transplantation for aplastic anemia/leukemia in 2004, which was complicated by severe acute and chronic GVH. This was managed with tracrolimus. Barium studies showed severe proximal 2 cm and 9cm mid-distal esophageal strictures which progressed over time despite oral GVH therapy. She had been on a liquid only diet for 2 years, following an unsuccessful attempt at dilation in 2007 at NIH. Since then symptoms progressed and esophagectomy or gastrostomy were recommended. Initial EGD showed typical esophageal GVH changes, with areas of mucosal slough, friability and severe structuring precluding passage past the proximal esophagus. Biopsies confirmed GVH. Fluoroscopic wire guided Savary dilation to 7mm resulted in severe proximal slough and deep ulceration, with post procedural odynophagia, but no perforation. This was treated with oral liquid sucralfate. Patient remained severely symptomatic with difficulty maintaining hydration and taking her oral medications for GVH which had to be given in elixir form. 9 weeks later at repeat EGD, the stricture had recurred. This time we injected triamcinolone 40mg/2cc in 0.25-0.5cc/injection via sclerotherapy needle in the reachable strictured areas, followed by fluoroscopic wire-guided dilation to 8mm. Over the subsequent 3 years a total of 15 endoscopic sessions, with 4 to 8 0.25-0.5ml endoscopic injections of 40 mg of triamcinolone/session, followed by progressive fluoroscopic wire-guided Savary dilation. There was gradual improvement in the endoscopic appearance. After the 5th session we could dilate the entire esophagus the the point where the endoscope could be advanced into the stomach. By 2012 the esophagus was dilated to a 14 mm diameter, the mucosal GVH changes were much improved/resolved.


[797A] Figure 1. Blackening of the distal esophagus, which classically stops at the GE junction.

798 Pooling of Barium at Mucosotomy Site After Peroral Endoscopic Myotomy For Achalasia Madhusudhan Sanaka, MD, FACG, Siva Raja, MD, PhD, Andrei Purysko, MD. Gastroenterology, Cleveland Clinic, Cleveland, OH. Introduction: A 24-year-old woman with achalasia underwent Peroral endoscopic myotomy (POEM). POEM was performed in standard steps including vertical mucosotomy on the anterior wall in the mid esophagus, creation of submucosal tunnel by submucosal dissection, selective myotomy of circular muscle starting 3cm distal to mucosotomy site extending 4cm into the cardia and closure of mucosotomy using endoscopic clips. The mucosotomy was about 2 cm long and 8 endoscopic clips (Wilson Cook, NC, USA) were used to close the mucosotomy site. Patient was kept nil per oral along with intravenous antibiotics and a barium swallow study was performed next day. It showed free passage of barium into stomach without a leak, however, there was pooling of small amount of barium in the submucosal space at upper end of the mucosotomy site adjacent to endoclips, without passage down the tunnel (figure 1). Patient was afebrile with normal white count except for mild chest discomfort as expected post-procedure. Patient was continued nil per oral for an additional day and a barium swallow study was repeated. It


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Abstracts did not show any further pooling of barium at the mucosotomy site and it passed freely into the stomach without a leak (figure 2). Clear liquid diet was started and she was discharged home. Pooling of small amount of barium at the mucosotomy site was likely due to passage of barium into submucosal space between the clips as they might not have caused water tight closure of mucosotomy. However, this finding is usually of no clinical consequence especially if barium does not leak out through the tunnel into the mediastinum. Meticulous and water tight closure of mucosotomy site might have prevented this. It is also important to start myotomy at least 2-3 centimeters distal to mucosotomy site such that the submucosal space closes off above the myotomy site and acts as a safety cushion.

799 Acute Esophageal Necrosis in Alcohol Abuse and Diabetic Ketoacidosis Xi Chen, MD, Daniel Eshtiaghpour, MD, Anuj Datta, MD, Sofiya Reicher, MD, Viktor Eysselein, MD. Harbor UCLA Medical Center, Torrance, CA. Introduction: Acute esophageal necrosis (AEN) is a rare disorder with approximately 112 cases reported. AEN has a mortality rate of over 30% and most commonly presents with signs of upper GI bleed. AEN is caused by hypoperfusion of the esophagus leading to mucosal damage. Some risk factors include age, male gender, diabetes mellitus, alcohol ingestion and malnutrition. Here we present a case of severe esophageal necrosis in the setting of diabetic ketoacidosis (DKA) and alcohol abuse. A 55-year-old male with poorly controlled diabetes and alcohol abuse presented with chest pain, nausea and vomiting, and severe DKA. He subsequently developed upper GI bleed with melena requiring blood transfusion. Urgent EGD showed large hiatal hernia with severe diffuse LA class D esophagitis with black exudates (Figures), involving the entire esophagus. Patient improved clinically with aggressive PPI and topical therapy. EGD 3 weeks later demonstrated healing of the esophagitis. Our case is an example of classic AEN. Patient’s ongoing alcohol abuse, poorly controlled diabetes, and large hiatal hernia most likely contributed to severity of the disease with involvement of most of the esophagus. Current therapy for AEN includes supportive treatment such as hydration and antacids and management of underlying conditions. In this case, despite the high mortality rates associated with AEN, our patient’s condition resolved within 3 weeks of diagnosis after supportive treatment and management of DKA.

[798A] Figure 1.

[799A] Figure 1.

[798B] Figure 2. [799B] Figure 2. © 2014 by the American College of Gastroenterology


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800 High-Grade Dysplastic Villous Adenoma Arising from Barrett’s Esophagus Alexander Schlachterman, MD, Dennis Yang, MD, Dennis Collins, MD, Anand Gupte, MD. Gastroenterology, University of Florida, Gainesville, FL. Introduction: An 83-year-old woman with a history of Barrett’s esophagus (BE) and low grade dysplasia was referred to our institution for evaluation of dysphagia. Esophagogastroduodenoscopy (EGD) revealed an irregular Z line. A ten mm nodule was seen at the GE junction, 41 cm from the incisors (A). The nodule was resected by hot snare. Four quadrant biopsies were also obtained along the Z line in the

area of previously noted Barrett’s esophagus. Histologic evaluation of the esophageal nodule revealed a villous adenoma with extensive high-grade dysplasia arising from BE (B). Remaining esophageal biopsies were consistent with low-grade dysplastic Barrett’s esophagus. Villous adenomas arising from BE are extremely rare and less than a dozen cases have been reported in the literature. These polypoid dysplastic lesions appear to share similar clinical, pathologic and molecular features as the more commonly seen flat dysplastic lesions associated with BE. These lesions are often associated with adenocarcinoma and definite management has included esophagectomy or polypectomy with close surveillance. We report a rare case of villous adenoma in the setting BE and highlight the important role of close endoscopic inspection during BE surveillance.

801 Black Esophagus: A Case of Acute Esophageal Necrosis Secondary to HSV2 Infection Christopher Hodnette, MD, Oleana Lamendola, MD, Venkat Banda, MD. Internal Medicine, Baton Rouge General Medical Center, Baton Rouge, LA. Introduction: Acute esophageal necrosis (AEN) is a clinical disorder characterized endoscopically by circumferential, black appearing esophageal mucosa. We describe a case of AEN with biopsy proven Herpes Simplex Virus (HSV) infection. A 45-year-old male, with past medical history of AIDS, diabetes mellitus, hypertension and medication noncompliance, presented with a 2 week history of a bilateral frontal headache. The patient was diagnosed with of aseptic meningitis and briefly treated with empiric acyclovir. During his hospitalization patient began to complain of dysphagia and odynophagia. EGD revealed severe, circumferential, black-pigmented esophageal mucosa extending to the Z-line. Biopsies were obtained and empiric therapy began. Histology showed marked esophagitis with dense inflammatory infiltrate. Immunochemistry was positive for HSV type-2 and acyclovir was resumed. Despite therapy dysphagia persisted. During the placement of a gastrostomy the esophagus was again examined. Diffuse mucosal granularity was noted throughout the esophagus without ulceration. The patient ultimately was discharged on acyclovir. The pathogenesis surrounding AEN is likely multifactorial. Tissue ischemia, gastric outlet obstruction, impaired barrier defenses, and infection have been sited as causes. Presentation is similar to upper GI bleed with review of system significant for epigastric pain, nausea, vomiting, fever, dysphagia, and syncope. Physical examination and laboratory findings are nonspecific. Diagnosis is via endoscopy, with findings of circumferential black pigmentation of the distal esophagus abruptly ending at the gastroesophageal junction. The treatment is generally supportive. Mortality is approximately 6%.

[800A] Figure 1. A 10 mm nodule was seen at the GE junction, 41 cm from the incisors.

802 Colonic Metastasis of a Primary Esophageal Adenocarcinoma Michael Green, MD, Najla Itani, MD, Mustapha El-Halabi, MD, Ransom Kilgore, MD, FACG, William Salyers, MD, MPH, FACG. University of Kansas School of Medicine, Wichita, KS. Introduction: The incidence of adenocarcinoma of the esophagus is increasing in the United States, representing nearly 50% of esophageal cancers. This is a significant increase from 10% in the 1970’s. The most likely sites of metastasis of primary esophageal adenocarcinoma are regional lymph nodes, liver, lung, bone, and brain. While extremely rare cases of colonic metastasis of squamous cell carcinoma of the esophagus have been reported in the literature, colonic metastasis of esophageal adenocarcinoma has never been previously described. We herein report the first known case of esophageal adenocarcinoma with metastasis to the colon. An 80-year-old Caucasian female presented with a several year history of GERD. The patient reported increasing nausea, vomiting, early satiety, and unintentional weight loss. Esophagogastroduodenoscopy identified an exophytic mass at 25 cm from the incisors with circumferential ulcerations that extended into the fundus of the stomach. Biopsies were consistent with invasive poorly differentiated adenocarcinoma. Endoscopic Ultrasound (EUS) showed a hypoechoic mucosalbased lesion extending 2.03 cm in depth with breakthrough of the muscularis propria but no surrounding organ involvement, consistent with a T3 lesion. Two peritumoral lymph nodes were suspicious for malignancy. CT scan of the chest, abdomen, and pelvis showed an area of wall thickening located within the distal transverse colon. The patient subsequently underwent colonoscopy that revealed a large ulcerating mass within the transverse colon. Biopsies showed poorly differentiated adenocarcinoma which was morphologically identical to the patient’s esophageal tumor. Furthermore, esophageal and colonic specimens were considered to be an immunohistochemical match and were positive for CK7 and AE1:3, focally positive for CK20, and weakly positive for CDX2. The strong positivity of the CK7 stain in the transverse colon in addition to focal positivity of CK20 are both more characteristic of esophageal adenocarcinoma and atypical of a primary colonic tumor, identifying the mass as a metastasis. The patient was not considered to be a surgical candidate given the presence of her colonic metastasis. She is currently undergoing FOLFOX chemotherapy. Patients identified with Stage IV esophageal adenocarcinoma with documented distant metastasis are currently incurable, and treatment should be palliative in nature. Given the poor prognosis, it is essential that physicians, and more specifically radiologists, practice a consistent and systematic evaluation of all organ systems of patients presenting with a primary esophageal tumor. Particular attention must be paid to uncommon locations of metastasis such as the colon.

803 Eosinophilic Esophagitis Presenting as Massive Upper Gastrointestinal Bleeding Treated With Esophageal Stent Manajyoti Yadav, MD,1 Fritz-Henry Volmar, MD,2 Michael Cashman, MD,2 Sonu Dhillon, MD,2 Srinivas Puli, MD2. 1. University of Illinois College of Medicine at Peoria, Peoria, IL; 2. OSF St Francis Hospital, Peoria, IL.

[800B] Figure 2. High power (200x) villous adenoma demonstrating high-grade dysplasia at the surface characterized by crowded hyperchromatic nuclei with cribriform architecture. The American Journal of GASTROENTEROLOGY

Introduction: Eosinophilic Esophagitis (EoE) is a rare cause of gastrointestinal bleeding. Esophageal tears due to EoE causing massive bleeding have not been described in literature. This case report depicts treatment of such tear and massive bleeding with self expandable esophageal stent. An 88-year-old female


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[801A] Figure 1.

with a history of osteoporosis was referred with massive upper gastrointestinal bleeding. On the day before admission she had one episode of vomiting of bright red blood and dark colored stool followed by light-headedness. Upon admission patient underwent aggressive fluid resuscitation and intensive care. Physical exam revealed tender epigastrium. Labs showed normocytic anemia. Upper endoscopy was done and it revealed a circumferential blood clot in esophagus starting at 25cm mark and extend-

ing the entire length of esophagus. Source of bleeding beneth the clot could not be localized. Next day a fully covered esophageal stent was placed. She stayed in hospital for 7 days, gradually improved and was discharged home on PPI with instructions to stop taking alendronate. At a follow up endoscopy 8 weeks later, patient was completely asymptomatic, the esophageal stent was removed and three biopsies were taken from esophagus. The biopsy specimens showed acute erosive esophagitis with increased intraepi-

[803A] Figure 1. (Clockwise from top left) EGD at presentation showing large blood clot in esophagus; after the placement of stent; EGD 8 weeks later after removal of stent and esophageal biopsies; biopsy depicting acute erosive esophagitis with increased intraepithelial eosinophils (20-50 per hpf). © 2014 by the American College of Gastroenterology


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thelial eosinophils (20-50/hpf) consistent with a diagnosis of Eosinophilic esophagitis. The prevalence of EoE is on the increase. Majority of affected adults are men in their second or third decade of life. Very late presentation of the disease and with gastrointestinal bleeding as a presenting complaint is rarely encountered. Rare cases of spontaneous esophageal tear and esophageal dissection have been described in the adult and pediatric literature. This case report is an import reminder to keep EoE as a rare differential when evaluating patients with esophageal mucosal tears and perforations and also to keep novel methods like stenting in mind while managing such patients.

806 Esophageal Hyperkeratosis and Multiple Esophageal Rings in a Patient With Recurrent Dysphagia Jason Mader, DO, Maen Kamal, MD, Rezwan Ahmed, MD, Yaser Rayyan, MD, FACG. Marshall University - Joan C. Edwards School of Medicine, Huntington, WV.

Introduction: To report 3 cases of achalasia found in patient with malignancy on preliminary review and seen over a period 2 years at our institution. Primary achalasia is estimated to occur in 1:10,000 patients. Patients’ age at diagnosis of achalasia, sex, type of cancers and their statuses, time interval between cancers and achalasia, treatments’ and their responses were recorded and are summarized in tablular format. Median age of diagnosis of these patients was 58 years. There were all female. All patients had breast cancer and were active on treatment at the time of diagnosis of achalasia. All patients were diagnosed with barium swallow, endoscopy and confirmed by esophageal manometry. Median time duration between diagnosis of primary cancers and achalasia was one year. None of the patient presented with achalasia at the time of primary cancers. All patients showed improvement in the clinical symptoms in response to treatment for cancer. Achalasia secondary to malignancy may be caused by a) direct infiltration of lower esophageal sphincter or b) as pseudoachalasia, following neoplastic infiltration of esophageal myenteric plexus or c) as a paraneoplastic process related to distant neoplasm suggested by the presence of antiANNA-1 antibody. Achalasia as a paraneoplastic process appears to present with a more rapid onset of symptoms, such as weight loss, than primary achalasia and hence distinction should be made in treating these patients for achalasia as opposed to monitoring them for improvement that may occur after treatment of the primary cancer. Larger retrospective studies are planned to enhance our understanding about this important entity.

Introduction: The purpose of this case presentation is to describe a patient with recurrent dysphagia who was found to have Esophageal Hyperkeratosis (EH), which remained stable over a period of 5 years. This is an 87-year-old female who presented in 2009 with worsening solid dysphagia without heartburn, with no history of smoking, ETOH use, asthma, skin lesions, or weight loss. An EGD revealed whitish plaques in the upper esophagus, multiple partial rings at the mid/lower third of the esophagus, a non-obstructive Shatzki’s ring, and a small hiatal hernia. Balloon dilation was performed and biopsy of the whitish plaques revealed keratinized esophageal mucosa with rare intraepithelial eosinophils. The patient was treated with 40 mg Omeprazole for 2 years. She returned in 2012 with similar complaints and had a repeat EGD revealing persistent white plaques of the upper esophagus. Balloon dilation was performed and biopsies demonstrated normal esophageal mucosa without eosinophils or hyperkeratosis. She remained asymptomatic off PPI therapy until she returned with recurrent dysphagia in 2014. A repeat EGD showed whitish plaques in the upper third of the esophagus, a Shatzki’s ring at the GE junction, and gastritis. Biopsies from the proximal third of the esophagus were taken and revealed squamous mucosa with hyperkeratosis and hypergranulosis. A review of all endoscopic pictures and histology slides revealed stability of these white plaques over a 5 year period. Esophageal Hyperkeratosis is a rare entity that reflects complete keratinization of the esophageal epithelium. Patients typically have heartburn and dysphagia, and a biopsy typically confirms the diagnosis. Multiple references describe esophageal hyperkeratosis as a complication of GERD. Our case highlights a patient with symptoms of EH, multiple esophageal rings requiring palliative therapies, and stable lesions over a 5 year period. It’s important for gastroenterologists to be able to differentiate various whitish lesions as they may represent a spectrum of conditions from benign mycotic exudates and Human papilloma viral infection, to dysplastic syndromes and squamous cell carcinoma. Association with cutaneous syndromes like Tylosis and Darier’s disease, Vitamin A and E deficiency, and alkali ingestion have also been reported. The relation of these lesions with esophageal rings is not clear, but may be attributed to GERD induced inflammation. Esophageal hyperkeratosis is a rarely described process that should be considered in patients with dysphagia or GERD. It is important to be knowledgeable of EH and able to differentiate it from other similar appearing lesions both on EGD and histologically.

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807

A Case of Eosinophilic Esophagitis With Achalasia Requiring Myotomy

Lymphocytic Esophagitis in Crohn’s Disease: Understanding the Significance

Diana Snyder, MD, Yomari Gonzalez, BA, Mukund Venu, MD. Loyola University Medical Center, Maywood, IL.

Satyajit Reddy, MSci,1 Edward Feller, MD, FACG,1 Li Juan Wang, MD,PhD,2 Samir Shah, MD, FACG1. 1. Alpert Medical School of Brown University, Providence, RI; 2. Roger Williams Medical Center, Providence, RI.

804 Achalasia in Patients With Malignancy Shamim Ejaz, MD, MPH, John Stroehlein, MD, FACG, Mehnaz Shafi, MD, FACG. Gastroenterology, Hepatology and Nutrition, UT MD Anderson Cancer Center, Houston, TX.

Introduction: Eosinophilic esophagitis (EoE) is a clinicopathological disorder defined by esophageal dysfunction and eosinophilic infiltration of the esophagus with more than 15 eosinophils per high power field (hpf) on microscopy after ruling out other causes of eosinophilia. Dysphagia is the most common symptom first described in a 1978 case report. Esophageal dysmotility on esophageal manometry has been described in EoE patients. Only one case report documented successful management of EoE with concomitant achalasia via Heller’s myotomy. Our patient demonstrates EoE in the presence achalasia with persistent symptoms despite medical management requiring Heller myotomy for symptomatic improvement. A 48-year-old female presented to clinic with difficult, painful swallowing and food regurgitation. She was diagnosed with EoE one year prior and treated with PPI followed by swallowed fluticasone, but did not achieve reduction in eosinophil count until she started a six food elimination diet. Despite histologic improvement, her symptoms persisted. She underwent upper endoscopy at our institution revealing a narrow-caliber esophagus that was subsequently dilated. Mucosal features were consistent with EoE. Biopsies showed up to 18 intraepithelial eosinophils per hpf from the proximal esophagus. She subsequently underwent high resolution esophageal manometry (EM) revealing achalasia. The esophagus exhibited failed peristalsis without relaxation of the lower esophageal sphincter (LES). The patient underwent laparoscopic Heller myotomy with Nissen fundoplication providing nearly complete resolution of symptoms. There are few reports of achalasia in the setting of EoE since the 1978 case. One case series reported most patients with EoE have abnormalities on EM. Only one patient had achalasia, which resolved with inhaled fluticasone. Another case series identified that 4 of 512 cases of achalasia had concomitant EoE. Two patients were treated for achalasia with Heller myotomy, but symptoms recurred. A recent study evaluating EoE with high resolution EM shows that esophageal body motility abnormalities, namely weak or failed peristalsis, are most common. It is unclear if our patient has type 1 or type 2 achalasia as stratified by the Chicago Classification since panesophageal pressurization may be seen in EoE alone. EoE with achalasia may be resistant to medical management and require myotomy for symptom improvement. EoE patients may benefit from early EM studies to identity concurrent esophageal motility abnormalities.

[804]

Table 1.

Age at diagnosis of Achalasia

Sex

Weight loss

1

58

F

2

58

3

70

Patient #

Introduction: Lymphocytic esophagitis (LE) is a rare, recently described entity of undetermined etiology or significance. We report an adult man with Crohns disease (CD) controlled with anti-TNF therapy but with refractory nausea and vomiting attributed to LE. A 49-year-old man with a 23-year history of CD reports persistent nausea, vomiting, and diarrhea for several years. He has peripheral arthritis that is worse with CD flares, GERD treated with omeprazole, and recently quit smoking. He had 2 prior surgeries 15 years apart, first for enterovesical fistula and later ileocecal resection. Three years ago, evaluation of symptoms and weight loss with colonoscopy and EGD showed active ileitis on biopsy, no UGI CD, and a transient ringed esophagus, but was negative for eosinophilic esophagitis or LE. He is currently on adalimumab 40mg weekly, which has improved pain, diarrhea, and weight; nausea and vomiting persist. He had not responded to mesalamine, 6MP, or a lower dose of adalimumab, had a partial response to steroids with severe side effects, and a delayed hypersensitivity reaction to infliximab. One year ago, MR enterography and colonoscopy revealed no evidence of active CD. Two months ago, upper and lower endoscopy were grossly normal. However, biopsies revealed esophageal LE at 35cm and increased lymphocytes in the duodenum. Despite swallowed Flovent for 2 months, nausea and vomiting persist. LE was first described in 2006 by Rubio et al as increased intraepithelial lymphocytes near the peripapillary fields without increased granulocytes. The less than 10 published studies to date have noted few associations without a dominant theory to its clinical significance. Data suggest an association of LE to pediatric CD, but 4 separate studies have found no association in adult CD. Dysphagia, the most common presenting complaint, is present in about half of LE cases. Interestingly, patients with LE may be half as likely to have GERD than patients without LE. Another reported association has been esophageal rings, as in our patient. In one large retrospective review, the esophageal mucosa was visually normal in as many as 91% of cases. Thus, clinicians with a degree of suspicion should consider performing blind esophageal biopsies to look for LE. Our patient has severe CD tried on multiple therapies. His current regimen has improved weight, diarrhea and abdominal pain. Recent endoscopic evaluation was negative for active CD. His refractory nausea and vomiting is puzzling; our hypothesis is that LE is contributing. Further studies, including prospective observational studies and additional retrospective reviews of esophageal biopsies, are needed to characterize the significance, natural history and management of LE.

Cancer status at the diagnosis of achalasia

Time interval between the two diagnosis

Treatment

Response to treatment

Breast

Active and mets were found in the Bones and Brain

3 months

Chemo and Botox

Good

Barium, endoscopy manometry,

Breast

Active and mets were in the Bones

8 years

Hormonal therapy and Botox

Partial


Breast

Active/T3N0M0

1 year

Chemo, radiation and Botox

Good

Methods of diagnosis

Type of Primary cancer

Yes


F

No

F

Yes



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Abstracts 808 Cytomegalovirus-Associated Esophagopulmonary Fistula in an AIDS Patient Successfully Treated with Esophageal Stenting James Araujo, MD,1 Alina Iuga, MD,2 Amrita Sethi, MD1. 1. Division of Digestive and Liver Diseases, Columbia University Medical Center, New York, NY; 2. Department of Pathology and Cell Biology, Columbia University Medical Center, New York, NY. Introduction: A 46-year-old man with AIDS and poor antiretroviral adherence presented with a 12-day history of chest pain, dyspnea, cough, and fever. Examination revealed tachycardia, cachexia, and thrush. One month prior, CD4 count was 9/mm3 and HIV viral load was 57,647 copies/mL. Chest CT noted a dominant cavitary mass in the right upper lobe, several smaller pulmonary cavitations, and proximal esophageal dilatation. Treatment for bacterial pneumonia and candidiasis was started. Initial infectious studies, including acid-fast sputum smears, were negative. Despite 7 days of broad-spectrum antibiotics, his cough worsened, serial chest imaging noted disease progression, and sputum culture grew MRSA and commensal bacteria. Three weeks into his course, he developed dysphagia and odynophagia. Serum

PCR for Cytomegalovirus (CMV) was 701 copies/mL. EGD noted a cratered 5-cm longitudinal ulcer in the proximal esophagus (Figure 1A) and a 1-mm fistulous opening within the ulcer (Figure 1B). Barium esophagram revealed a communication between the proximal esophagus and right hemithorax (Figure 1C). Chest CT demonstrated tracking of barium from the esophagus into the dominant pulmonary cavity (Figure 1D). These findings were consistent with the diagnosis of an esophagopulmonary fistula. On repeat EGD, biopsies of the ulcer were obtained, followed by placement of a 12-cm fully-covered metal stent across the fistula. Pathology showed esophageal squamous epithelium, inflamed reactive stroma, and acutely inflamed columnar respiratory-type mucosa with scattered CMV-positive cells, confirmed on immunohistochemistry (Figure 1E). The patient received valgancyclovir for 21 days and the stent was removed 35 days after placement with resolution of the ulcer. Repeat barium esophagram showed no structural abnormalities. We present the first reported case of a CMV-associated esophagopulmonary fistula successfully treated with antiviral therapy and a fully-covered metal esophageal stent. Esophagorespiratory fistulas are rare and usually associated with malignancy or post-operative complications. Use of fully-covered metal stents has been described in the treatment of esophageal fistulas and leaks with variable success.

809 That Diet Is Amazing David Martin, MD, FACG. Gastroenterology, Pinehurst Medical Clinic, Pinehurst, NC. Introduction: Demonstrate that dietary treatment of small intestinal bacterial overgrowth effectively treats gastroesophageal reflux disease without medication. Patients presenting to a private gastroenterology practice, who had gastrointestinal complaints were tested using the lactulose breath test for small intestinal bacterial overgrowth. These patients were also given dietary advice to avoid sugar except for honey, since bacteria don’t grow in honey; and to avoid starches except for whole grains. Many of the 1,740 patients with gastrointestinal complaints, particularly those patients with symptoms of gastroesophageal reflux disease, tested with the lactulose breath test for small intestinal bacterial overgrowth, and advised to follow a diet designed to clear small intestinal bacterial overgrowth had relief of their reflux symptoms; as well as relief of abdominal pain, nausea, bloating, belching and flatulence with diet alone. The need for acid suppression decreased as well. Many patients with gastroesophageal reflux disease have small intestinal bacterial overgrowth as demonstrated by the lactulose breath test. Treatment with a diet designed to eliminate the small intestinal bacterial overgrowth often eliminated the reflux symptoms and decreased or eliminated the need for acid suppression with medications.

810 Massive Gastrointestinal Hemorrhage Due to Candida Esophagitis: An Unusual Presentation Alicia Alvarez, MD, Leyla Maric, MD, Alison Schneider, MD. Cleveland Clinic Florida, Weston, FL.

[808A] Figure 1.

Introduction: There has been a decrease in opportunistic infections among HIV-infected patients since the widespread use of highly active antiretroviral therapy (HAART); however, the incidence of Candida esophagitis (CE) still remains high. Dysphagia and odynophagia are both a common manifestation of CE but rarely it can present as a massive gastrointestinal (GI) bleed. A 46-year-old male presented to the emergency department (ED) with reported fevers, chills, and generalized weakness. GI ROS revealed some mild abdominal discomfort for the past week. There was no reported dysphagia, odynophagia, or retrosternal chest discomfort. On arrival he was found to be hypotensive with BP 74/49, febrile and tachycardic. He appeared cachectic and abdominal exam was soft with no tenderness. While in the ED during the initial evaluation, he had a large melanotic bowel movement followed by massive hematemesis. On labs, WBC was 4.0, Hgb 4.6, Hct 14.3, INR 1.6 and plts 99. After patient resuscitation, an emergent esophagogastroduodenoscopy was done revealing extensive hemorrhagic Candida esophagitis in the mid esophagus. There was severe esophageal necrosis, ulceration with circumferential confluent plaques causing luminal narrowing. Surrounding uninvolved mucosa appeared normal. Stigmata of bleeding was seen throughout the esophagus. The patient required 6 units of packed red blood cells and 2 units of frozen plasma over the first 24 hours. Further history revealed a diagnosis of HIV/AIDS. Histopathologic diagnosis revealed pseudohyphae and true hyphae consistent with Candida species. Findings were negative for cytomegalovirus and herpes simplex virus infection. Treatment with blood product and intravenous fluconazole resulted in resolution of his GI symptoms. Since the introduction of anti-retroviral agents in the 1990s, the clinical presentation of HIV/AIDS has changed with less hospitalization for acute presentations of opportunistic infections. Massive upper gastrointestinal bleeding due to CE in AIDS patients is rare with only a few case reports in the literature. Gastroenterologists should be aware of this rare cause of severe GI bleeding so that therapies can be administered in an appropriate and timely manner.

[810A] Figure 1.



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811 Transepithelial Esophageal Brush Sampling Detects Adenocarcinoma Missed Twice With Forceps Biopsies Emily Walzer, BA,1 Jennifer Maranki, MD,MS,1 Howard Guss, DO,2 Michael Smith, MD,MBA1. 1. Temple University School of Medicine, Philadelphia, PA; 2. Coastal Healthcare, Ocean, NJ. Introduction: Barrett’s esophagus is a precancerous condition involving intestinal metaplasia of the tubular esophagus. Development of dysplasia or neoplasia often is focal; therefore, detection is dependent on sampling the specific site of histologic abnormality. Tissue acquisition via forceps biopsies (FB), the current standard of care, leaves a large area unsampled. To reduce sampling error, adjunctive methods can be used. These include Wide Area Transepithelial Sampling with 3-dimensional computer assisted analysis (WATS3D, CDx Diagnostics, Suffern, NY). This technique obtains full-thickness mucosal samples, which are analyzed using a neural network that identifies the most abnormal cells or cell clusters for pathologist review. Studies have shown that WATS3D increases detection of metaplasia and dysplasia in Barrett’s esophagus, both in an academic and community setting. Most studies, however, have focused on evaluation of cases where visual examination has not identified nodularity or other concerning focal findings. A 68-year-old white male underwent upper endoscopy by a community gastroenterologist for evaluation of dyspepsia. Findings included distal esophagitis with a nodule at the esophagogastric junction (EGJ). FB of this region revealed chronic esophagitis with extensive low grade glandular dysplasia; high grade dysplasia could not be excluded. Daily proton pump inhibitor was prescribed, and a repeat examination was recommended in two months. However, treatment of colon cancer diagnosed the same day delayed a follow-up endoscopy for 16 months. Once performed by the same community gastroenterologist, the procedure showed ulcerated nodules at the EGJ, which were sampled with both WATS3D brushes and FB. While FB revealed only chronic esophagitis with atypical small glandular proliferation, WATS3D samples showed at least high grade dysplasia. Additional sampling was obtained, as advised on the pathology reports, after titration of his anti-reflux regimen. The follow-up FB showed no evidence of either dysplasia or neoplasia, though WATS3D specimens demonstrated adenocarcinoma via atypical glandular cells with increased nuclear staining, cytoplasmic ratio and crowding. Subsequent endosonography and crosssectional imaging confirmed a T3N1 junctional adenocarcinoma. Despite targeting visually abnormal tissue during two separate endoscopies, FB failed to detect neoplasia, which was identified with WATS3D. Improved detection could be due to a greater surface area and depth of tissue sampled and/or the computer technology to identify and present the most abnormal cells for review. This case underscores the ability of WATS3D to improve care beyond current standard practices in a community setting. Disclosure - Dr. Smith - Advisory Board Member and Research Support: CDx Diagnostics.

812 Esophageal Variceal Band Ligation as a Means of Eradicating Barrett’s Esophagus Erin Toto, MD, Michael Smith, MD, MBA. Temple University School of Medicine, Philadelphia, PA. Introduction: Barrett’s esophagus (BE) is a precancerous condition involving intestinal metaplasia of the tubular esophagus. Eradication of BE can decrease the risk of progression to esophageal adenocarcinoma. Currently available endoscopic therapies for BE include band-ligation endoscopic mucosal resection (EMR), which has been used to excise focal areas of concern as well as entire BE segments. It is believed that, following removal of the metaplastic mucosa, neosquamous epithelium is generated in the absence of further acid exposure. We describe a case of band ligation without resection leading to partial BE eradication. A 61-year-old Caucasian male with known BE and a strong family history of esophageal cancer (2 brothers) presented for evaluation. Past history was notable for liver transplantation to treat alcoholic cirrhosis, complicated by portal vein thrombosis (PVT) and subsequent portal hypertension with development of varices. Upper endoscopy revealed ultra-long segment BE (C8M10 by Prague classification) without any dysplasia present on transepithelial brush biopsies performed in place of forceps sampling due to the presence of large esophageal varices and moderate thrombocytopenia. A gastric varix and portal hypertensive gastropathy also were seen. Given his BE segment length and family history, the decision was made to first eradicate his esophageal varices and then ablate his BE once the risk of variceal complications was minimized. A first round of endoscopic variceal band ligation was performed without difficulty. Within six days of the second banding procedure, the patient presented with acute upper gastrointestinal bleeding manifested by hematemesis and melena. Upper endoscopy demonstrated circular ulcerations at the banding sites without active bleeding. No intervention was performed at that time. Over the course of five weeks, recurrent life-threatening bleeding was treated with additional band placement, ethanolamine injections, and insertion of two Blakemore tubes. PVT precluded standard radiologic interventions, and ultimately an emergent surgical shunt was placed, followed by radiologic decompression of his portal vein and obliteration of his gastric varices. After these interventions, his bleeding ceased. Repeat endoscopy one month later showed resolution of the ulcerations with circular neosquamous islands at the banding sites. It is unclear if the band ligation itself or subsequent ulceration ultimately led to formation of the neosquamous epithelium. Further investigation is required to evaluate whether band ligation, which does not involve energy-mediated tissue trauma, could be an alternate method for BE eradication when more standard techniques are not possible.

813 A Fishy Case of Upper Gastrointestinal Bleeding Vikas Khullar, MD,1 Alexander Schlachterman, MD,2 Anil Sharma, MD, FACG2. 1. University of Florida - Department of Medicine, Gainesville, FL; 2. University of Florida - Division of Gastroenterology and Hepatology, Gainesville, FL. Introduction: A 66-year-old male with hypertension, hyperlipidemia and diabetes presented to the emergency department complaining of central chest discomfort after having ingested a piece of fish bone a few days prior. On examination, patient was in moderate discomfort and febrile (100.9 F); blood pressure was 132/59 with heart rate of 124 bpm with saturation of 99% on room air. Rest of the physical exam was unremarkable. Laboratory data showed leukocytosis of 17.7 THO/uL with 84% neutrophils. Hemoglobin was 12.6 g/dl and serum creatinine was elevated at 1.8 mg/dL. Troponin I was normal. Remaining results were unremarkable. The patient was admitted for further workup however the next


morning developed melena with a drop in hemoglobin to 8.6 g/dL. CT-scan of the chest/abdomen/pelvis with IV contrast revealed a pseudo-aneurysm of the distal aortic arch with mass effect and compression of the esophagus. Vascular surgery was emergently consulted and performed thoracic endovascular aortic repair (TEVAR). Gastroenterology was consulted and did not recommend endoscopy given a high risk of esophageal perforation. An aorto-esophageal fistula (AEF) was suspected and the patient was transferred to our institution. Upon transfer, a repeat CT with IV contrast was ordered; however, the patient became hypotensive, and started vomiting copious amount of blood. He was intubated and taken emergently to the operating room where vascular surgery performed a second TEVAR and gastroenterology was emergently consulted for placement of an esophageal stent to stabilize the bleeding. The post-operative course was complicated by mediastinitis, respiratory failure, pulmonary embolus, and decision was made to withdraw care. Accidental ingestion of foreign bodies is common, and rarely causes severe complications. Less than 1% of ingested foreign bodies cause perforation of the gastrointestinal tract. AEF is a rare life-threatening complication of esophageal foreign body ingestion and is associated with high morbidity and mortality. The typical presentation of an AEF is chest pain particularly with swallowing, sentinel hematemesis followed by massive upper gastrointestinal hemorrhage often resulting in exsanguination. Early recognition and prompt intervention may be the only effective management of AEF. Initial goals should focus on control of massive bleeding, achieved either through esophageal intervention (stenting, Sengstaken-Blakemore tube) combined with thoracic endovascular aortic repair or through open-thoracic surgery. Although, AEF continues to have a high fatality rate, a multidisciplinary approach involving gastroenterology, cardiothoracic and vascular surgery and radiology may help provide life-saving therapy.

814 Metastatic Breast Cancer With Odd Presentations Justin Cochrane, DO, Gregory E. Schlepp, MD, Wichit Srikureja, MD. Providence Sacred Heart Medical Center, Spokane, WA. Introduction: Breast cancer is one of the leading causes of death in the female population in the United States. Relapse after primary treatment occurs in 10-60% of cases, common sites include bone, lymph nodes, lung, liver, and brain. Gastrointestinal metastases are rare, accounting for less than 3%. Literature review shows few case reports of metastatic breast cancer with pancreatic involvement or hematogenous spread to the esophagus. A 70-year-old female with jaundice, nausea, vomiting and 10 pound weight loss. Diagnosed with breast cancer in 1992 with 1.0 cm mass in her left breast, hormone receptor positive and was treated by lumpectomy, radiation, and one cycle of chemotherapy. She declined adjuvant hormonal therapy with the primary diagnosis. Local recurrence occurred in her left breast in 1994 with solitary mass. She declined surgical resection and opted for hormonal therapy with aromatase inhibitor. Physical exam revealed scleral icterus with yellowing of the skin, no abdominal tenderness and no abdominal mass found. Labs showed total bilirubin 8.1, AST 121, ALT 115, and ALP 297 and CT abdomen/pelvis showed a 1.8 cm mass in the head of the pancreas. EUS with biopsy confirmed metastatic breast cancer. A 77-year-old female with metastatic breast cancer to the liver 8 years ago with worsening jaundice over the previous month. Initial breast cancer was treated with multiple rounds of chemotherapy. Physical exams showed no distention of abdomen with scleral icterus and profound jaundice. Labs showed total bilirubin 11.2, ALT 37, AST 163, ALP 199, ALB 2.2, and INR 1.4. EUS/ERCP were performed and showed common bile duct proximal dilation of 12-14 mm near solid mass. Fine needle aspiration of proximal mass showed metastatic breast cancer. A 83-year-old female with worsening dysphagia, and diffuse chest pain. She was diagnosed with breast cancer in 1993, and treated with lumpectomy and radiation. PET scan showed metastasis at the level of the carina being treated with chemotherapy. Esophageal dilation were performed every 6 months with good relief until the last 6 months which only gave minimal relief with multiple dilatations. EGD/EUS showed stricture at 27 cm with esophagus biopsy and fine needle aspiration of esophageal lymph nodes showing metastatic breast cancer. Breast cancer can spread to many different organ systems. Rarely does it affect the gastrointestinal system, but as shown in these three cases, a patient with a history of breast cancer and a pancreatic mass or dysphagia without improvement with typical treatments requires further exploration.

815 Leukemic Infiltration of the Esophagus, a Rare Etiology for a Common Disease Yaseen Alastal, MD, Tariq Hammad, MD, Muhammad Ali Khan, MD, Muhammad Bawany, MD, Osama Alaradi, MD, Ali Nawras, MD, FACG. University of Toledo, Department of Internal Medicine, Division of Gastroenterology, Toledo, OH. Introduction: The etiology of esophagitis in patients with acute leukemia is usually related to infections, reflux, or chemotherapy toxicity. Esophageal leukemic infiltration is a rare potential cause. Here we present a case of severe diffuse esophagitis secondary to leukemic infiltration. An 87-year-old male patient presented with jaundice for 10 days and worsening hiccups. He denied nausea, vomiting, abdominal pain or fever. He was recently diagnosed with acute myelocytic leukemia and underwent 1 cycle of chemotherapy 1month prior to presentation. Vital signs were stable. He had icteric sclera. Abdominal examination revealed mild right upper quadrant tenderness. Bowel sounds were present. Laboratory work showed white blood cell counts of 3.4 Thou/mm3, hemoglobin of 10.4 g/dL, platelets of 53 K/mm3. Total bilirubin was 11 mg/dL. Alkaline phosphatase, aspartate and alanine aminotransferase levels of 506 U/L, 439 U/L and 791 U/L respectively. Abdominal ultrasound showed intra and extrahepatic biliary dilatation and gallbladder stones. Patient underwent ERCP. During esophageal evaluation by the scope he was found to have severely ulcerative panesophagitis with yellow exudate covering parts of the esophagus and multiple submucosal hemorrhages (Figures). Multiple biopsies and brushing were done. Evaluation of the biliary tree showed long common bile duct stricture which was stented. Biliary duct brushing and endoscopic ultrasound guided fine needle aspiration of a lesion surrounding CBD were negative for malignancies. Pathology study of esophageal specimens revealed heavy leukemic infiltration which was confirmed by immunohistochemical stains. Viral as well as fungal stains and cultures were negative. Leukemic infiltration of the esophagus is a rare potential etiology of severe esophagitis in patients with disseminated leukemia.


| OCTOBER 2014

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Abstracts

[815A] Figure 1. Endoscopic manifestations of leukemia on mid esophagus.

[815B] Figure 2. Endoscopic manifestations of leukemia on lower esophagus.

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817

Black Esophagus in the Setting of Alcohol Abuse and Hemothorax: A Rare Phenomenon

An Interesting Case of Esophageal Intramural Pseudodiverticulosis With Tract Formation in an HIV Patient

Meira Abramowitz, MD,1 Garrett Lawlor, MD2. 1. SUNY Downstate Medical Center, Brooklyn, NY; 2. VA NY Harbor Healthcare System, Brooklyn, NY. Introduction: “Black esophagus,” or acute esophageal necrosis (AEN), is a rare endoscopic finding with an incidence of only 0.0125-0.2%. Possible causes include ischemia, severe GERD, alcohol abuse, and trauma. We present a unique case of “black esophagus” that occurred in the setting of alcohol use and hemothorax. A 58-year-old male with a history of GERD, CAD, HTN and EtOH abuse presented with coffee ground emesis and hematochezia. The patient drank 0.5 liters of vodka daily for several weeks. Three days prior to arrival, he had nausea, vomiting, and multiple falls; hematochezia started two days later. Upon arrival, the patient was unstable and obtunded, with a soft tender abdomen; chest was clear. His Hb was stable (11.8) and lactate was 21. On EGD, the esophagus looked circumferentially necrotic and friable from 21 to 40cm; no esophageal or gastric varices seen. Repeat EGD after 4 days was greatly improved. One week later, the patient had a large left hemothorax with fractures of the 10th-12th ribs (thoracic aorta intact). After a prolonged hospital course, the patient was discharged in stable condition. AEN was first described in 1990 as circumferential esophageal ischemia commonly presenting with hematemesis and melena. It usually occurs in the distal esophagus; a watershed area between the portal and azygos veins. Its mechanism is not well understood, but may involve tissue hypoperfusion, downregulation of protective esophageal mechanisms, and a rapid esophageal influx of gastric contents. In our case, the esophageal necrosis was likely due to a combination of a massive influx of gastric contents into the esophagus from prolonged vomiting and GERD, low systemic perfusion from lactic acidosis, and possible distal esophageal vasculature disruption from blunt trauma. After blood flow restoration, the ischemia rapidly reverses, which explained why the mucosa markedly improved in our patient after stabilization. Our case is unique because it shows the multifactorial nature of AEN and to our knowledge is the first case in the literature where AEN was present in the context of alcohol use, rib fractures, and hemothorax.


Victor Velocci, MD,1 Juan Blum-Guzman, MD,2 Bijo John, MD,2 Juan Munoz, MD, FACG2. 1. Internal Medicine, Providence Hospital, Southfield, MI; 2. University of Florida Shands Hospital, Gastroenterology, Jacksonville, FL. Introduction: Esophageal intramural pseudodiverticulosis (EIP) is a benign condition that presents as dysphagia in greater then 80% of patients. The condition is rare and pathogenesis is believed to be due to an obstruction of excretory ducts or motor disorders of the esophageal wall, each of which can lead to ductal dilation. We describe an interesting case of an HIV patient with complaints of dysphagia found to have EIP. The association of EIP with HIV is rare and has only been reported on a few occasions, but is a logical one given the propensity of HIV patients to develop esophageal Candidiasis, and the association of this fungal infection with the development of pseudodiverticula. Our patient, a 38-yearold male with HIV, presented with complaints of chest and abdominal pain. He had been experiencing progressive epigastric pain for the preceding 2 weeks described as burning, sharp, and without radiation. There was associated dysphagia to solid food, which was often followed by vomiting. Initial investigation with esophagram showed what were described as massive esophageal ulcers with fistulous communications and numerous pseudodiverticula. Upper endoscopy demonstrated multiple pseudodiverticula without any other gross abnormalities. Pathology from biopsies showed chronic inflammatory changes consistent with pseudodiverticula formation, but no evidence of infection. On repeat questioning the patient reported multiple episodes of Candidiasis in the past. Esophageal intramural pseudodiverticulosis presents as multiple flask-shaped dilations in the wall of the esophagus usually on esophogram or CT as visualization of EIP by EGD only occurs in about 20% of cases. Chronic alcoholism, diabetes mellitus, esophageal Candidiasis, and reflux disease are often reported in association with EIP, however an association with HIV has only been described a few times in the literature. We believe that difficulty visualizing pseudodiverticula on EGD and their resolution with treatment of the inciting pathology has led to underreporting of this association in the past. The extent of the tract formation seen in our patient was also very unique, as the outpouchings have generally been reported on the order of millimeters and not centimeters as seen in our case.


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818 A Case of Persistent Dysphagia Following Mesh Hiatal Hernia Repair Preethi Reddy, MD. Internal Medicine, University of Arizona Medical Center, Tucson, AZ. Introduction: Simple cruroplasty, or primary closure of an enlarged hiatus with sutures alone, has been noted to have a high failure rate of up to approximately 40%. As a result, the use of mesh for hiatal hernia repair has become increasingly popular given its lower recurrence rate. However, the use of mesh near hollow organs is not without complications. A case of dysphagia secondary to surgical mesh migration and erosion is presented. The potential complications of hiatal hernia repair with prosthetic reinforcement are reported with particular emphasis placed on its most significant complication, visceral erosion of the prosthesis. An 80-year-old Caucasian man presented with complaint of dysphagia to solids and to near-complete dysphagia to liquids for 7 months. He was experiencing associated nausea, vomiting, regurgitation and a 5-lb weight loss. He has a past medical of history of a large type I paraesophageal hernia for which he underwent Nissen fundoplication with mesh repair, subsequent mesh incisional hernia repair and later, revision for sinus tract formation. Physical exam revealed no evidence of malnutrition, palpable neck masses, thyromegaly, lymphadenopathy, peritoneal signs or neurological deficits. Laboratory studies showed no metabolic derangements, leukocytosis or anemia. An esophagram showed irregularity of the esophageal mucosa and a computed tomography scan of the neck and soft tissue was unremarkable without lymphadenopathy or esophageal masses. However, esophagoduodenoscopy (EGD) revealed esophageal and duodenal foreign bodies with suture-like material eroding into the lumen of the esophagus and duodenum, respectively. As a result, the patient underwent surgical removal of mesh and subsequent esophagectomy. This case highlights the potentially catastrophic complication of mesh repair: visceral erosion. Dysphagia in the absence of peritoneal signs in a patient following mesh placement necessitates EGD to rule out mesh-related complications such as intraluminal erosion which may lead to bleeding, perforation, bowel obstruction and death.

819 Asymptomatic Colonic Tuberculosis Nimah Jamaluddin, MD,1 Guy Weiss, MD, FACG,2 Wendy Ho, MD, MPH2. 1. Department of Internal Medicine, University of California Los Angeles, Los Angeles, CA; 2. Division of Digestive Diseases, David Geffen School of Medicine at UCLA, Los Angeles, CA. Introduction: There has been a resurgence of colonic tuberculosis in the United States over the past two decades. This disease presents with diverse clinical manifestations and mimics other clinical disorders, including tumors, periappendiceal abscess, Crohn’s disease, and other infections, making its diagnosis challenging. Therefore, investigation of risk factors for tuberculosis as well as endoscopic and histological features is essential. We present a unique case of an immunocompetent and asymptomatic woman that required the collaborative work of gastroenterology, infectious disease, and pathology to successfully diagnose and treat. Our case involves a nurse with history of hypothyroidism who underwent her first average risk screening colonoscopy at age 53. She was born in the Philippines and moved to the USA at age 31. She denied nausea, abdominal pain, diarrhea, constipation, rectal bleeding, fever, chills, and weight loss. During her colonoscopy there was an ascending colon stricture with erosions and erythema, with appearance concerning for Crohn’s disease (A). However, pathology showed moderate to severe active colitis with multiple confluent necrotizing and non-necrotizing granulomas without features of chronic mucosal injury. She tested positive for Mycobacterium tuberculosis (MTB)-Quantiferon-Gold ELISA and on further questioning, reported a history of PPD seroconversion years ago that was not treated for unclear reason. Chest x-ray was normal. The presumptive diagnosis of colonic tuberculosis was made, despite the negative acid-fast bacilli staining and MTB complex PCR of colonic biopsies. She was started on standard four drug therapy with isoniazid, rifampin, ethambutol, and pyrazinamide. After one month, this was simplified to isoniazid and rifampin, which she took for 3 months only, due to peripheral neuropathy despite daily pyridoxine. Repeat colonoscopy 1 month later revealed complete resolution of the colonic stricture and biopsies showed no granulomas. Repeat CT 5 months later continued to show resolution of the ascending colon stricture.

[816A] Figure 1.

[817A] Figure 1. Pseudodiverticulum of the middle third of the esophagus.


[819A] Figure 1. Stricture with erosions in the ascending colon.


| OCTOBER 2014

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Abstracts 820

821

Aorto-Esophageal Fistula Fatal Complication Status Post Esophageal Stent For Esophagojejunostomy Anastamosis Leak

Stage IV Squamous Cell Carcinoma of Esophagus With Multi-Loculated Cystic Metastasis to Pancreas: A Rare Presentation

Lakshmi Yarlagadda, MD, Belen Tesfaye, MD. Howard University Hospital, Washington, DC.

Arun Nagabandi, MBBS, Abhishek Matta, MBBS, Rajesh Kunadharaju, MBBS, Kyle Regsiter, MD. Savio Reddymasu, MD, FACG, Creighton University Medical Center, Omaha, NE.

Introduction: We are reporting a case of aortoesophageal fistula, rare and fatal complication after esophageal stenting for anastomotic leak after malignant tumor resection. Very few cases are reported so far. A 76-year-old black female admitted to the hospital with diagnosis of stage 1 gastric adenocarcinoma underwent gastrectomy with roux-en-y esophagojejunostomy. After 3 weeks post op she had abdominal tenderness, CT with oral contrast revealed small anastamotic leak subsequently she had endoscopy and esophageal stent was placed. Ten weeks after surgery she had massive upper GI bleed along with 2 episodes of maroon colored stool. She underwent upper endoscopy and was found to have migrated stent and a large clot was seen at 40 cm from entry site and the attempt for removal of stent led to profuse (torrential) bright red bleeding. Despite all resuscitative efforts, she died due to profuse bleeding from aortoesophageal fistula. (see FIG 2). Aortoesophageal fistula is a fatal and rare complication after esophageal stent placement for anastomotic leak. Evident clinically by classic chiari triad with mid thoracic pain, sentinel arterial hemorrhage (bright red blood) and exsanguination after symptom free interval. On those who have high index of suspicion, confirmation with endoscopy and aortography showing sub mucosal hematoma and fistula are reasonable. However, both stable and unstable patients should undergo immediate surgery with Thoracic Endovascular Aortic Repair with stent (TEVAR) with esophageal reconstruction surgery and antibiotics therapy for 4 weeks to prevent aortic stent infection. Aortoesophageal fistula is a rare and devastating complication. One should have a high index of suspicion in such patients as prompt recognition and appropriate management will decrease mortality.

Introduction: A 60-year-old male with no significant medical history presented to the gastroenterology clinic with dysphagia. Patient did not have any odynophagia, weight loss, hematemesis, malena or abdominal pain. He did not have any family history of malignancy. He had history of tobacco and alcohol abuse. Physical examination was unremarkable. EGD was performed which showed a hemi circumferential thickening between 29-34 cm in the esophagus and another nodularity at 37cm. Biopsies from the lesions revealed a moderately differentiated invasive squamous cell carcinoma. CT chest revealed a circumferential thickening of the mid esophageal wall corresponding to the EGD findings. CT abdomen revealed multiple cysts in the pancreas, the largest measuring 5.3 x 4 cm. It was multi-loculated with macrocysts in the tail of the pancreas with thickened septum and a central calcification. The pancreatic lesion was found to be mixed solid and cystic in nature on endoscopic ultrasound. Two enlarged peritumoral nodes were also identified. USG guided aspiration of the pancreatic cyst revealed that the fluid had a CEA level of 41.1 ng/ml and an amylase level of 13 U/L. Fluid cytology revealed malignant cells consistent with metastatic squamous cell carcinoma. As per the TNM staging system, the patient was found to be in stage T3N1M1 and was started on chemotherapy with carboplatin and paclitaxel. Primary squamous cell carcinoma in pancreas is extremely rare of all pancreatic malignancies as the pancreas does not have squamous epithelium. Pancreatic metastasis occurs in 0.12% of all primary esophageal carcinomas. Only 4 cases of squamous metastasis to pancreas from esophagus have been reported in literature. Of them 2 patients had synchronous metastasis and 2 patients had metachronous metastasis. Our patient had the pancreatic metastasis at the time of presentation. Esfehani et al reported a case of pancreatic squamous metastasis that presented 4 years after the removal of esophageal primary. The pancreatic lesion was noted to be cystic on a CT abdomen but gross examination after surgery revealed a hard mass. All the other reported cases had solid metastases. Our patient is unique as he had a mixed solid and cystic metastasis.

822 Is Endovascular Stenting as Benign as Proposed? Jayakrishnan Krishnakurup, MBBS,MD, Lauren Bleich, MD, Andrew Bedford, MD. Gregory Soloway, MD, Venkata Gourineni, MBBS, MD, Pietro Andres, MD, Bridgeport Hospital/Yale University, Bridgeport, CT.

[820A] Figure 1.

Introduction: Aortoesophageal fistula (AEF) is a potentially fatal complication that seldom ensues after endovascular repair of a thoracic aortic aneurysm. The initial symptoms can be very subtle. Early recognition can limit disastrous complications. A 70-year-old male with hypertension and, recent thoracic endovascular aortic repair (TEVAR) 15 days prior, was admitted with worsening of recent dysphagia. He denied any hematochezia, hematemesis, hemoptysis or melena. A CT chest done two months prior revealed an 8.8 cm saccular lower thoracic aortic aneurysm, following which he underwent a TEVAR. A repeat CT chest during the current admission displayed the stent with in the thoracic aorta without residual aneurysm or contrast leak. The esophagus exhibited apparent distal mucosal thickening with irregularity and an air fluid level. An endoscopy revealed a large ulcerated defect without any bleeding in the lower third of the esophagus, through which the outside wall of TEVAR graft could be visualized protruding into the esophageal lumen. The patient underwent staged resection and repair of thoracic aorta with axillo-femoral bypass. On day-1, he underwent a laparoscopic J-tube insertion with defunctionalization of esophagus and cervical esophagostomy. This was followed by extra anatomic arterial bypass (right axillary to right iliac-left iliac bypass) on day 2 and, removal of thoracic aorta and distal esophagectomy on day-3. His post-operative course was complicated by anuric renal failure, quadriplegia due to spinal cord ischemia post aortic resection and, sepsis with hafnia alvei (Gram-negative rod, which is a commensal in the human gastrointestinal tract). He is currently dialysis dependent, undergoing rehab in a special care unit. Aortoesophageal fistula (AEF) is a rare but serious complication of TEVAR with a reported incidence rate of 0.5- 1.7% in the literature. Suggested mechanisms of AEF in TEVAR includes direct perforation of the aorta and esophagus by the stent, ischemic esophageal necrosis, pseudo aneurysm formation or endoleak into the aneurysm with subsequent esophageal pressure and finally, infection of the prosthesis (5% of the reported cases). The Chiari’s triad comprising midthoracic chest pain, sentinel arterial hemorrhage and, subsequent massive hemorrhage is the most common presentation of AEF. The presentation with dysphagia alone as in our patient is extremely rare. Definitive treatment of AEF is resection or repair of the fistula with repair of the esophageal, aortic walls and stent removal. Depending on the extent of lesion the surgery can have devastating effects as in our patient.

823 Esophageal Cancer in Patients With Cystic Fibrosis Kevin Rank, MD, Alexander Khoruts, MD, Joanne Billings, MD, MPH, Jordan Dunitz, MD. University of Minnesota, Minneapolis, MN.

[820A] Figure 2.


Introduction: Incidence of gastrointestinal malignancies (GIM) is increased in patients with Cystic Fibrosis (CF), and development of GIM is further accelerated by immunosuppression. This is an issue of increasing concern for CF patients as their life expectancy has significantly increased over the recent decades and they often become recipients of solid organ transplants. We have previously published that initiation of screening colonoscopies at age 40 results in a high yield of advanced adenoma detection. However, CF patients are also at risk for other GIM, including esophageal cancer. We report two cases of esophageal cancer identified within the cohort of 95 CF patients age 40 and above and discuss the associated implications. Case 1: A 40-year-old male with history of CF s/p lung transplant presented for EGD to evaluate for odynophagia. He was found to have a large, partially obstructing esophageal tumor. Biopsies showed adenocarcinoma and staging revealed widely metastatic disease. He was started on palliative chemotherapy with initial response, but has unfortunately had disease progression resistant to additional chemotherapy.


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Case 2: A 52-year-old male with history of CF (not transplanted) presented for EGD to evaluate for dysphagia and weight loss. He was found to have a large, fungating mass in the middle third of the esophagus extending to the lesser curve of the stomach. Biopsy showed adenocarcinoma. Staging again revealed metastatic disease. The patient started on palliative chemotherapy but ultimately passed away from worsening disease. Although pulmonary complications are still the primary cause of death in CF patients, GIM are increasingly becoming important contributors to CF morbidity and mortality as this population ages. We have previously suggested earlier initiation of colorectal cancer screening in adult CF patients, especially since detection and removal of precursor polyp lesions has the potential of cancer prevention. Similarly, anecdotal data suggest that incidence of Barrett’s esophagus, the precursor lesion of esophageal adenocarcinoma, may be increased in CF. Identification of two advanced esophageal cancers within a relatively small patient cohort suggests that a more systematic evaluation of upper gastrointestinal tract screening standards may be warranted in CF. At the minimum these should be considered in the pre-transplant evaluation.

vessels that form an abnormal communication between the arterial and the venous systems. The typical locations of these lesions in the gastrointestinal tract are the stomach, the small intestine, and the colon. Atypical locations such as the esophagus have been rarely reported in the literature. A 63-year-old male with a past medical history of cirrhosis secondary to chronic hepatitis C and alcohol who underwent esophagogastroduodenoscopy (EGD) for variceal screening. The patient had no prior history of varices and was asymptomatic at the time of the procedure. EGD was negative for varices but did reveal the unusual finding of an AVM of 5 mm size that was found in the proximal esophagus at 17 cm from the incisors. Given no reported history of gastrointestinal bleeding or anemia, the AVM was not ablated. Discussion: AVMs in the GIT are frequently seen in the stomach, the small intestine, as well as the colon. In the esophagus, AVMs are mainly found distally, less frequently in mid- esophagus, and rarely proximally. Since angiodysplasia is the most common type of vascular lesions that inflicts the GIT and can present as an incidental finding in asymptomatic patients or can be a source of chronic bleeding leading to anemia, endoscopists have to be particularly vigilant to not overlook unusual sites of this abnormality, and thus careful examination of the proximal esophagus is recommended.

824 Spontaneous Paraesophageal Hematoma Jessica Yan, MD, Courtney Walker, DO. Internal Medicine, University of Arizona, Tucson, AZ. Introduction: Gastrointestinal bleeding is an uncommon but potentially lethal complication of hemophilia. Intramural hemorrhage of the gastrointestinal tract has been described in hemophiliacs. However, spontaneous paraesophageal hematomas, an uncommon cause of chest pain, have yet to be reported. We report a case of a 24 year old man with hemophilia B who presented with acute retrosternal chest pain. He endorsed a long history of gastrointestinal esophageal reflux but denied record of emesis, trauma, NSAID or alcohol use, or gastrointestinal bleeding. Previous hemophilia complications included hemarthrosis and intramuscular bleeding. Vital signs were stable and physical examination revealed right wrist ecchymosis. Laboratory analysis was significant for partial thromboplastin time of 126 and factor IX activity of 42% (normal 60-160%). Hemoglobin was 13g/dL. Chest computed tomography (CT) showed a paraesophageal hematoma surrounding the distal esophagus with mural thickening and inflammatory changes. He was treated with coagulation factor IX infusion, antacids, and clear liquid diet. Symptoms resolved and esophagram showed no evidence of perforation. He was unfortunately lost to follow-up upon discharge. We suspect this rare paraesophageal hematoma resulted from spontaneous bleeding of a paraesophageal vein triggered by his underlying coagulopathy. A clinical history of atypical chest pain is suggestive. Imaging studies such as CT, magnetic resonance imaging, and oral contrast studies are diagnostic. Differential diagnoses include: spontaneous intramural esophageal hematomas, peptic ulcer disease, Mallory-Weiss syndrome, myocardial infarction, or Boerhaave syndrome. Without a history of previous emesis, however, these diagnoses are unlikely. Regression typically occurs with control of the bleeding diathesis and conservative medical management. We highlight an uncommon complication of hemophilia, which to the best of our knowledge, is the first case reported in the literature.

[825A] Figure 1. Proximal esophageal AVM.

826 Epiphrenic Diverticulum Mimicking Hiatal Hernia Roopa Gandhi, MD,1 Sangeeta Agrawal, MD, FACG2. 1. Wright State University, Dayton, OH; 2. Dayton VAMC, Dayton, OH.

[824A] Figure 1. Coronal CECT showing ematoma collection adjacent to esophagus.

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Introduction: Epiphrenic diverticula of the esophagus are associated with concomitant esophageal motility disorders. The primary differential is a hiatal hernia, which is far more common. Symptomatic patients with epiphrenic diverticula exhibit dysphagia, regurgitation and aspiration. While most patients are treated conservatively, some may require diverticulectomy and esophageal myotomy to address the underlying motility disorder. We herein present a case of patient with esophageal perforation due to a large unrecognized esophageal diverticulum. A 48-year-old healthy woman found down at a social gathering was intubated on site and transported to a level one trauma center for acute respiratory distress. On radiology report, the CT PE protocol suggested a large portion of the stomach was in the right chest. There were no signs of acidosis, pneumatosis or pneumomediastinum. Family reported a longterm history of dysphagia for solids and liquids with regurgitation of food for the past six years. Previous workup included a CT of the chest indicative of a large paraesophageal hernia. EGD subsequently was attempted and was incomplete twice due to retained stomach contents, despite preparation with a clear liquid on the day prior to procedure. No esophagram or manometry was found in the patient record. A surgical referral had been provided for symptomatic paraesophageal hernia but he was unable to pursue further evaluation due to financial limitations. An emergent thoracotomy was performed for suspicion of gastric volvulus shortly after the patient was admitted. A large 10 cm perforated epiphrenic diverticulum was found during surgery for which myotomy with resection of the diverticulum was performed. Epiphrenic diverticulum is a pulsion diverticulum, usually located in the distal 10 cm of the esophagus. It is due to the herniation of mucosa and submucosa through the muscle layers of the esophageal wall due to increased pressure in the area of the diverticulum. Misdiagnosis of an epiphrenic diverticulum as a hiatal hernia results in a missed opportunity to address a treatable esophageal disorder. Epiphrenic diverticula are thin walled on CT; in contrast the thick walled hiatal hernias which often exhibit the presence of gastric mucosa and rugae. In addition, epiphrenic diverticula do not cause widening of the esophageal hiatus that is seen in the setting of hiatal hernia. Early recognition and diagnosis of epiphrenic diverticulum is crucial to prevent life threatening complications such as malignancy, obstruction, bleeding and esophageal perforation, as seen in this case.

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Incidental Arteriovenous Malformation in the Proximal Esophagus: A Rare Finding Ashraf Almashhrawi, MD, MSc, Mohamad Yousef, MD, Harleen Chela, MD, Khulood Ahmed, MD, Murtaza Arif, MD. Gastroenterology, University of Missouri, Columbia, MO. Introduction: Angiodysplasia, also known as arteriovenous malformation (AVM), is the most common type of vascular abnormality that involves the gastrointestinal tract (GIT), and consists of aberrant blood


Mediastinal Gastrointestinal Stromal Tumor in a Patient With Esophageal Colonic Interposition Zainab Shahnawaz, MD, Muhammad Arif, MD, Savio John, MD. Upstate Medical University, Syracuse, NY. Introduction: Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumors of the gastrointestinal tract. They typically arise in the stomach, but can also be found in the small intestine,


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Abstracts colon, rectum, and uncommonly in the esophagus and omentum. Colonic interposition is a procedure done for the therapy of esophageal injury from trauma, ingestion, strictures and cancer. We present the case of a 50-year-old male who presented with hemodynamically significant hematemesis and hemoptysis. The patient had a history of esophageal injury due to lye ingestion 34 years ago for which he underwent esophageal resection with colonic interposition and gastric pull up. Three years ago the patient presented with weight loss and chest pain. CT of the chest showed a large mediastinal mass measuring 12 x 11 cm which was encasing the aorta. Multiple liver lesions were also found suggestive of metastatic disease. Upper endoscopy with biopsies revealed colonic mucosa in the interposed segment of esophagus and a large, friable, ulcerated mass which was obstructing 75% of the esophageal lumen. Biopsies revealed highly atypical cells, hyperchromasia with increased mitotic activity, which stained positive for CD 117 and CD34 consistent with GIST. Biopsies of the liver lesions had similar findings and were consistent with metastatic GIST. The patient was treated with Imatinib with palliative intent but the size of the tumor continued to increase. The upper endoscopy performed on the current admission revealed a large, bleeding, fungating mass in the upper esophagus with complete obstruction of the esophageal lumen, which could not be traversed. Repeat CT revealed that the mass had increased in size to 18 cm and extended up to the neck and contained pockets of air, raising concern for a tracheo-esophageal fistula. The patient and family did not want to pursue aggressive medical therapy and hence palliative care measures were initiated. There are rare reports of adenocarcinoma developing in a colon graft. To our knowledge, this is the first report of GIST developing in a colonic interposition graft in the esophagus.

measures. We present a case of a 78-year-old male with coronary artery disease, hypertension, and unresectable, treatment deferred, pancreatic adenocarcinoma presenting with new onset odynophagia for 4 days. Upper endoscopy revealed severe, circumferential necrotic appearing esophageal mucosa with progressive worsening towards the distal end. Pathology confirmed diffuse ulceration and necrotizing inflammation, which is consistent with AEN. The patient was treated conservatively with high dose proton pump inhibitors and elected to pursue hospice care. Acute esophageal necrosis, or “black esophagus” is an exceedingly rare, poorly described esophageal disorder. Of the 88 cases reported to date, the majority of patients (>90%) present with gastrointestinal (GI) bleeding. Dysphagia/odynophagia alone occurs in less than 5% of reported cases. AEN is associated with high mortality of approximately 30%, mostly attributable to underlying co-morbidities. AEN itself carries a mortality rate of 6%. This is due to AEN occurring in the setting of advanced age and multiple medical derangements including cardiovascular disease, diabetes mellitus, and malignancy. The endoscopic findings in this case were classic for AEN, suggesting that recent esophageal insult and odynophagia was a reflection of AEN development. Due to underlying pancreatic malignancy and increased thrombotic predilection in the setting of malnutrition with decreased capability of reparative mechanisms, we theorize an acute vascular insult as the triggering cause for AEN. This case demonstrates typical endoscopic findings of AEN with a highly uncommon presenting complaint: odynophagia in the absence of GI bleeding. The diagnosis of AEN is an often ominous sign, indicating poor prognosis with limited treatment options.

829 Absolute Dysphagia Caused by Severe Esophageal Stricture Complicating Radiofrequency Ablation of Short Segment Barrett’s Esophagus Yaseen Alastal, MD, Tariq Hammad, MD, Muhammad Bawany, MD, Osama Alaradi, MD, Ali Nawras, MD, FACG. University of Toledo, Department of Internal Medicine, Division of Gastroenterology, Toledo, OH.

[827A] Figure 1. Endoscopic view of esophagus infiltrated by GIST tumor.

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Introduction: Esophageal stricture is a known complication of radiofrequency ablation procedure for Barrett’s esophagus, but it is unusual to complicate ablation of short segment Barrett’s esophagus. Here we present a case of severe esophageal stricture that developed 2 weeks after radiofrequency ablation of short segment Barrett’s esophagus. A 54-year-old Caucasian female with history of gastroesophageal reflux disease (GERD) and hiatal hernia underwent endoscopic evaluation for severe reflux symptoms. Esophagogastroduodenoscopy (EGD) showed 1.5 cm segment of Barrett’s esophagus and histopathology didn’t show dysplasia. Family history was significant for esophageal cancer in her father and Barrett’s esophagus in her son and two sisters. After ruling out esophageal dysmotility by high-resolution manometry and confirming GERD by 24 hour pH monitoring, the patient underwent hiatal hernia repair and Nissen fundoplication. GERD symptoms improved after surgery. In view of the strong family history of Barett’s esophagus and esophageal malignancy and the patient concerns about the risk of malignancy, she underwent radiofrequency ablation of Barrett’s esophagus. A total of 10 applications of 12 joules were done using Halo 90 ablation catheter. There were no acute complications. Two weeks after the procedure, the patient developed nausea and dysphagia with lower chest discomfort. EGD showed distal esophageal ulceration consistent with previous radiofrequency ablation. The patient was discharged on proton pump inhibitor. However, her symptoms have worsened and 5 days later she presented to emergency department with absolute dysphagia associated with nausea and vomiting and inability to swallow even liquids. Esophagogram showed persistent contrast column in the distal esophagus with no transit into the stomach, which was consistent with esophageal obstruction at the gastroesophageal junction. EGD showed severe distal esophageal stricture with ulceration and edema. The stricture was dilated up to 15 mm by CRE balloon. The procedure was repeated after 10 days with dilation up to 18 mm. Patient tolerated the procedure without further complications. On follow up her symptoms completely resolved. Severe esophageal stricture is a potential complication of radiofrequency ablation even of short segment Barrett’s esophagus. Endoscopic dilation is quite effective in treating this complication.

Acute Necrotizing Esophagitis in a Patient Without GI Bleeding Andrew Weber, BA,1 Alia Hasham, MD,3 Bassem Khalil, MD,2 Thomas Mahl, MD, FACG1. 1. University at Buffalo School of Medicine and Biomedical Sciences, Buffalo, NY; 2. MedStar Union Memorial Hospital, Baltimore, MD; 3. University at Buffalo Division of Gastroenterology, Hepatology, and Nutrition, Buffalo, NY. Introduction: Acute esophageal necrosis (AEN), also referred to as “black esophagus”, is a rare endoscopic finding marked by circumferential, blackening of the esophagus. The incidence is estimated at 0.01% to 0.28%. AEN most commonly involves, but is not limited to, the distal portion of the esophagus with a clear transitioning at the gastroesophageal (GE) junction to healthy mucosa. The etiology is likely multifactorial, resulting from hemodynamic compromise, corrosive injury, decreased barrier and/or regenerative functions and malnourished or debilitated states. Treatment is limited to supportive

830 Dysphagia in a Post-Surgical Patient Without a Stricture: Treatment With a Novel Large Caliber Fully Covered Self-Expanding Metal Stent Jerry Yu, MD, Zachariah Chandy, Bsc, Shawn Kaye, Bsc, Avanka Lowe, MD, Joshua Steichen, MD, John Lee, MD, Kenneth Chang, MD, FACG, Jason Samarasena, MD. University of California - Irvine, Orange, CA. Introduction: Fully covered self-expanding metal stents (FCSEMS) have been shown to be beneficial in the treatment of symptoms in malignant esophageal strictures. However, their use in benign disease remains under investigation. The Merit Medical EndoMAXX FCSEMS (Utah, USA) is a novel large

[829A] Figure 1. (A) Esophagogram revealed distal esophageal obstruction. EGD: distal esophageal stricture before (B) and after dilation (C). © 2014 by the American College of Gastroenterology


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caliber esophageal stent with specially designed “struts” that mitigate stent migration. This stent is the largest caliber esophageal stent available in the U.S. with a diameter up to 23 mm. The following is a case where this novel stent was used for relief of dysphagia symptoms related to a special case of benign disease. The patient is a 55-year-old female who underwent esophagectomy for esophageal cancer 6 months prior complicated by esophageal leak, abscess and sepsis and further surgical revision. Patient was referred to our center for symptoms of severe solid and liquid phase dysphagia and weight loss. Endoscopy surprisingly revealed a wide open esophago-gastric anastomosis with no stricture noted. An EndoMAXX 10 cm x 23 mm FCSEMS was placed at the level of the anastomosis and symptoms were relieved immediately with excellent toleration of the stent. The patient gained 30 lbs in 4 months. Four months later, repeat endoscopy showed no stent migration and successful stent extraction was performed without any complications. Patient reported recurrent symptoms of dysphagia within 1 day of stent removal. Upper GI series was performed which revealed hang up of contrast near the GE anastomosis and evidence of a sharp angulation at the GE anastomosis. The patient then underwent stent placement with the same model stent and immediately symptoms of dysphagia resolved. At the time of this writing, the patient has had stent in-situ for 3 months and continues to do well with no symptoms of dysphagia and no adverse effects of the stent. Currently esophageal FCSEMS are only FDA-approved for malignant strictures in the esophagus. There are a number of benign conditions of the esophagus that lead to strictures that can also be treated with FCSEMS, although their short and long term efficacy for relief of dysphagia has been questionable, and recent studies suggest migration rates in benign disease tend to be higher than with malignant strictures. This is a unique case where post-surgical anatomy led to severe dysphagia symptoms without a typical stricture. The EndoMAXX FCSEMS was used to “straighten the kink” seen on Upper GI series that was likely the cause of the patient’s dysphagia. The large caliber of the stent and its unique metal strut design likely aided in this stent not having an issue with migration. Further prospective study of this unique large caliber stent in benign disease is warranted.

831 Double Stenting for Malignant Broncho-Esophageal Fistula: A Viable Option for Palliation in Advanced Esophageal Cancer Prathab Devaraj, MD,1 Shashank Ponugoti, MD,2 Swati Pawa, MD1. 1. West Virginia UniversityDepartment of Digestive Diseases, Morgantown, WV; 2. West Virginia University- Department of Internal Medicine/Clinical and Translational Science, Morgantown, WV. Introduction: Broncho esophageal (BEF) fistula is reported in 5-10% of patients with esophageal cancer. In most of these cases, the insertion of a single stent, either a tracheobronchial or an esophageal stent is sufficient to seal off the fistula. In our case the esophageal stent failed to stop the contrast leak despite being in proper position due to lack of approximation secondary to a diseased esophagus. Thereafter, a bronchial stent was placed at the right intermediate bronchus and successfully stopped the contrast leak. A 50-year-old male with h/o hypertension was diagnosed with moderately differentiated squamous cell cancer of the mid esophagus. Endoscopic Ultrasound (EUS) showed invasion of tumor into descending aorta. Barium swallow showed fistulous communication between the esophagus and left main bronchus. BEF was complicated by recurrent pneumonia. Upper endoscopy showed a 7 cm circumferential friable mass with a fistulous tract in the mid esophagus. A fully covered Wallflex esophageal stent was placed under fluoroscopic guidance bridging the fistula. Repeat barium swallow after stent placement showed persistent fistula. Patient subsequently underwent bronchoscopy, which confirmed fistula between esophagus and left main bronchus. A metal stent was placed in the left bronchus covering the fistula. He was discharged home with tube feeds. He was evaluated 4 weeks later with a repeat barium swallow that showed complete resolution of the fistula. He is currently tolerating oral feedings. Malignant BEF is a devastating complication of advanced esophageal or lung cancer. Treatment should be aimed towards limitation of airway contamination and adequate nutrition. These can be effectively achieved by esophageal bypass and stenting. Bypass should be reserved for patients who can tolerate a major operation. Stenting promotes swallowing and also limits aspiration. Endoscopic management of BEF is challenging and can be achieved either by esophageal stenting or bronchial stenting or double airway and esophageal stenting. Stenting in both the esophagus and airways should be considered when both are severely invaded by malignancy, when the airway is compressed or when the fistula is insufficiently sealed by an esophageal stent. Studies have shown that survival and quality of life were much better in double stenting than single stenting. Early closure of fistula improves survival. Endoscopists should be aware of late complications like tissue necrosis, stent migration and inversion of stent flange after double stent placement causing obstruction. Prompt diagnosis and successful treatment with stenting will improve survival and quality of life in advanced cancer patients.

832 A Case of Esophageal Intramural Pseudodiverticulosis Due to Chronic GERD Xiao Jing Wang, MD,1 Anthony Gamboa, MD,2 Sonali Sakaria, MD2. 1. Internal Medicine, Emory University School of Medicine, Atlanta, GA; 2. Emory University School of Medicine, Digestive Disease Department, Atlanta, GA. Introduction: Esophageal intramural pseudodiverticulosis (EIP) is a rare disease thought to be due to chronic inflammation of the excretory ducts of submucosal esophageal glands. While diagnosis of EIP was previously made using barium esophagrams, esophagogastroduodenoscopy (EGD) has become the predominant modality for detecting this abnormality. Endoscopic features of EIP can be localized or diffuse and are characterized by multiple pinhead-sized outpouchings of the esophageal wall. Most patients present with esophageal stenosis with a history of multiple prior EGDs. We present a case of EIP diagnosed by EGD after numerous prior scopes with dilation of esophageal stenosis. A 60-year-old woman with diabetes mellitus and GERD presented with dysphagia to solids and liquids leading to decreased oral intake and regurgitation. She reported midline burning despite twice daily esomeprazole but denied weight loss. She had at least six prior EGDs with dilation but none within the past three years. An EGD was performed for suspected esophageal stricture. Esophageal intubation suggested a tight upper esophageal sphincter without mucosal lesion. The sphincter was traversed revealing multiple, very small punctuate lesions throughout the esophagus as well as small whitish plaques in the mid-esophagus (Figure 1). Biopsies and brushings ruled out eosinophilic and candida esophagitis, respectively. Barium swallow showed multiple small curvilinear outpouchings along the outer margin of the mid and distal esophageal lumen consistent with EIP. Pathology showed epithelial chronic inflammation with basal cell hyperplasia consistent with reflux esophagitis. Though pathophysiology remains largely unknown, EIP is associated with inflammation of the excretory ducts of submucosal esophageal glands and is frequently associated with chronic inflammatory states as esophageal candidiasis, achalasia, GERD, and diabetes mellitus. Alcohol and tobacco abuse have also been strongly implicated in pathogenesis. With the technological advancement and increasing ability to detect small alterations in esophageal architecture, the incidence of EIP is likely to increase. EIP has been implicated in development of esophageal stenosis, esophageal squamous cell carcinoma, spontaneous esophageal perforation, esophagobronchial fistulas, and pulmonary or mediastinal abscesses. Increased recognition of characteristic findings on EGD may allow further study into disease pathogenesis and prevent complications.

833 Watch It Grow: Esophageal Impaction With Chia Seeds Rebecca Rawl, MD, MPH, Lauren Browne, MD. Carolinas Medical Center, Charlotte, NC. Introduction: A 39-year-old male with asthma and seasonal allergies presented with the acute onset of persistent, severe dysphagia. The patient had a long history of intermittent dysphagia to solids which had worsened over the preceding 2 weeks. Twelve hours before presentation, he swallowed a tablespoon of dry chia seeds followed by a glass of water. He immediately experienced epigastric discomfort and was unable manage his oral secretions. Glucagon did not relieve his symptoms. Emergent EGD showed complete distal esophageal obstruction with a gel of hydrated chia seeds. Attempts at traversing or advancing the bolus using an adult diagnostic upper endoscope were unsuccessful. Removal of the seeds using a Roth net and grasping forceps was also unsuccessful due to a semi-solid consistency. A neonatal gastroscope was advanced past the obstruction revealing a stricture at the GE junction. The neonatal gastroscope was then used to push small amounts of the chia seed gel into the stomach until the impaction was relieved. The patient was started on twice daily PPI, and a liquid diet was recommended until repeat endoscopy was performed. Chia seeds (Salvia hispanica) are small (2mm x 1.5mm), oval seeds native to Mexico and Guatemala. They have been used for food, medicine, and paint since Aztec civilization. They were initially introduced to the U.S. by terracotta “pets” on which the seeds would grow. Over the last 5 years, their use as a food product has been growing in popularity due to high protein, omega-3 fatty acid, and fiber content. Chia seeds are marketed to improve cardiovascular health, promote weight loss, and improve glycemic control. When added to liquid, dry chia seeds immediately begin to form a hydrogel capsule absorbing up to 27 times their weight in water. In the stomach, this process contributes to a feeling of satiety. In our patient, an underlying esophageal stricture resulted in the formation of a hydrogel in his esophagus causing complete esophageal obstruction. This is the first report of esophageal food impaction with chia seeds. With the increasing popularity of chia seeds, patients with a history of dysphagia or esophageal strictures should be cautioned about their use, especially in their dry form.



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Abstracts without any significant blood loss. Histologically, specimen demonstrated surface ulceration, acute inflammation, and lobular proliferation of capillary-sized vessels lined with endothelial cells. The final diagnosis identified the polyp as a late stage lobular capillary hemangioma, or a pyogenic granuloma. There was no evidence of malignancy. This case illustrates a rare clinical presentation of an esophageal hemangioma along with its gross, endoscopic, and pathologic features, and the utilization of various imaging and treatment modalities available for successful intervention. Although uncommon, these lesions have a high propensity to cause significant bleeding. Our case describes the distinctive endoscopic and endo-sonographic findings and demonstrates its amenability to endoscopic resection.

836 Endoscopic Risks of Paraesophageal Hernias and Incidental Transdiaphragmatic Herniation of the Pancreas Christopher Velez, MD,1 Akiva Marcus, MD,1 Paul Feuerstadt, MD,1 Arthur Harris, MD, FACG2. 1. Department of Medicine, Montefiore Medical Center, Bronx, NY; 2. North Bronx Health Network, Bronx, NY.

[833A] Figure 1.

834 Primary Paget’s Disease of the Esophagus: A Rare Presentation of Esophageal Adenocarcinoma Omar Shahbaz, MS, MD, Shounak Majumder, MBBS, MD. Medicine, University of Connecticut School of Medicine, Farmington, CT. Introduction: Paget’s disease was first described by Sir James Paget in 1874 as large round cells with clear cytoplasm and eccentric nuclei scattered within the epidermis. It is most classically recognized in breast tissue where the presence of these cells represent an underlying ductal carcinoma in situ. Extra-mammary Paget’s disease has also been reported in the vulva, anus, axilla, and eyelids. In fact, it is postulated that Paget’s disease can occur anywhere stratified squamous epithelium is present. One rare site of Paget’s disease is the esophagus. Compared to the sole presence of intraepithelial neoplastic paget cells with glandular differentiation found in primary disease, in secondary Paget’s there is also evidence of adenocarcinoma beneath the basement membrane. We present the case of a 51-year-old woman with past medical history of stage IIa, BRCA 2 positive, Her2neu positive, ER negative, PR positive breast adenocarcinoma status post lumpectomy, chemotherapy and radiation who was referred to gastroenterology for 2 years of intermittent dysphagia. Esophagogastroduodenoscopy (EGD) revealed irregular mucosa from the upper esophagus down to 35cm below the incisors, circumferential rings throughout and no discrete abnormal masses. Concern for eosinophilic esophagitis prompted biopsies from mid and distal esophagus. Pathology was consistent with intraepithelial pagetoid poorly differentiated adenocarcinoma at 18-30cm below the incisors. Distal esophagus and stomach biopsies were negative for carcinoma. Of note, recent breast MRI, mammography, and ultrasound showed no signs of malignancy. The patient was diagnosed with primary esophageal adenocarcinoma with pagetoid mucosal distribution pattern, or primary esophageal Paget’s disease. In accordance with previously described cases, she was referred for surgical resection of the esophagus and laryngectomy, which the patient ultimately refused. She was treated with Taxol, Carboplatin and radiation therapy. Follow-up PET scan and EGD revealed no evidence of recurrent malignancy. She remains alive and under surveillance 2 years post-therapy. Esophageal Paget’s disease is an extremely rare entity. To our knowledge, there are only 5 reported cases—2 of which are primary and 3 are secondary. The present case represents the third published case of primary Paget’s disease and it is the only one manifesting as circumferential rings on EGD. Further, it is the first patient managed medically as opposed to surgically. Although uncommon, paget cells may signify not only an underlying esophageal adenocarcinoma, but also may be the primary manifestation of malignancy.

835 Esophageal Hemangioma: An Unusual Cause of Upper GI Bleeding Joseph Salhab, DO, Saras Sharma, DO, Farhan Israr, DO, Cristina Marin, MD, Laritza Enriquez, MD. Larkin Community Hospital, Miami, FL. Introduction: Capillary hemangiomas are most commonly found on cutaneous tissue in the head and neck region and on the mucosa of the oral cavity. This case is a remarkable finding, as this type of vascular proliferation is rarely found within the alimentary tract or even as a cause of an upper gastrointestinal hemorrhage. This case reports a 62-year old Hispanic female afflicted with this benign tumor who was admitted to the hospital with severe anemia (Hgb of 6.1) and black tarry stools. A literature review of hemangiomas yielded less than 50 reported cases within the gastrointestinal tract, with a predilection for older males (mainly in their fourth to sixth decades of life). A 62-year-old female patient with a past medical history of hypertension and hyperthyroidism presented to the emergency department with the chief complaint of general malaise, subjective fever, palpitations, and a “pounding headache” of one days duration. After thorough history with full review of systems, the patient admitted to black tarry stools, worsening in frequency within the last few months. Her physical exam was mostly unremarkable, with only a faint 1/6 systolic murmur at heard at the left sternal border. Laboratory findings revealed that the patient was severely anemic, with a hemoglobin of 6.1 and hematocrit of 19.1. Medical management included a blood transfusion and an upper endoscopy which demonstrated a 1.5cm protruding, necrotic, pedunculated polyp at the distal esophagus about 0.5 cm above the GE junction. Although this lesion was highly vascular, the patient subsequently underwent endoscopic snare polypectomy with clip placement


Introduction: A 61-year-old woman with gastroesophageal reflux disease, peptic ulcer disease, and asthma was hospitalized with 2 days of abdominal pain and distention, nausea, and vomiting. Despite having undergone prior Nissen fundoplication, a large paraesophageal hiatal hernia (PHH) had been identified 6 years previously. At that time she was referred for surgery, but she was deemed “too high risk” and an operation was deferred. In the setting of her admission complaints, computerized tomography was performed which revealed a massive left sided diaphragmatic hernia containing not only the stomach, but portions of the spleen, jejunum, descending and transverse colon, as well as the pancreatic tail. Compressive atelectasis of the left lung and mediastinal shift also was noted. Surgery was re-consulted, with pre-operative endoscopy requested to assess for peptic ulcer recurrence. Esophagogastroduodenoscopy (EGD), tolerated without incident 2 years earlier for gastrointestinal bleeding, was performed in the standard fashion including patient placement in the left lateral decubitus position and air insufflation of the stomach. Prior to the EGD, the patient received fentanyl and midazolam. After the procedure, she became dyspneic, disoriented, lethargic and hypoxic; administration of naloxone and flumazenil reversed these symptoms. PHH’s represent only 5-10% of hiatal hernias, with large transdiaphragmatic hernias more often resulting from trauma (penetrating, blunt, or peri-operative) versus progressive hiatal defect enlargement. Herniation of the pancreas is exceedingly rare with only a dozen reports in the literature in the last half century. Even without symptoms, surgery should be offered to avoid the multiple possible adverse events associated with large PHH’s, including incarceration, strangulation, perforation, or as in this patient’s case, frank obstruction. In terms of endoscopy-related risks, patients with PHH have a greater likelihood of respiratory decompensation secondary to reduced lung function from atelectasis. Atelectasis of the left lung in this case was exacerbated further both by placement of the patient in the left lateral decubitus position and by subsequent air insufflation of the herniated stomach. In retrospect, endoscopic evaluation under general anesthesia immediately prior to surgical correction would have been preferable. This case demonstrates a severe presentation of a PHH, with rare involvement of the pancreas. When weighing the risks of endoscopy in any patient, it also reminds clinicians to consider specific clinical conditions, such as the effects of PHH-contents on the cardiopulmonary system, in addition to the more common cardiovascular and pulmonary diseases.

837 Black Esophagus: Complication of Colon Post-Polypectomy Bleeding Hemant Chatrath, MD,1 Sunitha Musuku, MD,1 Rita Kapoor, MD2. 1. University of Arizona, Tucson, AZ; 2. Jamaica Hospital Medical Center, New York, NY. Introduction: Acute esophageal necrosis or black esophagus is rare and caused by ischemia, back flow chemical injury, inadequate protective barriers and physiological reserve. To our knowledge, black esophagus secondary to post polypectomy bleeding has not been reported in literature before. We present a case of a 64-year-old male with history of hypertension and coronary artery disease that presented for routine screening colonoscopy. Multiple polyps in the ascending and descending colon less than 1 cm in size were resected with a combination of hot and cold snare. Patient presented 2 days later to the hospital with dysphagia, coffee ground emesis and bright red blood per rectum. On admission hemoglobin dropped from baseline of 13 gm to 8 gm. CT scan of the abdomen showed fluid consistent with blood in entire colon and esophageal wall thickening. Colonoscopy revealed bleeding from post polypectomy site, which was successfully treated with hemoclip. Upper endoscopy was remarkable for diffuse circumferential necrosis of the entire esophagus with sparing of the GE junction. Patient was treated with high dose PPI. Repeat upper endoscopy was performed in 4 weeks, which showed complete resolution with normal esophageal mucosa. Patient was doing well with no dysphagia. There were no stricture or infectious complications. The exact etiology of acute esophageal necrosis is unclear but ischemia plays an important role in the pathogenesis. Our case serves to increase awareness among endoscopists of acute esophageal necrosis as a potential complication of post polypectomy bleeding.

838 Alendronate: An Unlikely Cause of Intramural Esophageal Hematoma Meira Abramowitz, MD, Dimitrios Georgostathis, MD, Evan Grossman, MD, FACG. SUNY Downstate Medical Center, Brooklyn, NY. Introduction: Intramural esophageal hematomas (IEH) are a rare cause of esophageal injury. Precipitating factors of IEH usually include vomiting, straining, iatrogenic causes, and bleeding disorders. We present an unusual case of IEH in a patient who was taking a combination of antiplatelet medications and bisphosphonates. A 78-year-old woman with a history of coronary artery disease status post coronary artery bypass grafts, hypertension, hyperlipidemia, and osteoporosis presented to the ER with burning, retrosternal chest pain and hematemesis which started that morning. Her daily medications included aspirin, clopidogrel, and alendronate. On examination, the patient was hemodynamically stable with a


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2 months of upper and lower extremity bullous skin eruptions in addition to more recent odynophagia and melenic stools in the setting of ibuprofen use for analgesia. A diagnosis of bullous pemphgoid was confirmed by direct immunofluorescence which identified immunoglobulin G and complement 3 deposits at the dermoepidermal junction. Endoscopy performed the following day revealed, in addition to a 2 centimeter duodenal bulb ulcer, vertical linear fissures with sloughing of the superficial esophageal mucosa consistent with esophagitis dissecans superficialis. The patient was initially treated with intravenous methylprednisolone for 3 days, followed by a prednisone taper with improvement in his bullous skin lesions, odynophagia and melenic stools. With less than 10 cases of esophagitis dissecans superficialis associated with bullous pemphigoid described in the English literature, prompt endoscopic recognition is vital in corroborating a diagnosis and guiding therapy.

840 Upside Down Intrathoracic Stomach: A Case Report Laura Pestana, DO, George Saffouri, MD, Christopher Blevins, MD, Santhi Swaroop Vege, MD, FACG. Mayo Clinic, Rochester, MN.

[838A] Figure 1. Esophageal hematoma. large emesis basin filled with blood. An emergent EGD revealed a raised blue/purple area along the anterior wall of the esophagus, concerning for esophageal hematoma, along with a V-shaped mucosal defect at 23 cm from the incisors oozing blood. An esophagram and CT chest did not reveal signs of esophageal perforation or pneumomediastinum. The patient did well throughout her hospital course and was discharged without any further complications. IEH is defined as a dissection of the esophageal submucosa. It is part of a spectrum of esophageal injuries ranging from local mucosal tears to transmural esophageal rupture. Classic symptoms of IEH include chest pain, dysphagia, and hematemesis. Spontaneous IEH (SIEH) is more likely to occur in patients with bleeding disorders and those on anticoagulation. The cause of our patient’s IEH was probably her two antiplatelet medications and alendronate, which has been known to rarely cause esophageal rupture. On esophagram and CT scan, IEH may appear as abnormal intraluminal/intramural defects. EGD may reveal friable mucosa with a bluish longitudinal hematoma, with or without a mucosal break, similar to what was found in our patient. SIEHs usually resolve within three weeks with conservative management, which explains our patient’s uneventful hospital course and discharge. This case is unique as to our knowledge, it is the first in the literature where a SIEH was associated with a combination of two antiplatelet agents and a bisphosphonate.

Introduction: A 73-year-old male with a history of hiatal hernia and short-segment Barrett’s esophagus presented with complaints of nausea, vomiting, and acute, stabbing abdominal pain thirty minutes after eating. He also endorsed the sensation of food being stuck in his chest, but no hematemesis, melena, odynophagia, weight loss, fevers, or chills. On exam, vitals were within normal limits, abdomen was soft, non-distended, and tender to palpation in the upper epigastrium without rebound or rigidity. Cardiopulmonary exam was unremarkable. Laboratory studies revealed lactate of 3.32 mmol/L (ref 0.6-2.3 mmol/L) and lipase of 107 U/L (10-73 U/L). Further evaluation with CT abdomen revealed a very large hiatal hernia with an upside down intrathoracic stomach that was mildly to moderately distended and worrisome for delayed gastric emptying. He was admitted to the hospital, maintained nothing per os (NPO), and given intravenous fluids. Thoracic Surgery was consulted and performed thoracotomy with Belsey Mark IV fundoplication for gastric outlet obstruction secondary to the large intrathoracic stomach. At one month post-surgery, he was tolerating meals and doing well. Upside down stomach is a rare form of hiatal hernia (15 eosinophils/hpf). Pathologic analysis of endoscopic biopsies of esophageal nodule was consistent with GCT. Endoscopic ultrasound revealed esophageal nodule originated from deep mucosal (second esophageal wall) layer, an endosonographic characteristic consistent with GCT. The tumor was extracted using endoscopic mucosal resection (EMR) without complications. Histologic analysis of the resected specimen confirmed granular cell tumor. Patient underwent treatment with standard six food elimination diet for EoE resulting in symptomatic improvement. Case 2: A 15-year-old male with history of asthma presented with intermittent dysphagia, without heartburn or dyspepsia and with several episodes of esophageal food impaction during the prior 5 years. EGD revealed one 10-mm-wide, submucosal nodule with normal appearing overlying mucosa in upper esophagus at 25 cm from incisors without other endoscopic abnormalities. Pathologic analysis of superficial endoscopic biopsies of esophageal nodule were nondiagnostic. Histologic analysis of biopsies of middle esophageal mucosa was consistent with EoE (>20 eosinophils/hpf). Endoscopic ultrasound revealed esophageal nodule originated from deep mucosal (second esophageal wall) layer, an endosonographic feature consistent with GCT. The nodule was endoscopically extracted using EMR technique without complications. Histologic analysis of the resected specimen demonstrated GCT. Patient was recommended to undergo trial of daily omeprazole 20 mg therapy and follow-up with allergist for eventual six food elimination diet. This report adds 2 cases to the single previously published case of EoE with GCT. Although these two entities appear to have different pathophysiology and their concurrence may be coincidental, future large endoscopic studies are warranted to further investigate this potential association and determine its potential pathophysiology. Both entities should be considered in the differential diagnosis of dysphagia, particularly in young patients.

842 Post-SEMS Stricture Development: An Emerging Complication Munish Ashat, MD, Jayanta Samanta, MD, Saroj Sinha, DM, Rakesh Kochhar, DM. Department of Gastroenterology, Post Graduate Institute of Medical Education and Research, Panchkula, India. Introduction: Self expanding metallic stents (SEMS) are increasingly being used for the management of benign esophageal lesions such as leaks, and fistulae. However the long term outcome for such use remains unknown. The study is based on 6 patients of esophageal leaks who were treated with SEMS and subsequently developed esophageal strictures requiring another intervention. Data retrieved included their demographic profile, basic disease, type of stent placed, duration for which stent was kept in-situ, time interval for onset of dysphagia after stent removal, presence of tissue hyperplasia, site of stricture, number of dilations done, need for steroid injection or needle knife incision and the response to the therapy. The basic pathology in 6 patients (4 males) with age ranging from 27-77 years was Boerhaave’s syndrome (n=2), post-sleeve gastrectomy leak (n=2 ), caustic injury with perforation (n=1) and posttranshiatal esophagectomy leak (n=1). The stents used were Danis Ella® with shaft size 25 mm (n=2), Bona® stent with shaft size 18 mm (n=2) and Megastent® (Taewoong) with shaft size 28 mm (n=2). The stents were removed 6 weeks to 4 months after placement. In 1 of the patients, stent could not be removed, while one needed a SEMS in SEMS placement for removal. The onset of dysphagia ranged from 2 -4 weeks after stent removal while 1 patient had dysphagia within 2 weeks of stent placement because of stricture at upper end. However, only 3 patients had endoscopic evidence of tissue hyperplasia prior to stent removal. Strictures developed at lower end of the stent in 3 patients, at upper end in 2 while 1 had strictures at both upper and lower ends. The strictures were managed by serial dilations, requiring 2-8 dilatations, either by Savary Gillard dilator (5 patients) or CRE balloon dilator (1 patient). 1 patients required steroid injection while another required needle knife incision. On a follow up from 4-12 months, 4 patients are currently asymptomatic, while 1 patient is on serial monthly dilation and 1 patient is on self bougienage. Post SEMS stricture development can occur in patients with benign esophageal conditions even without the development of tissue hyperplasia. This complication should be recognized early and it can be treated successfully by serial dilation.

843 Verrucous Carcinoma of Esophagus: A Diagnostic Challenge Tarun Kukkadapu, MBBS, Bret Stysly, MD, Abul Rehman, MBBS, Sumanth Daram, MD. Georgia Regents University, Augusta, GA. Introduction: Verrucous carcinoma of esophagus (VCE) is a rare variant of squamous cell carcinoma; so far less than 23 cases have been reported in literature. VCE is a well-differentiated carcinoma that is slow growing, irregular and wart like in appearance and has a tendency for local invasion. Verrucous squamous cell carcinoma has been reported in the oral cavity, larynx, urogenital and anorectal regions. We present a case of VCE to highlight that high index of suspicion and evaluation with EUS are crucial steps in making an early diagnosis and management of disease. A 64-year-old man referred to our institution for further evaluation of dysphagia and esophageal mass on EGD. He presented with dysphagia to solids and 60 lb. weight loss over a period of 10 months. There was no history of alcohol or tobacco use or ingestion of caustic substances. He had hypertension, diabetes mellitus, and end stage renal disease requiring hemodialysis. Multiple endoscopic evaluations at outside facilities revealed an esophageal mass with inconclusive pathology; squamous atypia without definitive evidence for malignancy was reported.


At our institution, EGD and EUS were performed; conventional upper endoscopy revealed a 9cm long near circumferential obstructing mass with a warty/verrucous appearance. On endosonographic evaluation, diffuse thickening of the mucosa and sub-mucosa was noted with invasion through the muscularis propria, without any invasion of surrounding organs and no pathological lymph nodes were noted. Endoscopically obtained biopsy specimens using a jumbo forceps showed abnormally thick hyperplastic squamous mucosa with marked hyperkeratosis, cellular atypia, focal ulceration with heavy inflammatory cells and exhibiting verrucous growth pattern; suggestive of verrucous carcinoma. CT scan of thorax, abdomen and pelvis showed multiple hepatic lesions and lytic lesions in axial and appendicular skeleton suggestive of metastatic disease. EGD was repeated for new onset hematemesis, previously described long circumferential tumor was visualized; given the sub-optimal surgical candidature for palliation and the advanced metastatic disease, a partially covered self-expanding metallic stent was placed for palliation. Diagnosis of VCE is very elusive as is suggested by the current case as well as those described in the literature. A high index of suspicion on the basis of endoscopic features and EUS findings is helpful. Large biopsy specimens to include the sub-mucosa, such as those can be obtained by use of a jumbo forceps, are important for accurate diagnosis. The role of fine-needle aspiration (FNA) during EUS needs to be evaluated in cases with non-diagnostic pathology even with jumbo biopsy forceps.

844 Broncho-Esophageal Fistula: Diagnosed at Upper Endoscopy Reshi Kanuru, MD, Somashekar Krishna, MBBS, MPH, Peter Stanich, MD. Wexner Medical Center-The Ohio State University, Columbus, OH. Introduction: Dysphagia is a common symptom with a wide spectrum of potential etiologies. We report the presence of a benign broncho-esophageal fistula causing aspiration pneumonia that was not identified on initial imaging but was discovered during upper endoscopy. A 52-year-old male presented with respiratory distress and on review reported progressive dysphagia. He stated that over the past year he progressed from normal swallowing function to difficulty with swallowing pills and dysphagia with liquids. The frequency and extent of his symptoms continued to worsen more precipitously over the past three months and he now was unable to take in solids. He denied any difficulty initiating or completing swallows. Prior to the current admission, he developed shortness of breath after he tried to swallow his morning medications and was admitted to a local community hospital. He was treated for aspiration pneumonia. He developed sepsis and was briefly placed on pressors. He was transferred to our institution for further evaluation. A CT chest showed multifocal patchy opacities in both lung bases concerning for aspiration pneumonia without other identified abnormality. He then underwent an upper endoscopy that showed a defect in the middle third of the esophagus suspicious for a broncho-esophageal fistula secondary to active coughing when this area was examined. In addition there was a noted esophageal stricture measuring 1 cm in length with a 6 mm inner diameter just inferior to the fistula. A nasopharyngeal endoscope was able to traverse this stricture with no significant pathology noted in the remaining esophagus, stomach or small bowel. Biopsies of the fistula and stricture showed no evidence of malignancy. On secondary review of the CT scan, a defect was noted consistent with the suspected broncho-esophageal fistula. An esophagram was completed the next day that confirmed the fistula connecting the mid-esophagus to the proximal mainstem bronchus. An esophageal stent was placed over the fistula and his stricture was dilated. He was discharged after advancement of his diet. Two months later he underwent bronchoscopy showing that the broncho-esophageal fistula was reduced in size. Our case highlights the importance of endoscopy in evaluating dysphagia as many etiologies of dysphagia cannot be adequately identified on imaging. Even with the large number of patients who present with dysphagia, it is rare to identify a benign broncho-esophageal fistula with benign esophageal stricture as they are generally associated with malignant esophageal diseases and iatrogenic causes. Despite their rarity, a heightened suspicion is indicated in the clinical setting of aspiration pneumonia and esophageal dysphagia.

845 Lymphocytic Esophagitis: An Under-Recognized Entity by Gastroenterologists Ana Maria Crissien Martinez, MD, Walter Coyle, MD, FACG. Scripps Green Hospital and Clinic, San Diego, CA. Introduction: Lymphocytic esophagitis (LyE) is an uncommon, new clinical entity with an estimated incidence of 1/1000. It is becoming more widely recognized by pathologists but less so by gastroenterologists. We report 2 cases of LyE at our institution. The first is a 69-year-old female with a history of GERD, urticaria, HTN and rheumatoid arthritis evaluated for dysphagia with recurrent food impactions. Dexlansoprazole failed to improve her symptoms. Esophagram showed a barium pill retained at the C7 level without mucosal abnormality or external compression. On EGD her esophagus was narrowed and had concentric rings. Dilation was not performed as passage of the endoscope caused a mucosal rent. On histopathology, there was basilar hyperplasia with prominent lymphocytosis within the submucosa and the lower portion of the squamous epithelium. The second case is a 58-year-old female with a history of metastatic breast cancer and GERD status post Nissen fundoplication evaluated for progressively worsening dysphagia and new odynophagia. On EGD the mid-to-distal esophagus had a ringed appearance. She was dilated to 16.5 mm with a through-the-scope balloon with evidence of small mucosal rents. On histopathology she had squamous mucosa with peripapillary increased lymphocytes and spongiosis. Unlike the first patient she was not on a proton pump inhibitor. In both cases, symptoms had not recurred since their last EGD. LyE is defined as the presence of dense lymphocytic infiltrates in the peripapillary esophageal squamous mucosa (with lower numbers in the interpapillary fields) and marked spongiosis in the absence of significant numbers of neutrophils or eosinophils. LyE affects older women who present with dysphagia and odynophagia but GERD has been found to be unusual. Endoscopic findings suggestive of EoE have been reported in one third of patients diagnosed with LyE. Even though no definite clinical associations have been established in adults, studies agree that LE appears to be a disease localized to the esophagus, as biopsies taken from other GI sites have not shown increased lymphocytic infiltration. Initially there was believed to be an association with Crohn’s disease in children, but later studies have not found an association with inflammatory bowel disease. The pathophysiology of this entity remains


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unclear. In the largest series to date, most clinicians interpreted the histopathology of LE as somewhat equivalent to GERD. Increased awareness of this entity is required to better understand its natural history and long term implications, and to ultimately discover etiologic associations and therapies.

846 Endoscopic Mucosal Resection (EMR) for the Management of Solitary Extramedullary Plasmacytoma of the Esophagus Erik Rahimi, MD, Wayne Hofstetter, MD, Chelsea Pinnix, MD, PhD, Sheeba Thomas, MD, Sanam Loghavi, MD, L Jeffrey Medeiros, MD, Brian Weston, MD. The University of Texas MD Anderson Cancer Center, Houston, TX. Introduction: We present a first report of EMR for management of Solitary Extramedullary Plasmacytoma (EMP) of the esophagus. Case Report: A 50-year-old man with chronic intermittent dysphagia secondary to eosinophilic esophagitis (EoE) was referred for management of an incidental mid-esophageal mass which was biopsy proven to be an EBV+ plasma cell neoplasm. Extensive work-up for an underlying plasma cell dyscrasia including multiple myeloma confirmed this to be a solitary EMP. Endoscopic reassessment demonstrated an irregular sessile 1.0-1.5 cm mid-esophageal nodule at 25 cm. EUS showed a hypoechoic nodule involving the mucosa and submucosa with intact muscularis propria. The lesion was successfully resected by EMR using a multi-band mucosectomy device without submucosal injectate. The primary lesion was resected with a single band ligation although a second ligation was performed given a grossly close margin. No additional thermal ablation therapy was used. No endoclip closure was required. No immediate or delayed complications were observed. Pathologic and immunohistochemistry assessment was compatible with solitary EMP with marked expansion of the submucosa by sheets of large plasmacytoid cells without blastic appearance. Despite EBV+, there were no features of plasmablastic lymphoma. Peripheral and deep resected margins from the primary band ligation were free of tumor. Only 5-13% of EMPs occur in the gastrointestinal tract. Standard therapy for solitary plasmacytoma involving extramedullary sites involves definitive radiation therapy, followed by surgery if necessary with an overall good prognosis. Endoscopic management has not been well described given limited data. Only one prior case report has described successful endoscopic management of a subcentimeter mucosal EMP using endoscopic submucosal resection (ESD). However this technique is not yet widely performed and is associated with a higher risk for perforation. EMR is already widely used for the diagnostic and therapeutic management of mucosal and submucosal neoplastic lesions. EMR appears to be a feasible and less invasive alternative to radiation and surgery for select small, well defined EMP lesions limited to the mucosa and submucosa of the esophagus. EUS can help assess those lesions appropriate for EMR. Long term follow up of endoscopic treatment of solitary esophageal EMPs is needed. Surveillance EGD with biopsies will be repeated at three months. Repeat endoscopic management, radiation and surgery remain potential salvage therapeutic options.

847

[847B] Figure 2.

course was complicated by several episodes of hypotension and Hypoxia with Atrial fibrillation that was secondary to acute Pulmonary embolism. Throughout the hospital stay she had poor oral intake and complained of dysphagia so Esophagogastroduodenoscopy (EGD) was planned once her condition stabilized.EGD showed circumferential black discoloration of the whole esophagus worse in the lower third. Biopsies were not taken for the fear of esophageal perforation. The etiology of AEN is multifactorial, including ischemic insult due to any condition causing hypoperfusion, corrosive injury in the setting of esophago-gastroparesis and gastric outlet obstruction, and decreased function of the mucosal barrier in malnourished and acutely ill patients. Patients usually present with upper gastrointestinal bleeding, abdominal pain, vomiting and dysphagia. The hallmark on EGD is diffuse circumferential black mucosal discoloration in the distal esophagus that abruptly stops at the GE junction. Management includes treatment of the underlying illness, restoring hemodynamic stability, acid suppression with PPI’s to help mucosal healing and TPN. Complications include perforation, esophageal strictures and death with mortality approaching 32%. Acute esophageal necrosis is a rare entity with selective involvement of the esophagus. Timely diagnosis and treatment is crucial to improve survival in these patients.

Black Esophagus Dilhana Badurdeen, MD,1 Kenneth Brown, MD, FACG,2 Andrew Sanderson, MD,1 Adeyinka Laiyemo, MD2. 1. Howard University College of Medicine, Washington, DC; 2. Providence Hospital, Washington, DC. Introduction: The black esophagus, also known as acute esophageal necrosis (AEN) or Gurvits syndrome, is a rare clinical entity with a prevalence between 0.01%-0.2%. Our patient is an 86-year-old female with a history of diabetes, hyperlipidemia, hypertension and chronic kidney disease who was admitted with vomiting, diarrhea, and lethargy. At admission she was dehydrated with a sodium of 152 and creatinine of 3.2. She was treated for urosepsis and Clostridium difficile colitis. Her hospital

848 Hemoptysis Versus Hematemesis: Bronchoscopy or Upper Endoscopy? Rajesh Ramachandran, MD,1 Cherif El Younis, MD2. 1. SUNY Downstate Medical Center, Division of Gastroenterology and Hepatology, Brooklyn, NY; 2. Brookdale University Hospital, Brooklyn, NY. Introduction: Patients can occasionally present with anemia and bleeding of unclear origin. We present a case of a patient who was observed to have hemoptysis versus hematemesis. A 66-year-old male smoker and limited historian with a history of hypertension, dyslipidemia, traumatic brain injury, and emphysema was admitted to the hospital from neurology clinic after patient was found to have an episode of small volume hemoptysis. Since the patient was a heavy smoker, there was a high suspicion for lung cancer. CT scan of the chest showed moderate emphysematous changes, but no pulmonary nodule, pleural nodularity, or mass. On lung exam, the patient had bibasilar crackles with rhonchi. Labs revealed a normocytic anemia with hemoglobin of 8.8. Given that no obvious pulmonary etiology of hemoptysis was noted, there was no plan to pursue a bronchoscopy. The gastroenterology service was consulted after patient was noted to have a few additional episodes of small volume hemoptysis. The patient was never observed to have any hematemesis. He was noted to eat well, without obvious dysphagia or odynophagia. He did not have a history of NSAID use, and did not drink alcohol. The oral cavity did not reveal any evidence of tongue lacerations, gum disease, or bleeding oral ulcers. The patient remained hemodynamically stable. His stool did not reveal melena. Given the enigmatic nature of the patient’s anemia and his intermittent blood loss, a decision was made to perform an upper endoscopy. The EGD revealed an erythematous, ulcerated, friable area in the larynx that explained the etiology of the patient’s low grade hemoptysis. ENT service was consulted, and they performed a biopsy that revealed squamous cell carcinoma of the larynx. This case illustrates the need to consider non-pulmonary and gastrointestinal differentials in a patient that presents with questionable hemoptysis versus hematemesis. The consideration of an ENT malignancy was not a part of the differential diagnosis from either the pulmonary or the gastroenterological teams. Squamous cell carcinoma of the larynx is the most common head and neck cancer in Western countries. The larynx plays a key role for many essential functions, including breathing, voice production, airway protection, and swallowing. On further review of the patient’s symptoms, he did speak with a hoarse voice, and while this was noted in the consultation notes from multiple services, the symptom was attributed to long term smoking and possible reflux disease. This case highlights the fact that gastroenterologists should have a high suspicion for ENT malignancy in patients with blood per os that does not appear to be frank hematemesis.



| OCTOBER 2014

www.amjgastro.com

Abstracts 849

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Esophagitis Dissecans Superficialis as a Rare Clinical Manifestation of a Praneoplastic Syndrome

Incisional Therapy for Symptomatic Double Lumen Esophagus: A New Therapeutic Modality

Javed Sadiq, MD, Dimitrios Georgostathis, MD, Veronika Dubrovskaya, MD, FACG. SUNY Downstate Medical Center, Brooklyn, NY. Introduction: Esophagitis dissecans superficialis (EDS) is a rare finding that may present as part of a paraneoplastic syndrome. A 66-year-old female with no significant PMHx presented with new onset of ascites. Ascitic fluid was diagnostic for stage IV adenocarcinoma of unknown primary. Cancer markers were ordered and were notable for an elevated CA125 level with normal CEA and CA19-9 levels. Upper endoscopy was performed to rule out gastrointestinal malignancy. Upper endoscopy demonstrated normal stomach and duodenum. Endoscopic examination of the esophagus revealed active linear sloughing of the superficial mucosa of the entire esophagus, consistent with EDS (Figure 1). The patient denied any signs of dysphagia, odynophagia, GERD, or dyspepsia. Findings of EDS in this patient may represent a paraneoplastic syndrome from an occult malignancy. EDS is a rare endoscopic finding characterized by sloughing of large fragments of esophageal mucosal lining. Typical causes include medications (e.g. bisphosphonates, NSAIDs, potassium chloride), hot beverages, chemical irritants, celiac disease, collagen diseases and autoimmune bullous dermatoses. Close review of our patient’s social and medical history does not reveal any of the aforementioned precipitating factors. A review of the published literature brought up rare cases of paraneoplastic causes of EDS. The pathophysiology seems to be similar to that of paraneoplastic pemphigus. This case may represent as paraneoplastic EDS from occult malignancy.

Presidential Poster Harshit Khara, MD, Kimberly Fairley, MS, DO, Chuan Long Miao, MD, Amit Johal, MD, David Diehl, MD. Department of Gastroenterology & Nutrition, Geisinger Medical Center, Danville, PA. Introduction: Double lumen esophagus is a rare endoscopic finding with a handful of clinical cases described in the literature. Most of these patients were treated with conservative management involving acid suppressive therapy or esophageal dilation. With the advent of technology, we report a new management modality for symptomatic cases of double lumen esophagus. An 86-year-old male with gastroesophageal reflux disease (GERD), hypertension, coronary artery disease and diabetes, presented with history of recurrent dysphagia and meat impactions. EGD done at outside hospital showed esophagitis with distal esophageal stricture which was dilated up to 60 Fr Maloney bougie dilation. He was referred to our center for further management after aggressive treatment with oral PPI therapy. Upon repeat endoscopy, his esophagitis and esophageal stricture seemed to be improving but at the GE junction, he was found to have a mucosal bridge across the lumen creating a double lumen esophagus, leading into the cardia. This was appreciated both on forward and retroflexed views. Since the patient had failed medical management as well as repeated dilations, we decided to treat this mucosal bridge with incisional therapy. In order to prevent inadvertent bleeding, prophylactic endoclips, one at each end of the mucosal bridge, were placed first and then the bridge was incised with a needle knife using endocut settings. The endoclips stayed attached to each incised end. There were no procedure related complications and the patient recovered uneventfully and has not had any symptom recurrence at 9 month follow up. Incisional needle knife therapy for lumen-obstructing benign mucosal lesions should be considered as a first line treatment approach due to its one-step success rate. It would avoid repeated procedures related to gradual endoscopic dilation and help avoid persistent symptoms from conservative treatment options. Our patient not only presented with a unique endoscopic finding of double lumen esophagus, which is a rare complication of GERD, but was also successfully treated for it with a unique modality of incisional therapy which is reported for the first time for its treatment.

[849A] Figure 1. Esophagitis dissecans superficialis.

850 Lymphocytic Esophagitis: A Mystery Ankur Varma, MD,MPH,1 Yezaz Ghouri, MD,1 Pratap Singh, MD,1 Adeeb Dwairy, MD,2 Sushovan Guha, MD, PhD2. 1. Department of Internal Medicine, The University of Texas Health Science Center at Houston, Houston, TX; 2. Division of Gastroenetrology, University of Texas Health Science Center at Houston, Houston, TX. Introduction: Lymphocytic esophagitis (LE) is a histologic phenotype of esophagitis characterized by intraepithelial lymphocytes and spongiosis. It is diagnosed in one in a thousand patients who have esophageal biopsies for any reason. Its non-specific clinical and endoscopic presentation, makes it a diagnostic challenge for physicians. We hereby present a rare case of LE in a patient who presented with hematemesis. A 46-year-old male presented to the emergency room with sudden onset hematemesis, few hours after he had alcohol. BP was 155/95 mm of Hg, heart rate: 86 bpm, respiratory rate: 16 breaths/min and oral temperature of 98.1’ F; physical examination was unremarkable. Hemoglobin was 12.8 g/dL. Nasogastric suction revealed bright red blood. He was given intravenous rehydration and pantoprazole. Subsequently, he underwent an EGD which revealed a soft friable necrotic semi-circumferential mass with an adherent clot, suspicious for bleeding, in the mid-esophagus. The mass was biopsied. Argon plasma coagulation was applied to prevent further bleeding episodes. CT of the thorax and abdomen showed mucosal thickening of the mid to distal esophagus with no extra-esophageal lesions. Biopsy showed inflammatory exudates, squamous epithelium and rare minute aggregate of squamous cells with eosinophilic cytoplasm. Gross appearance of the mass was concerning for malignancy, so a repeat EGD was done 3 days later which showed endoscopic signs mimicking eosinophilic esophagitis (EoE) (“ringed” esophagus) along with disappearance of the soft friable mass, replaced by scar tissue. Random biopsies of the friable appearing mid esophageal region were taken . Histopathology showed infiltration of the squamous epithelium with lymphocytes, consistent with LE. The patient did not have any further episodes of hematemesis and was discharged on oral pantoprazole. A previous case report of EoE with similar presentation has been reported where eosinophilic infiltrate was believed to be associated with collagen deposition and subepithelial fibrosis (via TGF-B and IL-5 pathways) resulting in an esophageal mass (M. Fassan et. al, 2009; Endoscopy). Likewise LE could have similar lymphocyte mediated immune pathways which can explain the findings above. Our case adds a novel endoscopic finding to the emerging list of endoscopic features for LE and to the best of our knowledge this is the first case in which LE presented as an esophageal mass causing hematemesis.


[851A] Figure 1. Double lumen esophagus.

852 A Rare Case of Mixed Adenoneuroendocrine Carcinoma of the Esophagus John Anong, MD, John Litchfield, MD, Mark Young, MD, Thomas Borthwick, MD. Internal Medicine, East Tennessee State University, Johnson City, TN. Introduction: Most cancers of the esophagus are either adenocarcinomas arising from Barrett’s epithelium or squamous cell carcinomas from long-standing alcohol and tobacco abuse. Infrequently, tumors that arise in the esophagus stem from other tissues and these are usually primary cancers. Rarely, cancers can present in combination, either mixed or collision type tumors. One such phenomenon is esophageal mixed adenoneuroendocrine carcinoma (MANEC) which is exceedingly rare based on review of the literature. The pathophysiology is unclear and these tumors portend to very poor prognosis relative to other cancers. We herein present such a case. A 65-year-old male presented to our institution with progressive symptoms of dyspepsia and dysphagia. He had been a chronic smoker but had no prior history of radiation or alcohol abuse. Physical examination laboratory evaluation on admission revealed no pertinent abnormal findings. Initial evaluation barium esophagram revealed distal narrowing of the esophagus. Upper endoscopy was then performed and findings showed an irregular lesion with ulceration of the distal esophagus. Pathological examination and immunohistochemistry of a biopsy specimen confirmed adenocarcinoma of the esophagus with positive staining for Large cell neuroendocrine tumor; as such, the patient was diagnosed with MANEC of the esophagus. The patient was treated unsuccessfully with chemotherapy and is currently pending further work up. Our patient presented with a rare case of MANEC of the esophagus. To our knowledge, there are only three prior cases of MANEC reported in the literature. Indeed these cancers are extremely rare and as such recommendations for optimal management are lacking but surgery has been used in the past. Furthermore, these tumors have a very poor prognosis. Physicians should suspect MANEC in the setting of uncharacteristically rapid growth of previous esophageal metaplasia.


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CLINICAL VIGNETTES/CASE REPORTS - STOMACH

854 Gastric Diverticuli as a Cause of Obscure Gastrointestinal Bleeding

853 A Gastric Carcinoid and Fundic Polyps in a Patient on Chronic Proton Pump Inhibitor Therapy: A Diagnostic Challenge Veronica Baptista, MD, Anjali Basil, MD, Kaitlin Fitzpatrick, BS, David Cave, MD, PhD. Gastroenterology, UMass Memorial Medical Center, Worcester, MA. Introduction: Incidence of gastric carcinoid has risen from 2.4% to 8.7% over the past 3 decades. There are concerns about chronic proton pump inhibitors (PPI) use causing enterochromaffin-like (ECL) cell hyperplasia with increased gastrin levels and the development of gastric carcinoid tumors. We describe a case of fundic gland polyposis and gastric carcinoid associated with chronic PPI use. A 50-year-old woman with reflux had been on PPI for over 20 years. In 2008, upper endoscopy noted a few fundic gland polyps. In 2011, multiple 2-6-mm fundic gland polyps were seen. One of them appeared slightly more heterogeneous and erythematous, and was removed. Pathology revealed a well-differentiated gastric carcinoid with a mitotic index of 10%. Subsequent endoscopic ultrasound showed no residual lesions. Biopsies were negative for H. pylori infection. Gastrin level was mildly elevated at 105 pg/ml, vitamin B12 was normal at 369 pg/ml. She has done well since. Two cases of human gastric carcinoid tumors have been reported in association with hypergastrinemia leading to ECL hyperplasia induced by chronic PPI use of 10-13 years. In a study of sporadic Zollinger-Ellison Syndrome, ECL hyperplasia was noted in 99% cases, 7% with dysplasia. These occurred in the absence of atrophic gastritis, and with gastrin elevation less than 5 times normal. This suggests that chronic PPI use can lead to prolonged hypergastrinemia with the possibility of developing gastric carcinoid tumors. Our patient with over 20 years of PPI use has developed multiple fundic gland polyp related to PPI therapy. She has no evidence of chronic gastritis or pernicious anemia. Her gastrin level was minimally elevated. One can argue that she has spontaneous gastric carcinoid tumor, which is rare. However, as shown in other studies, ECL hyperplasia does not correlate with the degree of hypergastrinemia, and the progression of ECL dysplasia into carcinoid tumor from chronic low-level exposure to mildly elevated gastrin level in the setting of chronic PPI use has to be seriously considered. Chronic PPI use is a well-known cause of fundic gland polyps. Evidence also suggests a link between chronic PPI use and ECL dysplasia leading to gastric carcinoid formation. Patients on long-term PPI with fundic polyposis may need careful serial follow-up.

Jagpal Klair, MD, Arjun Vaid, MD, Shyam Dang, MD. University of Arkansas for Medical Sciences, Little Rock, AR. Introduction: Gastric diverticuli are a rare but life-threatening source of obscure gastrointestinal bleeding. Their insidious and sometimes catastrophic presentation underlies the need for increased awareness and prompt management. A 75-year-old white male presented with symptoms of pre-syncope and dyspnea on exertion after multiple episodes of melena. He denied hematemesis, abdominal pain, dysphagia, or NSAID use. His co-morbidities included hypertension, diabetes mellitus, and atrial fibrillation. On admission, he was hemodynamically unstable with a tachycardia of 120 beats/minute and systolic BP of 60 mm of Hg. His physical examination was remarkable for melena on digital rectal examination. Laboratory tests revealed a Hb of 6.2, INR of 5.7, and an elevated BUN of 71. He was administered intravenous fluids, large-volume blood and plasma transfusions, and started on a pantoprazole infusion. On transfer to the ICU, he underwent an emergent upper endoscopy (EGD) with a large amount of retained blood and no obvious source of bleeding seen. The fundus was not adequately visualized due to an inability to clear the blood clots. An emergent Nuclear Medicine bleeding scan did not reveal active blood loss. He remained transfusiondependent and subsequently underwent a second EGD. This revealed the presence of a gastric fundal diverticulum (Figure 1 a,b), about 1 cm in diameter, with no other source of bleeding identified. The patient was referred for surgical evaluation; however, his clinical status gradually improved and he was discharged to the medical floor. Due to an often dramatic and potentially fatal presentation, gastrointestinal bleeding secondary to gastric diverticuli (GD) requires a high index of suspicion. Some reports have indicated vague symptoms of burning sub sternal pain or nonspecific abdominal discomfort preceding the presentation; however, patients are mostly symptom free. Prevalence ranges from 0.04% on barium contrast studies to 0.01-0.11% on endoscopy. Surgical resection is advocated in the presence of persistent symptoms or with complications such as persistent bleeding or a perforation.

855 Proten Shakes: An Unusual Cause of Gastric Phytobezoar in a Health Obsessed Person Jagpal Klair, MD, Mohit Girotra, MD, Jonathan Dranoff, MD, FACG, Farshad Aduli, MD, FACG. University of Arkansas for Medical Sciences, Little Rock, AR.

[853A] Figure 1.

Introduction: Phytobezoars consist of components of indigestible plant and animal material, most commonly found in the stomach. They are usually asymptomatic, but may be brought to attention when become symptomatic with nausea, vomiting, abdominal pain, upper GI bleeding or in severe cases gastric outlet obstruction or perforation. Usual predisposing conditions include gastroparesis, hypothyroidism, other motility disorders and altered anatomy due to gastric surgeries or stomach ulcers. We present a case of gastric phytobezoar due to excessive intake of protein shakes. A 35-year-old man with no medical history presented for evaluation of gradually progressive abdominal pain and abdominal distention with occasional nausea, vomiting, early satiety and 10 lb. weight gain over 3 to 4 months. He led a healthy lifestyle, was a non-smoker, non-alcoholic, no history of illicit drug use and took no prescribed medications. His PCP obtained routine blood-work, thyroid panel, ultrasound and CT abdomen/pelvis which were unremarkable. He was referred for endoscopy (EGD) which revealed a large gastric phytobezoar extending from fundus to antrum of stomach, and gastric biopsies were unremarkable for any infiltrative process. Upon detailed discussion, he revealed his passion for exercising, intense gym regimen, high intake of protein shakes and other protein supplements over the past few months. It was hypothesized that protein shakes were probably making stomach contents stay for longer periods of time, decreasing gastric emptying and precipitating bezoar formation. Patient was advised to alter his diet by avoiding slow digestible substances like fiber, fruits and vegetables, while avoiding protein shakes, consumption of pineapple juice and coca-cola (assist in dissolving bezoars). Patient expressed strong interest in surgical removal of bezoar, but was appropriately counseled to try conservative measures. Repeat EGD was in 1 month revealed significant decrease in the size of gastric phytobezoar making endoscopic removal of residual phytobezoar possible. He remained asymptomatic thereafter on clinical follow-ups. Protein shakes consist of large proportions of protein content which takes longer to digest than carbohydrates, due to which food stays in stomach longer than usual. This effect is more pronounced with casein powder because casein is a very slow-digesting protein. This may precipitate undigested food hardening into solid



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Abstracts masses called bezoars. Our novel case intends to make physicians cognizant regarding this rare etiology of phytobezoars in modern day individuals, who often consume protein shakes and powders as health supplements to their exercise regimen, without understanding their possible adverse effects

856 Gastric Antral Web: A Case Series to Better Define a Rare Cause of Gastric Outlet Obstruction Neha Nigam, MD,1 Walid Chalhoub, MD,1 Dalia Abdelaziz, MD,1 Firas Al-Kawas, MD, FACG,2 Stanley Benjamin, MD, FACG1. 1. Medstar Georgetown University Hospital, Washington, DC; 2. Johns Hopkins Sibley Memorial Hospital, Washington, DC. Introduction: Gastric antral web (AW), or antral diaphragm, is a rare cause of gastric outlet obstruction (GOO). Etiology may be congenital or acquired from ulceration. We identified 33 patients with AW during 24,646 esophagogastroduodenoscopies (EGD) over a 7-year period (2006 to 2013). Only 4 cases (0.02%) presented with symptoms of GOO. Case 1: An 80-year-old female with dysphagia to solids and liquids and persistent vomiting underwent EGD with dilation of presumed pyloric stenosis without relief. Repeat EGD showed an obstructing AW. Sequential balloon dilation allowed passage of a 9.8 mm scope. Symptoms recurred in 2 weeks and the web was incised with needle-knife (NK). Case 2: A 72-year-old male with diabetes underwent EGD for a 10-year history of early satiety, intermittent regurgitation, and 100 lbs weight loss. Prior EGD with biopsy of antral “narrowing” was complicated by bleeding, but repeat showed an obstructing AW precluding passage of a 9-mm scope. Sequential balloon dilation from 8-15 mm was performed, allowing a 5 lbs weight gain in 2 weeks. Case 3: A 60-year-old female with dysphagia and nausea had an obstructing AW on EGD. Balloon dilation, 4-quadrant NK cuts, and steroid injection were performed without resolution of symptoms. Over a 5-year period, she underwent similar interventions with incremental improvement. Surgery was not offered. Case 4: A 74-year-old female with arthritis was admitted for 6 weeks of 10 loose, intermittently melenic, stools daily. Thickened antrum and pancolitis were noted on endoscopy. EGD performed after a 3-week steroid course showed an AW requiring a 6 mm scope to traverse. As per patient wishes, no intervention was performed. Cases 5 to 33: Twenty-nine patients were incidentally found to have a non-obstructing AW during EGD. Seventeen patients underwent EGD for gastroesophageal reflux not alleviated with long-term protonpump inhibitor use or presence of dysphagia, odynophagia, weight loss, or anemia. Twelve individuals were scoped for chronic abdominal pain, 2 of whom had melena of unclear etiology. Discussion: Non-obstructing AWs are incidental findings and frequently asymptomatic. Diagnosis is usually suspected during EGD, in which aperture size does not vary with peristalsis or ‘double bulb’ sign on upper GI series. Confirmation is made by demonstrating a normal pylorus distal to the AW. Symptoms of GOO are common with web aperture less than 1 cm. However, the association between GI bleeding when no other etiology is identified and reflux symptoms needs further study. Endoscopic balloon dilation is transiently effective. Endoscopic incision can be effective and safe in relieving symptoms, but repeat treatment may be needed. The role of surgery needs to be better defined.

857 Diarrhea With Severe Weight Loss Secondary to Gastrocolic Fistula (GCF) Don Esprit, MD,1 Nicholas Karamitsios, MD, FACG,2 Tokunbo Ajayi, MD,3 Nureddin Almaddah, MD3. 1. Internal Medicine, NSMC, Salem, MA; 2. North Shore Medical Center, Salem, MA; 3. North Shore Medical Center, Salem, MA. Introduction: Gastric resection for peptic ulcer disease has decreased over the past 2 decades and hence complications of surgery for peptic ulcer disease are seen less frequently in clinical practice. We report a case of a large GCF in a patient with a history of gastrectomy. Case Report: 54 year-old-female with a 30 pack year history of smoking, Billroth 11 gastrectomy for peptic ulcer disease and revision with a Roux-en-Y gastrojejunostomy for delayed gastric emptying presented with a 3-month history of severe weight loss and diarrhea. Her weight dropped from 130 lbs to 73 lbs. with passages of 10 to 20 watery pale stools a day, occurring 15 to 30 minutes after meals. She reported no melena or hematochezia nor vomiting. On examination, the patient was disheveled and emaciated (BMI 11.5). Vital signs were within normal limits. Mild periorbital edema was present. There was only mild abdominal tenderness and no organomegaly or ascites. There was 2+ pitting bilateral peripheral edema. Significant laboratory results: Complete blood count was normal. Basic metabolic profile was normal except for BUN 2 mg/dl, creatinine 0.2 mg/dl, albumin 1.5 g/dl, prealbumin 10 mg/dl, phosphorus 1.1 mg/dl. Stool specimen was negative. Gastroscopy revealed a large cleaned based gastric ulcer on the jejunal side of the gastrojelunal anastomosis with a severely stenotic jejunal orifice (1-2 mm opening); a large gastrocolic fistula (15 mm) which the scope easily traversed. Colonoscopy and ileoscopy were unremarkable except for the fistula which was identified in the transverse colon.The patient was placed on TPN and after 4 weeks underwent surgery with en bloc resection and primary anastomosis. Discussion: Gastrointestinal malignancies were reported previously as the most common causes of GCF. Recently, benign etiologies appear to be more common. These include complications of peptic ulcer disease and enteral feeding tubes. The most common presenting symptoms are diarrhea, weight loss and abdominal pain. Diagnosis is made by barium enema. Endoscopy are useful but may miss small fistulae. Treatment in most cases is surgical.


[857A] Figure 1. Gastroscopy revealing a large cleaned base gastric ulcer with a 2-mm stenotic jejunal orifice and a 15-mm gastrocolic fistula.

858 Acute Gastric Dysfunction After Catheter Ablation of Atrial Fibrillation Presidential Poster Alicia Alvarez, MD, Sandra Rodriguez, MD, Roger Charles, MD, FACG. Cleveland Clinic Florida, Weston, FL. Introduction: Gastroparesis is a chronic disorder characterized by slow gastric emptying in the absence of mechanical obstruction. Rarely, acute cases of gastroparesis can present as an extracardiac complication caused by vagus nerve injury following radiofrequency ablation for the treatment of refractory atrial fibrillation. Here, we report a case of acute delayed gastric empting as a consequence of percutaneous catheter ablation of atrial fibrillation. Case Report: A 47-year-old female underwent catheter ablation for drug refractory atrial fibrillation. No complications were detected during procedure and the patient was discharged after 24 hours. Seven days later, the patient was seen in the emergency department with symptoms of worsening fullness and abdominal distention. On admission, the patient denied any nausea, vomiting, and/or abdominal pain. Abdominal exam showed a non-tender but distended abdomen, bowel sounds were markedly decreased, and positive succussion splash during auscultation. The hematological profile, blood sugar, electrolytes, renal function, and LFTs were otherwise unremarkable. A CT of the abdomen showed severe distention of the gastric lumen containing heterogeneous congested material. However, there was not evidence of luminal obstruction, as contrast material was observed in the mid ileum. A scintigraphic 4-hour gastric emptying test (GET) was performed. Thirty-two percent of the meal was retained at the end of 4 hours (Normal 3 months. Conclusion: BBS is a serious but preventable complication. Patients should be educated to gently rotate and move the PEG about 1-2 cm once a day. The external portion should be monitored regularly and 2 cm of space should be allowed between the external bumper and skin.

Introduction: Cameron and Higgins first described Cameron lesions as linear gastric ulcerations or erosions in hiatal hernias in 1986. They can be associated with overt or occult gastrointestinal hemorrhage. Hypotheses regarding the pathogenesis include mechanical trauma to mucosa as the hernia slides through the diaphragmatic hiatus, pressure-induced mucosal ischemia at the diaphragmatic hiatus, gastric acid exposure, and lymphatic obstruction. We describe a 64-year-old woman with past medical history of anemia, pulmonary embolism (PE), and past alcohol abuse that presents with black stools and coffee ground emesis. Hemoglobin (Hb) on arrival was 14.6, and then went down to 10.8. Patient has a history of anemia first diagnosed at an outside hospital 3 years prior when she presented with a Hb of 4 with no overt gastrointestinal bleeding. She underwent multiple upper endoscopies (EGD) as well as colonoscopies, and capsule endoscopy over the last 3 years, all of which were normal. Despite treatment with iron supplementation and a proton pump inhibitor (PPI), she continued to have multiple admissions for symptomatic anemia with no cause identified. On this current admission, CT scan showed a large hiatal hernia, with most of the stomach present within the posterior mediastinum. Patient underwent EGD the following morning, which showed: normal esophagus, normal antrum and body, normal duodenum. 3 linear Cameron erosions that were friable to touch were seen in the hernial sac. Patient was placed on twice daily PPI and iron and referred to thoracic surgery. Cameron ulcers are an uncommon cause of severe UGI bleeding. Only a few reports about the clinical and endoscopic features of this lesion have been published. Our case confirms that Cameron ulcers can be a clinically significant cause of occult gastrointestinal bleeding. Cameron ulcers should be in the differential diagnosis of all patients with large hiatal hernias and severe anemia, whether overt or occult. Acid suppressants along with iron supplementation is the mainstay of treatment and surgery is reserved for refractory cases.

[866A] Figure 1.

[866B] Figure 2.

[865A] Figure 1.

867 A Rare Case of Hemorrhagic Gastritis Caused By Sevelamer-Induced Necrosis Syed Amer, MBBS, De Petris Giovanni, MD, Cuong Nguyen, MD. Mayo Clinic, Phoenix, AZ.

866 An Unusual Cause of Hematemesis: Buried Bumper Syndrome Anupam Aditi, MD, Aparajita Singh, MD, FACG. University of California, San Francisco, CA. Case Report: A 60-year-old man with embolic strokes presented with one day of hematemesis. A month prior, he underwent PEG placement for severe dysphagia. Exam revealed stable vitals and a non-tender abdomen. The PEG site was without erythema or drainage but the tube could not be rotated or advanced into the stomach. An upper endoscopy showed a deeply buried inner bumper in the gastric wall with raised epithelialized margins. Removal of the buried bumper was discussed but due to multiple comorbidities and development of pulmonary hemorrhage, the patient was managed conservatively. Given lack of tube dysfunction and no evidence of infection, the patient was reinitiated on PEG feeding. He continues to receive feeding through his PEG tube three months after the above presentation with no new PEG related complications. Discussion: BBS is a rare entity and occurs due to the overgrowth of gastric mucosa over the inner bumper of a gastrostomy tube. Vigorous tightening of the external bolster can lead to ischemic necrosis of the gastric wall and subsequent migration of the internal bolster into the gastric or abdominal wall. This can result in tube blockage, perforation, abscess or sepsis. Management of BBS is not standardized. Some have used endoscopic or surgical removal while others have left the PEG in situ and placed a second PEG


Case Report: A 64 year-old-male with history of ESRD, currently on hemodialysis presented with chief complain of nausea, bloody emesis and diffuse abdominal pain. His home medications were aspirin, hydralazine, gabapentin and sevelamer (4000 mg TID). He denied any history of NSAID use. On presentation, he was febrile, tachycardic and hypotensive. His labs were remarkable for Hb of 7.8, WBC of 10.3 and Cr of 7.7. The patient was resuscitated with normal saline and 1 unit of PRBC. CT abdomen showed pneumatosis with intramural air in the gastric fundus (Figure 1) Upper endoscopy revealed diffuse, severely friable mucosa in the gastric body, biopsy of which revealed pale yellow sevelamer crystals (Figure 2) deposited in the lamina propria of the body of the stomach. Sevelamer was discontinued and he was started on a low phosphate diet and a proton pump inhibitor. He was also advised to obtain a repeat EGD in 1 month. Discussion: Sevelamer is anion exchange resin used to treat hyperphosphatemia in patients with ESRD. On hematoxylin and eosin stain, the crystals are 2-toned in appearance with bright pink accentuations on a rusty yellow background. There is very little literature on the mechanism of sevelamer mediated gastric mucosal injury. Sodium polysyterene sulfonate, a cation exchange resin used to treat hyperkalemia, is known to cause mucosal ischemia and ulceration by direct toxicity. Being an exchange resin, it is likely that sevelamer crystals cause mucosal injury by a similar mechanism of direct toxicity. To our knowledge, this is the first reported case of hemorrhagic gastritis due to sevelamer induced necrosis in the literature.


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[867A] Figure 1. Pneumatosis with intramural air in posterior wall of the fundus of the stomach.

[868A] Figure 1. Attempt to break up the bezoar.

[867B] Figure 2. Hematoxylin and eosin stain of ulcer bed with sevelamer crystals.

868 Gastric Bezoar After Vagotomy and Billroth I Resection: An Intriguing Complication of a Historical Surgery Christine Boumitri, MD,1 Frank Gress, MD,2 George Abdelsayed, MD,1 Liliane Deeb, MD1. 1. Department of Medicine, Staten Island University Hospital, Staten Island, NY; 2. NewYork-Presbyterian Hospital/ Columbia University Medical Center, New York, NY. Introduction: Bezoars are collections of undigested food that accumulate in the GI tract. They could occur after gastric surgery due to low acid milieu and slow peristalsis. Vagotomy and Billroth resections are culprit surgeries. Patients are often asymptomatic or display symptoms indistinguishable from other GI disorders resulting in delayed diagnosis and potential complications. Case Report: 55-year-old man with vagotomy and Billroth I, 25 years ago presented with right upper quadrant (RUQ) pain, nausea and vomiting. Exam revealed RUQ tenderness. Chemistry revealed bilirubin of 1,4. Ultrasound showed gallbladder sludge and 7 mm common bile duct. HIDA, CT and MRCP were negative. Symptoms were attributed to biliary colic. A month later, pain recurred with vomiting of undigested food. Gastric outlet obstruction (GOO) was suspected. EGD revealed a large gastric bezoar. Fragmentation with a polypectomy snare failed due to hard consistency (Fig 1). Patient was referred for laparoscopic surgery where a 10x10x3 cm phytotrichobezoar was removed using an endobag (Fig 2). Patient did well thereafter. Discussion: Bezoars are a rare cause of GOO. They often present with vague symptoms. Large bezoars may lead to GOO, pressure ulcers and GI bleed. Recognition of highrisk patients and subtle clinical clues may assist in early diagnosis and prevention of complications. EGD is the test of choice and offers therapy like fragmentation or dissolution. If that fails, surgical extraction is recommended. Traditionally, bezoars were removed by laparotomy. Recently laparoscopic extraction through an anterior wall gastrotomy in an endobag, as in our patient, is slowly growing to be the intervention of choice.


[868B] Figure 2. Laparoscopic removal of gastric bezoar.

869 Inadvertent Gastric Stimulator Use During Pregnancy Avik Sarkar, MD,1 Brian Weiner, MD,1 Craig Rezac, MD,2 Sita Chokhavatia, MD, FACG1. 1. Rutgers - Robert Wood Johnson Medical School, Department of Internal Medicine, Division of Gastroenterology, New Brunswick, NJ; 2. Rutgers - Robert Wood Johnson Medical School, Department of Surgery, New Brunswick, NJ. Introduction: Gastroparesis is characterized by delayed gastric emptying in the absence of mechanical obstruction. The most commonly identified etiologies are diabetic and idiopathic. Symptoms include nausea, vomiting, postprandial fullness, bloating, weight loss, and abdominal pain. Gastric electrical stimulation (GES) may be considered in patients with refractory symptoms, particularly nausea and vomiting. Nausea and vomiting also frequently occur in pregnancy, with severe symptoms described


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as hyperemesis gravidarum (HG). Treatment options for HG are limited and mostly supportive. Safety for use of GES during pregnancy or delivery has not been established. All studies to date involving GES have current or planned pregnancy as an exclusion criteria. A 37-year-old woman with no past medical history was evaluated for epigastric pain, post-prandial nausea and vomiting. Extensive workup revealed markedly delayed solid phase gastric emptying on scintigraphy (EGD, CT abdomen and laboratory tests were normal). Dietary modification, erythromycin, metoclopramide, prochlorperazine, ondansetron, and pantoprazole provided only marginal symptom relief. The Enterra gastric stimulation system, an IRB approved humanitarian use device (HUD) at our institution, was implanted to treat refractory idiopathic gastroparesis. Patient’s vomiting frequency had significantly decreased within the first week. Prior to device implantation, she had been counseled on contraception and stated no current desire for pregnancy. Patient continued to do well at each of her 3 follow-up visits post-implantation. She missed her next appointment and a letter detailing the importance of follow-up was sent. She returned 6 months later (12 months from implantation) and was noted to be 14 weeks pregnant. Patient reported no gastroparetic symptoms but the Enterra system was turned off per manufacturer recommendations. Within the next 2 weeks, she noted worsening abdominal pain, post-prandial nausea, vomiting and weight loss despite medical treatment. Hyperalimentation therapy was initiated but she remained with continued symptoms for the remainder of her pregnancy. She had a planned Caesarean section at 39 weeks and delivered a healthy boy. Due to persistence of symptoms, the HUD was restarted at 1 week post-partum. To our knowledge, this is the first reported case of GES during pregnancy. Although inadvertent, our patient had no symptoms of gastroparesis or HG in the first trimester while the gastric stimulator was on. Further studies may be warranted to investigate safety of GES in pregnancy, especially in the subset of patients that have gastroparesis and hyperemesis gravidarum. Disclosure - Dr. Rezac - Speaker: Intuitive Surgical Inc.

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871 16-Year-Old Female With “Watermelon Stomach”? Amandeep Singh, MD,1 Anwaar Khan, MD, FACG,2 Robert Krall, MD,2 Zafar Mirza, MD, FACG2. 1. Crozer Chester Medical center, UPLAND, PA; 2. Olean General Hospital, Olean, NY. Introduction: Gastric antral vascular ectasia (GAVE) also known as “watermelon stomach” (WS) is an uncommon cause of gastrointestinal blood loss. It typically presents in middle aged females. We are presenting a case of GAVE at an unusually early age with atypical symptoms. Case Report: A previously healthy 16-year-old Caucasian female presented to the emergency department with a 1 month history of upper abdominal pain. She had no accompanying fever, nausea, vomiting or weight loss. Physical examination showed tenderness in the epigastric and right upper quadrant region. Complete blood/laboratory data showed normal cell counts, chemistry and liver function tests. Upper abdominal ultrasound showed gallbladder stones without any acute process. Upper endoscopy showed incidental findings of linear striae in the antrum indicative of GAVE. H.pylori was negative on biopsy. Histology showed mild chronic inflammation with few lymphocytes, plasma cells, dilated capillaries and venules. The patient eventually underwent cholecystectomy for her likely biliary colic. Discussion: GAVE is a poorly understood but treatable entity and an increasingly identifiable cause of chronic iron deficiency anemia or acute or occult upper gastrointestinal bleeding. It typically presents in middle aged and older females. The pathophysiology of GAVE remains unclear. Watermelon stomach (WS) as described above is an endoscopic finding of the longitudinal antral folds containing visible columns of tortuous red ectatic vessels (watermelon stripes), pathognomonic for WS. Treatment options for WS include endoscopic, pharmacologic, and surgical approaches. Endoscopic interventions including argon plasma coagulation and endoscopic band ligation are usually used when patients become severely transfusion dependent or there is evidence of any upper GI bleed. Failure to recognize GAVE can result in delayed treatment for years. Our patient with GAVE was unusually young and was diagnosed incidentally. Due to lack of anemia on laboratory examination we elected to monitor her clinically for any future development of anemia.

Unusual Presentation of a MALT Lymphoma as a Gastric Submucosal Mass Grace Yang, BA, MBS, Amy Tilara, MD. Rutgers Robert Wood Johnson Medical School, New Brunswick, NJ. Introduction: MALT lymphomas are the most common type of primary gastric lymphomas. Gastric MALT lymphomas tend to display indolent behavior, and usually present as a localized invasion of the mucosa with potential involvement of deeper layers of the stomach wall. It is rare to see MALT lymphoma present as an isolated submucosal gastric mass without involvement of the mucosa. Case Report: A 61-year-old female with no significant past medical history presented 7 months after a work-up for complaints of melena and hematemesis at an outside hospital and was found to have an obstructing distal subepithelial gastric mass with ulcerations and gastritis on EGD. Biopsies showed mild acute and chronic inflammation negative for H. pylori. An EUS FNA was completed at the outside institution, but the FNA was nondiagnostic. She was then referred to our institution for EUS and further evaluation. CT chest/abdomen/pelvis revealed a 3.6 x 2.1-cm gastric antral submucosal mass at the posterior wall. Upper endoscopy revealed a large subepithelial mass in the prepyloric antrum without bleeding. A heterogeneous round well-defined mass was identified endosonographically in the prepyloric region of the stomach arising from the submucosa without associated lymphadenopathy. FNA was then completed with a 22-gauge needle, and the specimen was sent for cytology and flow cytometry. In order to obtain more tissue for diagnosis, a 1-cm incision into the mass was then made with the needle-knife using a free hand technique. Jumbo biopsies were then taken from the submucosal tissue from the incisional site. An Endoclip was placed over the incision with good result. Biopsies from the submucosal lesion showed morphology and immunophenotype consistent with a marginal zone lymphoma. FNA of the submucosal mass showed an atypical lymphoid infiltrate. FISH showed the presence of t(11;18). A monoclonal kappa light chain expressing population of cells was positive for CD20/CD19 and negative for CD5/CD10. She was then referred for definitive radiation therapy after H.pylori treatment. The patient tolerated radiation therapy well, and complaints of abdominal pain, nausea, and vomiting resolved. A follow-up EGD with EUS exhibited that the submucosal lesion had resolved. Discussion: While MALT lymphomas are the most common primary gastric lymphomas, their presentation as a localized gastric submucosal mass remains extremely rare. The diagnosis of MALT lymphoma by endoscopic mucosal biopsy alone became challenging in this case due to the unusual presentation as a submucosal mass. Therefore, EUS with FNA and incision of the mass for deeper biopsies provided the most accurate diagnosis and may become an important way to evaluate submucosal gastric lesions.

872 A Case of Varicella Zoster Hemorrhagic Gastritis Kaartik Soota, MD,1 Brandon Sprung, MD,2 Aaron Huber, MD,2 Thomas Werth, MD, FACG2. 1. Unity Health System, Rochester, NY; 2. University of Rochester, Rochester, NY. Introduction: Hemorrhagic gastritis secondary to Varicella zoster virus (VZV) is rarely identified in immunocompromised patients, and we report such a case from our experience. An 82-year-old female with chronic lymphoid leukemia receiving chemotherapy, presented with 1 week of anorexia, abdominal pain, nausea and vomiting. Lab evaluation was significant only for thrombocytopenia, and abdominal CT scan was unrevealing. Her symptoms persisted despite hydration and pain control, and on hospital day 5 she developed worsening thrombocytopenia with transaminemia and leukocytosis. Viral hepatitis panel including HSV, CMV and EBV was negative, as was an abdominal ultrasound with doppler. An upper endoscopy performed to evaluate her symptoms revealed small, hemorrhagic, irregular shallow ulcerations and erosions throughout the stomach (Figure 1A). A diffuse vesicular rash developed on hospital day 10, and acyclovir was initiated empirically. Multi-organ failure rapidly ensued, and care was withdrawn. The endoscopic biopsies later revealed epithelial hemorrhage, ischemia and nuclear viral inclusions with a strongly positive immunohistochemical stain for VZV, consistent with acute hemorrhagic gastritis due to VZV (Figure 1B). Viral swab of a skin lesion was positive for VZV by PCR. Discussion: To our knowledge, this is one of a few cases of VZV hemorrhagic gastritis confirmed by endoscopic biopsy and PCR of cutaneous lesions. Reactivation of VZV is common in immunocompromised patients, usually presenting as a cutaneous eruption of vesicles. Rarely, visceral and gastric involvement can occur, usually concurrent with a hematologic malignancy and disseminated cutaneous involvement. The vesicular eruption can be absent initially and be first observed up to 10 days after abdominal symptoms develop. Presentation of visceral VZV is non-specific and may be characterized by nausea, vomiting, and abdominal pain with possible development of gastrointestinal hemorrhage, pancreatitis and hepatitis. While endoscopic evaluation is often unrevealing, gastrointestinal mucosal involvement can occur in the form of gastric ulcerations or punctate hemorrhages. Treatment is with antivirals. A high clinical suspicion is important to recognize this condition early in the proper clinical setting, as mortality rate can be 40-50%.

[872A] Figure 1. (A) Hemorrhagic, ecchymotic shallow ulcerations and erosions with exudate. (B) Immunohistochemical stain for VZV demonstrates diffuse and strong positivity within viral inclusions.



| OCTOBER 2014

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Abstracts 873 Gastric Adenocarcinoma Presenting as a Solitary Metastatic Bone Lesion in the Scapula Larry Carter, DO, Jennifer Phemister, MD, Pranav Patel, MD, Chakradhar Reddy, MD, Mark Young, MD. East Tennessee State University, Johnson City, TN. Introduction: It is well known that most patients with gastric adenomcarcinoma in the United States already are symptomatic and have advanced incurable disease at the time of diagnosis. The most common sites of metastasis are liver, peritoneal surfaces, and nonregional or distant lymph nodes. However, gastric adenocarcinoma with bony metastases is uncommon and it is even rarer to have solitary bone metastases as the presenting sign at the time of diagnosis. A 76-year-old male that presented to his primary care with a chief complaint of right shoulder pain. The pain would wax and wane, but progressively became more persistent. He was treated with non-steroidal anti-inflammatory drugs initially with no relief. He was referred to an orthopedist that treated the patient with oral steroids and steroid injections with only partial relief. He subsequently was sent for evaluation with an MRI of the right shoulder that revealed a mass destroying the scapular spine and invading the adjacent soft tissues. The mass measured 2.7 x 3.0 x 2.1 cm. He then went for a CT guided biopsy of the mass and pathology revealed poorly differentiated adenocarcinoma that stained positive for cytokeratin 7. CT scan of the chest, abdomen, and pelvis revealed a cavitary mass in the left upper lobe of the lung as well as a right middle lobe nodule. He underwent transbronchial biopsies of the left upper lobe lung mass that revealed only benign cells. Given the high index suspicion for an upper aerodigestive disease primary the patient was referred to gastroenterology for a possible upper endoscopy to evaluate for a gastric primary. EGD was performed and a 2-3 cm mass in the body of the stomach was found and multiple biopsies were taken. Pathology revealed invasive, moderately differentiated gastric adenocarcinoma that stained positive for cytokeratin-7. Most bony metastatic lesions are found concomitantly with other more common sites of metastases. However, there is only a scant amount of data that have shown solitary metastatic bony lesions at presentation. Furthermore, it seems that bony metastases from gastric adenocarcinoma has a propensity for spread to flat bones. Interestingly, in this patient he presented with metastases to the scapula. Finally, bony metastases in gastric adenocarcinoma carries a poorer prognosis compared to other primary malignancies with bony metastases.

colitis. Subsequently, the patient improved after cessation of this drug. Previously, collagenous colitis has been divided into 2 types: type 1 in young people with nodular gastric mucosa and anemia. Type 2 has erythematous gastric mucosa in middle aged to elderly people and is associated with collagenous colitis. Our patient had significant overlap as she had erythematous gastric mucosa then nodular mucosa later along with colitis. Many medications have been linked to collagenous colitis, and olmesartan is the only medication linked to collagenous enteritis. Collagenous gastritis, however, has not been previously linked to any medications. The mechanism of action for olmesartan to induce the enteropathy is unknown, but the presence of HLA-DQ2 might predispose patients to developing it. Although causality cannot be definitively proven in this case, the resolution of her symptoms after stopping olmesartan supports an association.

[875A] Figure 1.

874 Metastatic Non-seminomatous Germ Cell Tumor (Choriocarcinoma) Presenting With Hematemesis and a Gastric Mass S. Bashar Almadani, MD, MPH,1 Sohrab Mobarhan, MD,1 Shriram Jakate, MD2. 1. Rush University Medical Center, Division of Digestive Diseases, Chicago, IL; 2. Rush University Medical Center, Department of Pathology, Chicago, IL. Introduction: Approximately half of the patients with nonseminomatous germ cell tumors (NSGCT) present with disseminated disease, typically to the retroperitoneal lymph nodes and, less frequently, lungs, liver, and brain while GI involvement remains extremely rare. We report a rare case NSGCT presenting as gross hematemesis. Case Report: A-34 year-old man with no significant past medical history presented with an intracranial hemorrhage. Prior to admission, he had reported hematemesis daily for the prior 2 weeks as well as hematochezia and dark stools. He denied any abdominal pain. He was not on any medications and had no allergies. Family history was unremarkable for malignancy. On exam, he was hemodynamically stable, but somnolent. Chest x-ray as concerning for multiple mass-like opacities suspicious for metastatic disease. Head imaging was remarkable for a large posterior lobe hematoma and evidence of midline shift and herniation. He was taken for urgent craniotomy and hematoma evacuation and found to have a mass which was resected. Ultrasound of the scrotum showed a large heterogeneous solid part cystic mass replacing the right testicle and bHCG level was > 275,000 MIU/mL. GI was consulted given the history of possible hematemesis. Hemoglobin on admission was 9.7 (prior baseline unknown), however INR, MCV, RDW, and iron studies were normal. BUN/Cr was normal as well and no overt bleeding had been noted. He was started on an empiric PPI continuous infusion and EGD was performed and revealed a 2 cm firm, exophytic, polypoid, friable, umbilicated mass (Figure 1) in the antrum just proximal to the pylorus. It was biopsied multiple times and then prophylactically injected with diluted epinephrine and hemoclips. Pathology revealed pleomorphic tumor cells including cytotrophoblasts and multi-nucleated syncytiotrophoblasts and was strongly positive for B-HCG on immunohistochemistry staining (Figure 2), consistent with metastatic choriocarcionoma. He underwent right radical orchiectomy with plans to initiate chemotherapy. Discussion: Extragonadal metastatic involvement is commonly found in brain, bones, and liver. Gastric involvement, however, is exceptionally rare. In a study of 990 testicular tumors, fewer than 5 were associated with GI metastasis. The prognosis of patients with GI metastases in NSGCT is generally quite poor and, in the case of choriocarcionoma, typically results as a result hematogenous spread and portends poorly due to its rapid proliferation and excessive vascularity. These patients are at risk of significant morbidity and mortality from GI bleeding as a result of necrosis resulting from chemotherapy as well and merit close follow up and a low threshold for intervention.

[875B] Figure 2.

875 Olmesartan-Induced Collagenous Gastritis, Duodenitis, and Colitis Robert Taylor, MD,1 Casey Chapman, MD2. 1. Internal Medicine, LSU - Baton Rouge, Baton Rouge, LA; 2. GI Associates, Baton Rouge, LA. Introduction: Collagenous gastritis is a rare, possibly under recognized entity with histological similarities with collagenous sprue and collagenous colitis. It was first reported in 1989 by Colletti and Trainer. Due to having a nonspecific presentation, lack of clear etiologies and no specific treatment recommendations, it is a difficult pathologic result to find. We present a case of a 53-year-old female who developed collagenous gastritis and duodenitis 1 to 2 months after starting olmesartan then delayed collagenous


[875C] Figure 3. The American Journal of GASTROENTEROLOGY

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876 Blurry Vision in Patient With Watery Diarrhea: Serendipitous Diagnosis of Neurocysticercosis Javier Lopez Moncayo, MD,1 Normi Dessalines, MD,1 Sita Chokhavatia, MD,2 Salman Muddassir, MD1. 1. St Francis Medical Center, Hamilton, NJ; 2. Robert Wood Johnson University Hospital, New Brunswick, NJ. Introduction: Neurocysticercosis, also known as disease of swine, is a common helminthic infection estimated to occur in 50,000 people worldwide. In 2013, 148 cases from United States were reported to the WHO. Humans become intermediate hosts of Taenia solium by ingesting its’ eggs from contaminated food specially undercooked pork. Common presentations of gastrointestinal involvement are abdominal pain, nausea, diarrhea or constipation which arise within 6-8 weeks after cyst ingestion. Neurologic symptoms including headaches and seizures may precede GI symptoms. A 26-year-old Guatamalan male without past medical history had lived in the U.S. for 13 years. He had not traveled abroad during this period. He was evaluated in the ED for a 3 day history of severe headaches, nausea, nonbloody emesis and watery diarrhea. Symptoms accompanied by blurry vision. On enquiry, he had suffered from headaches for over 2 years but these had not been associated with visual symptoms, fever, back pain, paresthesias, seizures, or a skin rash. He did not have recent exposure to sick contacts or animals. Physical examination including neurologic and fundoscopic exams were unremarkable except for mild diffuse abdominal tenderness. Laboratory data including CBC, CMP, ESR, HIV and viral hepatitis serologies, urine toxicology were all negative. Head CT scan detected low attenuation in the paramesencephalic cistern, along the basilar cisterns and extending into the left sylvian fissure reported as suspicious for gelatinous pseudocysts of cryptococcal meningitis. MRI imaging showed cerebral calcifications with multiple cystic lesions with widening of the left sylvian fissure and prominent lateral ventricle with the floor of the third ventricle depressed into the sella turcica suggesting a communicating hydrocephalus secondary to racemose neurocysticercosis. Serum ELISA for cysticercus antibody was weakly positive (>0.90). Stool tests were negative for ova and parasites. Cryptococcal antigen was negative. Dexamethasone, albendazole and antiseizure prophylaxis medications were initiated to treat neurocysticercosis. At two month follow up, patient was doing well with resolution of GI symptoms and improved vision. Taeniasis continues to be a serious public health problem especially in patients from Mexico, Guatemala and Peru. A high index of suspicion for neurocysticercosis is important in patients from these endemic areas who present with persistent GI and neurologic symptoms. In addition to praziquantel or albendazole, neurocysticercosis treatment includes supportive therapy with corticosteroids and seizure prophylaxis. Taeniasis is one of the top neglected tropical diseases of this decade whose eradication is a current challenge of the WHO.

[877B] Figure 2.

in primary cancers of the lung, breast, prostate, bladder and kidneys, among others. Bone metastasis from gastric cancer is quite rare, with a variable incidence of anywhere from 1% to as high as 20% seen on autopsy studies. Prognosis of gastric cancer with bone involvement is particularly poor. The incidence of gastric cancer with bone involvement is low, and therefore, treatment modalities have yet to be established. This case demonstrates the need for a wide differential diagnosis even in regards to common complaints in otherwise healthy-appearing patients.

877 A Rare Cause of Back Pain: Metastatic Gastric Signet Ring Cell Adenocarcinoma Jason Rubinov, MD, Sunny-Skye Keppel, MD, Jonathan Mazurek, MD, Jonah Shulman, MD, Gil Ascunce, MD, FACG, Gabriel Levi, MD. Mount Sinai Beth Israel, New York, NY. Case Report: A 60-year-old female with a past medical history of COPD presented with recurrent back pain over several months. Physical exam was notable for morbid obesity, lumbar paraspinal tenderness, and decreased motor strength and sensation in bilateral lower extremities. Lab analysis was significant for a 5-fold elevation in alkaline phosphatase (750 U/L). CT scan of the lumbar spine revealed a large lytic lesion involving the L2 vertebral body with associated compression of the thecal sac. Lytic lesions were also noted in the right sacrum and right iliac bones. A biopsy of the L2 lesion was performed which returned as metastatic signet-ring cell adenocarcinoma. The patient underwent an endoscopy which showed a 20 mm gastric ulcer in the anterior wall of the gastric body with a clean base. Biopsy of the ulcer revealed poorly differentiated invasive adenocarcinoma, with signet ring features. Giemsa and H&E stains were positive for Helicobacter pylori. The patient was eventually discharged to receive chemotherapy with palliative intent. Discussion: We present a case in which a common complaint of back pain was found to be caused by atypical metastatic spread of a signet ring cell gastric adenocarcinoma. Bone metastasis typically occurs

878 Ovarian Cancer Metastatic to the Stomach: A “Reverse Krukenberg” Tumor John Guido, MD, Peter Stanich, MD, Edward Levine, MD. Ohio State University Wexner Medical Center, Columbus, OH. Introduction: Gastric cancer is a common cause of mortality in the United States, but metastatic tumoral involvement of the stomach is rare, with an estimated prevalence of 0.7-5.4% of all gastric malignancies. Breast, lung, esophagus, and malignant melanoma represent the most common primary sites. Metastatic ovarian carcinoma comprises less than 2% of all secondary gastric cancers. Case Report: A-52 year-old female with a past medical history of metastatic serous epithelial ovarian carcinoma was admitted with a 1 week history of dull epigastric pain, nausea with small volume hematemesis, dark stool output from her colostomy, and fatigue. Her course had been complicated by perforation of the splenic flexure due to tumor invasion 2 months prior to presentation and she was status-post cytoreductive surgery and transverse loop colostomy. Laboratory testing showed her hemoglobin to be 6.5 g/dL, compared to 11.1 g/dL 1 week prior, and fecal occult blood testing was positive. CT scan showed significant thickening of the gastric wall as well as a peritoneal fluid collection adjacent to the greater curvature. Given her presentation gastroenterology was consulted to evaluate for acute gastrointestinal bleeding. She underwent EGD with findings of LA Grade A esophagitis as well as extrinsic compression on the stomach with overlying erythema and granularity of the mucosa in the gastric body. Multiple biopsies were taken and were pathologically shown to contain focal atypical glands suggestive of metastatic ovarian carcinoma. The atypical cells were located near the base of the biopsy, coursing through the muscularis mucosae with an infiltrative configuration. Immunophenotyping showed AE1/3, CK7, and PAX8 positivity and CK20 negativity, consistent with a tumor of Muellerian origin. Her bleeding resolved with PPI therapy and she was restarted on palliative chemotherapy. Discussion: Although rare, ovarian metastases to the stomach need to be on the differential diagnosis in the proper setting. This likely occurs through malignant ovarian cells being disseminated throughout the abdominal cavity by peritoneal fluid. Luminal tumor invasion begins at the serosa and progresses inward to the mucosa as shown by the pathology in our case. Diagnosis is made by endoscopy and biopsy. Immunohistochemical staining can be used in cases where it is difficult to differentiate ovarian from gastrointestinal origin, as serous ovarian carcinomas are often CK7 positive and CK20 negative, whereas gastrointestinal carcinomas tend to be CK7 negative and CK20 positive.

879 Intra-abdominal Myxoid Liposarcoma as a Cause of Isolated Gastric Varices Daniel Eshtiaghpour, MD, Xi Chen, MD, Ann Pham, MD, Anuj Datta, MD, Sofiya Reicher, MD, Viktor Eysselein, MD. Harbor UCLA Medical Center, Torrance, CA.

[877A] Figure 1.


Introduction: Gastric varices are present in 20% of patients with portal hypertension and may occur with esophageal varices. Gastric varices have a comparatively reduced risk of bleeding (incidence 25% in 2 years) but have higher rates of rebleeding and mortality.


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Abstracts Liposarcomas are the second most common soft tissue sarcoma in the U.S. with myxoid as the most common variant. These low-grade tumors generally present in the fourth to fifth decade as a large mass in the extremities. We report a case of bleeding from isolated gastric varices (IGV) caused by intra-abdominal myxoid liposarcoma. A 46-year-old female with history of gastric varices, and anemia status post 7 units pRBC presented with fatigue and melena as well as headache and chest pain. Physical exam was unremarkable except for a small amount of black stool on rectal exam. CBC showed Hgb 4.7 with MCV 74.6, platelets 193, and comprehensive metabolic panel, LFTs, and coags WNL. Her Hgb improved to 6.6 after 2 units of pRBCs and octreotide and protonix drips. EGD found significant bleeding from multiple large IGV and antral erosions but no esophageal varices. CT revealed a 10.5x10x10.1 cm lobulated mass between the stomach, spleen and pancreatic tail with perigastric varices. The splenic artery and vein were encased by the tumor and the splenic vein did not opacify suggestive of obstruction/thrombosis. A hyperdense lesion was seen in the R liver lobe. After 2 more bleeding events requiring transfusion of 6 units pRBC and ICU care, splenic artery embolization was performed. CT-guided liver biopsy diagnosed myxoid liposarcoma. IGV are subclassified by location: type 1 are fundal and type 2 are ectopic in the antrum, corpus and pylorus. Both gastric and esophageal varices can be a consequence of portal hypertension, however IGV can also result from splenic vein pathology. IGV do not respond well to the therapeutic modalities used for esophageal varices ligation but can respond to endoscopic variceal obturation, splenectomy, or splenic artery embolization. This case demonstrates the challenges of managing IGV as they are not a homogenous entity and tend to be more life-threatening compared to esophageal varices, with greater severity of bleeding, higher risk of rebleeding (34-89%) and higher mortality. Risk factors include fundal location, presence of red spots, advanced Child’s score and large size. This is an unusual presentation of myxoid liposarcoma which is characterized by translocation t(12;16)(q13;p11), consists of mesenchymal cells and lipoblasts, typically involves the lower extremities and has a 30% local recurrence rate and distant metastasis. Treatment is based on the extent of disease and includes surgery/ radiation or chemotherapy.

880 An Atypical Manifestation of SLE Waheeb Ahmed, MD, Muhammad Zulqarnain, MD, Alicia Findlay, MD, Bishara Rizvi, MD, Asha Chakka, MD. Internal Medicine, Canton Medical Education Foundation, Canton, OH. Introduction: We describe a rarely reported GI manifestation of SLE: gastroparesis. Case Report: A 51-year-old African American woman with the past medical history of gastroesophageal reflux disease (GERD), idiopathic thrombocytopenic purpura, hypertension, iron deficiency anemia, rheumatoid arthritis, and SLE presented to the ER with 3 days of nausea and vomiting. She was unable to keep any food down. She also complained of abdominal distension, and 9/10 abdominal pain. Bowel habits were normal and she had no fever. She had presented 16 days prior with similar history, along with dehydration and acute kidney injury. During that admission, she also complained of dysphagia prompting a GI referral, esophagogram, and upper GI endoscopy were done which were consistent with moderate-severe GERD. An EGD was performed which showed mild gastroparesis. A provisional diagnosis of viral gastroenteritis was given at that time. During the following admission, a gastric emptying study (GES) was performed demonstrating mild gastroparesis, with more than 66% residual after 2 hours. Her medications did not include any associated with gastroparesis. Surgical causes were ruled out and the patient’s dominant symptoms were thought to be due to the gastroparesis. The duration of the symptoms prompted suggestion of a sub-acute cause, in this case SLE gastroparesis. ReglanTM and ProtonixTM were given to address the patient’s symptomatology. Conclusion: Discussion: Gastroparesis is characterized by delayed gastric emptying in the absence of mechanical obstruction, causing nausea, vomiting, early satiety, bloating, and or upper abdominal pain. The etiology of gastroparesis includes diabetes mellitus, post viral syndrome, medication side effects, postsurgical, neurological, autoimmune, and mesenteric ischemia. Determining the etiology in a patient with SLE is complicated as several of the above mentioned potential etiologies may be present at the same time. Nearly one-third of patients with gastroparesis the cause is idiopathic. In our patient all the usual causes of gastroparesis were ruled out, so it was suggested that she developed this secondary to SLE. Therefore any patient who has SLE with gastrointestinal symptoms, a differential diagnosis should include gastroparesis. SLE as a cause for gastroparesis has been described in literature, but only one case has been reported so far to the best of our knowledge. Current treatment modalities for gastroparesis include dietary modifications such as small meals, prokinetic agents such as metoclopramide and erythromycin, antiemetics, antidepressants, and gastric electrical stimulator implantation in refractory cases.

881 A Rare Case of Squamous Cell Carcinoma of the Stomach Mark Pence, DO, Amy Stratton, DO, Dawn Torres, MD, FACG. Internal Medicine/Gastroenterology, Walter Reed National Military Medical Center, Bethesda, MD. Introduction: To describe a case of gastric squamous cell carcinoma, marked by significant upper gastrointestinal bleed resulting in anemia and dysphagia. Case Report: The patient was a 64-year-old male with a history significant for alcoholic cirrhosis awaiting orthotopic liver transplant, hepatocellular carcinoma (HCC) and grade I esophageal varices who was admitted to the ICU with hypotension after two episodes of large volume hematochezia, in the setting of progressive dysphagia and fatigue for one month. The patient’s past medical history also included resolved Los Angeles (LA) grade D esophagitis and stage IV (T1N2M0) uvular squamous cell carcinoma (SCC) status-post curative uvulectomy/tonsillectomy with chemotherapy and radiation six years prior with no evidence of disease recurrence. Physical exam revealed a cachectic male, with 3+pitting edema of the lower extremities bilaterally and scant amount of blood in the rectal vault. Vitals: Temperature 98.5, Pulse 64, Blood pressure 87/56, Respiratory rate 17, SpO2 100% on 2L NC. Laboratory data was significant for: Hemoglobin 8g/dL, INR 1.2, Total bilirubin 0.8mg/dL, Serum creatinine 0.82mg/dL with a MELD score of 8. Esophagogastroduodenoscopy (EGD) revealed LA grade D esophagitis, grade II


esophageal varices and a new gastric cardia mass with active oozing and no evidence of extension to the esophagus. Biopsy results were remarkable for SCC. CT chest/abdomen/pelvis revealed new metastasis involving lung, liver and numerous lymph nodes. Given his comorbid conditions and poor functional status treatment options were limited. He completed palliative radiation and died while in hospice care. Discussion: SCC of the head and neck typically is treated with multi-modality therapy using surgery, radiation, and chemotherapy. Distant metastasis is uncommon and recurrence is usually local. It is unclear if this represents a late recurrence or a new primary SCC. The patient had a PEG tube placed at the time of initial SCC diagnosis which was removed 5 years prior and PEG tract seeding would be another albeit less likely cause for his recurrence. This case is an unusual presentation of either a new second SCC or a distance recurrence in an alcoholic cirrhotic awaiting liver transplant for HCC.

882 Rare Case of End-Stage Gastric Signet Cell Adenocarcinoma that Metastasized to the Colon Deepak Sharma, DO,1 Varun Jain, MD,1 Sandeep Jubbal, MD,1 Vimala Ramasamy, MD,2 Ava Anklesaria, MD,1 Zoran Bogdanovic, MD2. 1. Icahn School of Medicine at Mount Sinai (Bronx) - James J Peters VA Medical Center, Bronx, NY; 2. North Central Bronx Hospital, Bronx, NY. Introduction: A 63-year-old female with medical history of hypertension, type 2 diabetes mellitus and hyperlipidemia presented with intermittent abdominal pain, nausea, vomiting, poor appetite and weakness. Vital signs were normal and physical exam was remarkable for dry mucous membranes and right lower quadrant and suprapubic abdominal tenderness. Labs showed mild leukocytosis, hypokalemia, contraction alkylosis, elevated anion gap and acute kidney injury. Intravenous fluids, metoclopramide and potassium supplements were given. CT with oral contrast revealed severe left hydronephrosis, diffuse colonic wall thickening with regional adenopathy and soft tissue stranding. Colonoscopy revealed a hard mass in the right colon and cecum, flat sessile soft polypoid lesion in the transverse colon and a flat, hard 5 cm long polypoid circumferential area 20 cm from the anal verge. Pathology report concluded poorly differentiated adenocarcinoma with signet ring cell features in the colonic submucosa. Upper endoscopy exhibited pre-pyloric thickening, which prevented the endoscope from entering the duodenum. Biopsies of the stomach were unremarkable, but a signet ring cancer in the deeper layers could not be excluded due to the thickened wall. The patient later developed obstructive bowel symptoms. Abdominal CT was remarkable for intussusception. She underwent exploratory laparotomy and gastrojejunostomy, during which the gastric wall was biopsied and sent for immuno-histochemical staining. Results were more consistent with adenocarcinoma of upper GI tract origin (positive CEA, CDX2, AE1/ AE3, mucicarmine, negative CK7 and CK20). These results and the observation of colonic signet ring deposits in the submucosa instead of the mucosal surface supported the diagnosis of a primary gastric signet ring cancer in the deeper tissues, which metastasized to the colon. The patient had an uneventful recovery and was discharged home with oncology and surgery follow-up. She returned with symptoms of small bowel obstruction. Her hospital course was complicated by development of small bowel perforation secondary to ileoceacal disease involvement, after which she deteriorated and died. Signet ring cell carcinoma originates in the stomach in 99% of cases. Endoscopy and biopsy has 95% diagnostic accuracy for gastric cancer, CT scan is useful for staging, and endoscopic ultrasound helps in delineating depth of tumor invasion. Treatment of choice up to stage III cancers is subtotal or total gastrectomy. Five-year survival in end-stage gastric carcinoma is 3% in the United States. It is very rare to see a primary gastric cancer with metastasis to the colon, which makes our case unique.

883 Rare Case of Metastatic Gastric Cancer Loveleen Sidhu, MD, Samarth Patel, MD, Ramin Bagheri, MD, Melik Tiba, MD, Joshua Aron, MD. Elmhurst Hospital Center, Elmhurst, NY. Introduction: Gastric carcinoma is a common malignancy worldwide. Advanced stages of the disease may result in metastases to liver, peritoneal surfaces, lymph nodes, ovaries, or pulmonary tissue. We report a rare case of metastatic gastric carcinoma presenting with symptoms of abdominal pain and weight loss. Case Report: A 64-year-old male with diabetes and recent diagnosis of multiple myeloma, presented with abdominal pain. He described it as cramping densation in lower abdomen accompanied by multiple episodes of vomiting. He had similar symptoms on and off for the past year with decreased appetite in the last few months. History was significant for a recent unintentional weight loss and 20 pack years of smoking. Patient had no family history of cancer and a normal screening colonoscopy 6 years ago. Physical exam revealed pale and cachectic male without any lymphadenopathy. Labs were notable for microcytic anemia with hemoglobin of 8.9g/dl, iron studies were consistent with iron deficiency anemia. Patient underwent upper and lower GI endoscopy for further evaluation. EGD showed indistensible stomach with non-obstructive circumferential mass suspicious for malignancy, while colonoscopy revealed 3 separate semi circumferential polypoid lesions in ascending, sigmoid colon and rectum. CT scan of chest and abdomen was pertinent for gastric wall thickening. Immunohistologic exam of the gastric biopsy specimens revealed adenocarcinoma while all colonic lesions were noted to be poorly differentiated adenocarcinomas originating from upper GI tract. Conclusion: Adenocarcinoma of stomach accounts for more than 90% of malignant neoplasias of stomach. Metastasis by hemotogenous route usually involves liver. Intestinal metastases are rarely reported from gastric adenocarcinoma. Primary gastric tumors with intestinal metastases are mostly of the scirrhous type and poorly differentiated, with or without signet ring-cell differentiation. The probable route of metastasis involving the gastrointestinal tract is hematogenous, however longitudinal intramural spread or direct invasion of peritoneal implants is also possible. To our knowledge, the metastatic lesions reported in literature were segmental strictures. Our case is unique in that it is one of the very few reported cases of metastases of a gastric adenocarcinoma presenting as multiple colon polypoid lesions.


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884 Primary Gastric Melanoma: Wait, I Thought the Stomach Did Not Have Any Melanocytes! Daniel Eshtiaghpour, MD, Danny Lee, MD, Sofiya Reicher, MD, Anuj Datta, MD, Viktor Eysselein, MD. Harbor UCLA Medical Center, Torrance, CA. Introduction: We report a case of a patient who presented with abdominal pain and decreased ability to tolerate food, and was found to have melanoma in the gastric mucosa. We highlight the difficulty of diagnosing primary gastric melanoma with certainty, given its rarity and theoretical implausibility, as normal gastric epithelium lacks melanocytes. We also briefly review several pathophysiologic and embryologic hypotheses for this phenomenon. A 50-year-old Hispanic male presented to our clinic with epigastric pain and decreased ability to tolerate food. An EGD revealed a large, irregular ulcerated gastric mass extending 1.5 to 2 cm from the gastroesophageal junction to the antrum. The mass was biopsied, and immunohistochemical stains showed the tumor cells were positive for melan-A, HMB45 and vimentin, confirming melanoma. A thorough search for another possible primary lesion, consisting of a complete skin examination and positron emission tomography (PET), did not identify a clear primary site of melanoma. The PET scan revealed uptake involving the gastric walls and lymph nodes in the perigastric, retroperitoneal and left supraclavicular regions. BRAF analysis was positive for a V600 mutation. The patient subsequently underwent palliative jejunostomy placement and was evaluated by medical oncology. Primary gastric melanoma is extremely rare (with only a handful of cases reported in the literature), likely due to the lack of melanocytes in normal gastric epithelium. Therefore, when melanoma is encountered in the stomach, it is crucial to search for a primary melanocytic lesion that may have metastasized to the stomach. While gastrointestinal involvement by melanoma has been found in up to 60% of autopsies of patients who have died with primary cutaneous melanoma, melanoma located primarily in the gastric mucosa is an uncommon occurrence. Several pathophysiologic mechanisms have been suggested. Ectopic migration of melanocyte precursors or differentiation of the APUD cells to melanocytes have been suggested as possible mechanisms. Spontaneous regression of primary melanoma has also been recognized, and it is possible that our patient’s gastric melanoma may have represented a metastasis from primary lesion that had spontaneously regressed. The median overall survival for primary melanoma of the GI tract is 17 months; for primary melanoma of the stomach, 5 months. There is little consensus on therapy for patients with primary GI melanoma, but treatment with complete excision may provide long-term disease-free survival. Vemurafenib, a BRAF kinase inhibitor, has been shown to improve both overall and progression-free survival in patients with metastatic melanoma with the BRAF V600E mutation

[885B] Figure 2. Gross pathology of bi-lobed gastric mass.

equally affected. Presenting symptoms depend on location and size of the tumor. Diagnosis is primarily based on histopathology which is the gold standard as clinical features and imaging play a limited role. The most effective treatment modality is complete surgical resection. To our best knowledge, we present the first case of gastric SFT of the angiofibromatous variant presenting with profound anemia.

886 Upper Gastrointestinal Bleeding as a Manifestation of Metastasis From Laryngeal Cancer

885 An Unexpected Cause of Profound Iron Deficiency Anemia John Erikson Yap, MD, Ashutosh Gupta, MD, Bashar Attar, MD, PhD, FACG, Satya Mishra, MD, FACG, Meron Teshome, MD, Frances Manosca, MD. John H Stroger Hospital of Cook County, Chicago, IL. Introduction: Solitary fibrous tumors (SFTs) are rare spindle cell tumors that usually arise from the pleura. In a few case reports, they have been found in other sites. We present a rare case of gastric SFT presenting with bloody emesis. A 50-year-old female presented with coffee ground emesis associated with melena for 6 days. Physical examination was significant for pallor and tachycardia. Abdominal examination was benign. Laboratory results revealed iron deficiency anemia with a hemoglobin of 1.8 but otherwise unremarkable. EGD showed a 4-5 cm bilobed mass near the junction of the stomach antrum and body. Biopsy was inconclusive. Radiographic staging confirmed gastric mass without evidence of metastasis. Laparotomy with wedge resection of the stomach showed a 5.0 x 3.8 x 3.1 cm, exophytic mass with central ulceration. Pathology showed gastric wall containing spindle cell tumor ulcerating through the mucosa. Histologic and immunohistochemistry picture (diffuse CD34 and bcl2 positivity) fit the diagnosis of angiofibromatous variant of SFT with insufficient histological criteria for malignancy. Klemperer first described SFTs in 1931. Only 15-20% are malignant. The median age of occurrence is 45 to 50 years with both sexes

Amandeep Singh, MD, Hammad Nazeer, MD, Nayere Zaeri, MD, Kshitij Thakur, MD, Monica Zeitz, MD, FACG. Crozer Chester Medical Center, Upland, PA. Introduction: Neoplasms of the upper gastrointestinal (GI) tract account for less than 5% of all cases of severe upper GI bleeding. There are many case reports of metastatic tumors to the stomach causing upper GI bleed as their initial presentation. We are describing the first case in the literature of upper GI bleed as a manifestation of metastatic laryngeal cancer to the stomach. Case Report: A 75-year-old Caucasian male with past medical history of peptic ulcer disease, hypertension, coronary artery disease, recent abdominal aortic aneurysm repair and stage IVa squamous cell laryngeal cancer diagnosed in July 2009 status post combined failed chemoradiation x 3, presented to the emergency room with complaints of nausea, vomiting and lower back pain for 1 day. While in the ER, the patient started having bloody vomitus, and became lethargic. Emergent intubation was performed for airway protection. Stat CT abdomen and pelvis was obtained which showed no leak or rupture of AAA. Incidentally, the patient was found to have an irregularly shaped 6.2 x 2.9 cm stomach mass along the left posterior wall of the gastric body. Initial vital signs were: temp 97.5°F, pulse 81/min, RR 16/min, bp 99/38 mm Hg and SaO2 100% on mechanical ventilation. Physical examination was benign. Initial labs were: Hb 4.8 g/dL, Hct 15.4, WBC 12.5, platelet 205,000/cmm, PT 14.9 sec, INR 1.2, aPTT 28 sec, BUN 36 mg/dL, creatinine 2 mg/dL. Emergent EGD was performed which confirmed a large friable mass in the gastric fundus, which was biopsied, and the pathology revealed fragments of oxyntic type gastric mucosa showing metastatic squamous carcinoma consistent with laryngeal cancer. The patient received 8 units of blood products, with repeat hemoglobin of 9.4 g/dL. The patient had no further bleeding, was successfully extubated, and eventually discharged with instructions to follow up for palliative radiotherapy. Discussion: Typically, gastric cancers are adenocarcinoma, squamous cell carcinoma, lymphoma, or gastrointestinal stromal tumors. Rarely, tumors in the stomach may be from distant metastases. The tumors that metastasize to stomach most commonly are lung, breast and malignant melanoma, and can present with abdominal pain, nausea, vomiting and bleeding. Laryngeal cancer usually presents as hoarseness, difficulty swallowing, or a lump in the neck. The most common site of metastasis in laryngeal squamous cell cancer is the lung. This is the first report of metastatic squamous cell laryngeal cancer to the stomach presenting as an upper GI bleed. This case is not only an unusual presentation of laryngeal cancer, but also highlights an exceedingly uncommon site for laryngeal metastasis and a rare cause of upper GI bleeding.

887 Helicobacter heilmannii: A Rare Cause of Abdominal Pain Azfar Niazi, MBBS, Omar Khokhar, MD, FACG. Department of Medicine, Division of Gastroenterology, University of Illinois-Peoria, Bloomington, IL.

[885A] Figure 1. Gastric bi-lobed mass. The American Journal of GASTROENTEROLOGY

Introduction: A 44-year-old female was referred to gastroenterology clinic for abdominal pain for 6 months. The pain was aching in quality, 5/10 in intensity, and aggravated by oral intake. The pain was associated with belching. Past history included partial hysterectomy for enlarged uterus, a caesarean section and mitral regurgitation. Physical exam was unremarkable. Mild leukocytosis was seen on laboratory investigation. An upper endoscopy was performed, which revealed patchy erythema, friability, and granularity in the antrum (Figure 1-2). Histopathology confirmed chronic active gastritis, positive for Helicobacter organisms. H. Pylori immunostain highlighted numerous well-defined corkscrew


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Abstracts organisms that were longer than typical H. pylori organisms, consistent with Helicobacter heilmannii. Helicobacter heilmannii (H. heilmannii) infection is a relatively rare causative agent of gastroduodenal diseease. However, H. heilmannii frequently colonizes gastric mucosa of animals, primarily cats and dogs, from where it can be transmitted to humans. Patients usually present with longstanding epigastric pain, nausea, vomiting, and heartburn. The patient was successfully treated with antibiotic therapy with resolution of symptoms.

unusual gastric and colonic appearance, biopsies were sent to tertiary care facility pathology department for expert consultation. Final pathologic examination confirmed MCL from the duodenal and gastric biopsies without H. pylori identified on Giemsa stain. Tissues from the terminal ileum and the whole colon were also tested positive on immunohistochemistry for MCL. His follow-up computed tomography scan of the abdomen and pelvis showed large tissue abnormality in the distal stomach and extensive adenopathy. The patient was referred to oncology and received 6 cycles of rituxan and bendamustine with interval scans showing favorable response. Despite general poor prognosis of MCL, our patient had good clinical response at one year follow up and returned to his baseline with resolution of anemia. Mantle cell lymphoma has an incidence of approximately 4 to 8 cases per million persons per year. The disease occurs in older individuals with a median age around 68 and male predominance. It can present as lymphomatous intestinal polyposis in any region of gastrointestinal tract. To our knowledge, there are limited case reports, which suggest association between mantle cell lymphoma and gastric and duodenal ulcers in absence of H. pylori infection. Therefore, although peptic ulcer disease can be benign especially with history of aspirin intake, we should not exclude the possibility of lymphoma. Edge biopsies should be obtained if the ulcer and mucosa appear to be atypical.

889 A Case Report: Bridging the Gap in Understanding “Non-Celiac Gluten Sensitivity” Presidential Poster Bhaumik Brahmbhatt, MD,1 Meghavi Brahmbhatt, MBA,2 John Cangemi, MD1. 1. Mayo Clinic, Jacksonville, FL; 2. London Metropolitan University, London, United Kingdom.

[887A] Figure 1.

Introduction: A 27-year-old male with no significant past medical history presented with sub-acute onset of severe, intermittent, sharp epigastric pain, lasting for hours and disturbing his sleep. There was no association with meals and he denied constitutional symptoms, acid reflux, nausea, vomiting or change in bowel habits. Review of systems was unremarkable. He had mild relief with antacids. He denied use of non-steroidal anti-inflammatory drugs or supplements. He had no significant past surgical, family, or social history. There was no history of smoking or alcohol and caffeine use. His BMI, vitals, and physical exam were normal. On workup, he had normal blood count, electrolytes and liver tests. Stool studies were negative for lactoferrin, ova and parasites, and cultures. He was empirically started on 14 days of twice daily proton pump inhibitors (PPI), with resolution of symptoms in 2 days. After completion his symptoms recurred. H. pylori stool antigen was negative. PPI therapy was restarted with resolution of symptoms in 2 to 3 days. At this time his TTG Ab was negative and his EGD was unremarkable, including gastric and small bowel biopsies. Diagnosis of non-ulcer dyspepsia was given and he was continued on PPI twice daily indefinitely. At home, he had his asymptomatic wife and his first degree cousin with similar symptoms started 2 months later than him. A very careful diet history revealed that only difference in diet from his asymptomatic wife was their daily morning 2 slices of whole wheat bread of same brand for about 3 months. One of the potential causative ingredients was azodicarbonamide. To prove the correlation, he stopped his PPI with recurrence of symptoms. Then they changed to a brand without this food additive and their epigastric pain resolved. With reintroduction of this food additive all had recurrence of symptoms. Azodicarbonamide is an odorless, crystalline powder, used for strengthening the flour, to increase its shelf life. It is most commonly used for making “foamed” plastics (i.e. various rubbers, such as gym mats, etc.). Although available in the US, this “food additive” is banned in Australia and Europe and is illegal in Singapore, incurring time in prison and a fine of $450,000. Conclusion: The use of food additives to prolong the shelf life has increased and patients may be at risk for an adverse reaction. Although the mechanism for gastrointestinal intolerance is unknown, this case demonstrates a clear association between symptoms and exposure to azodicarbonamide. A thorough evaluation of diet for non-ulcer dyspepsia and other non-specific gastrointestinal symptoms is essential to avoid unnecessary and expensive testing and treatment.

890 A Unique Case Presentation of Symptomatic Gastric Telangiectasia in Isolated Granulomatous Gastritis Bhaumik Brahmbhatt, MD, Mark Stark, MD. Mayo Clinic, Jacksonville, FL.

[887B] Figure 2.

888 Gastric and Colonic Mantle Cell Lymphoma With History of Peptic Ulcer Disease Tanya Dam, DO, Nathaniel Krogel, DO, Duane Moise, DO, Brent Smith, MD, Todd Ogrodowczyk, MD. Gastroenterology, Blue Ridge Digestive Health, Morganton, NC. Introduction: Mantle cell lymphoma (MCL) is an aggressive B-cell neoplasm in mantle zone of the lymph node with poor prognosis. There are not many case reports to link between peptic ulcer disease and mantle cell lymphoma. Therefore, we present a case of mantle cell lymphoma in setting of gastric and duodenal ulcers. A 68-year-old Caucasian male presented with chronic anemia from “Goody Powder” use (powder form of aspirin, caffeine, and acetaminophen). The patient had workup with esophagogastroduodenoscopy a year ago with diffuse ulcers in the stomach and the duodenum. Since the diagnosis, he was started on proton pump inhibitor and discontinued aspirin. His esophagogastroduodenoscopy after 8 weeks showed partially healed ulcers. He returned to our office because of weight loss and recurrent iron deficiency anemia without melena or blood in stool. His repeat esophagogastroduodenoscopy revealed congestion in the stomach and non-healing ulcers in the duodenum. His colonoscopy showed abnormal vascularity, erythema, and nodular mucosa of the whole colon. Due to the presence of


Introduction: Literature has associated granulomatous gastritis with gastric ulcers but not with arteriovenous malformation, leading to transfusion dependent anemia. Case Report: A 32-year-old male patient with chronic blood transfusion and IV iron dependent anemia from chronic gastrointestinal blood loss for 7 years despite repeated cauterization of angiodysplasia in his stomach. He has intermittent melena, one episode of scant hematemesis in past, 40 lbs weight loss, no other GI symptoms, no NSAID/anticoagulants, no coagulopathy; no symptoms to suggest systemic vasculitis, sarcoidosis or inflammatory bowel disease. No contributing past medical, surgical or family history. He denies use of alcohol or recreational drugs; smokes half a pack of cigarettes/day. Uses carafate and omeprazole twice a day. BMI 26.5, unremarkable vitals and physical exam. He has had several endoscopies. Cumulative findings on EGD: several clean base superficial and irregular shaped antral ulcer, multiple spider telangiectasia on all mucosal surfaces of stomach, central portion bled with touch. Stomach biopsy: moderate active gastritis with noncaseating epithelioid granulomas, no microorganisms. Special stains: H. pylori, fungus and AFB were negative; Fungal and AFB cultures of biopsies are negative (3 months). Esophagus and small bowel biopsies were normal. Twice colonoscopy: normal, including terminal ileum. Capsule endoscopy: multiple AVM in stomach, antral ulcer, old hematin in distal small bowel, otherwise normal small bowel. Serology: negative for HIV, normal haptoglobin and ristocetin cofactor; W/u for Von Willebrand syndrome, factor 8 activity 225%; VWF ag normal. Doppler US: no portal vein thrombosis; ESR: 2. Infectious causes: negative for syphilis and schistosomiasis, PCR for Whipple’s bacillus negative, H. pylori IgG Ab positive; Histoplasma Ab negative (no eosinophilia and no eosinophillic granulomas). Normal serum protein electrophoresis. Vasculitis: negative autoantibodies to proteinase 3, myeloperoxidase, ANA. Sarcoidosis: CT chest/abd/pelvis: no lung infiltrate or signs of sarcoidosis; few tiny visible retroperitoneal nodes; normal liver/spleen, ACE level is normal. Assessment:


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isolated granulomatous gastritis, without recognizable infection, systemic sarcoidosis, or small bowel/ colon Crohn’s disease. Plan is aimed to eradicate H pylori, treat with steroids, similar to treatment of Crohn’s disease; if repeat endoscopy shows improvement then slow taper of steroids, if has recurrence then consider azathioprine. Conclusion: This case report will contribute to the limited literature on isolated granulomatous gastritis, with a unique association of symptomatic AVM’s.

891 Gastric Metastasis From Renal Cell Carcinoma Causing Upper Gastrointestinal Bleeding 18 Years After Curative Tumor Resection: A Case Report and Review of the Literature Hassan Dakik, MD,1 Deborah Fisher, MD,2 Mafuzul Haque, MBBS2. 1. Duke University, Durham, NC; 2. Veterans Affairs Hospital, Durham, NC. Case Report: Our patient was an 83-year-old male with a prior history of renal cell carcinoma (RCC) treated with a radical nephrectomy and chemotherapy 18 years prior. He was reported to be in full clinical remission at the time of presentation. He presented to our emergency department with complaints of one day of lightheadedness and melena. His triage vital signs were significant for orthostatic hypotension. His physical exam was notable for melena. Hemoglobin was 12.9 gms from a prior baseline of 14. A proton pump inhibitor infusion was initiated and he was admitted to the hospital ward. He underwent upper endoscopy that revealed a 1.5 cm irregular shaped and inflammatory appearing polyp on the lesser curve. Further inspection revealed an area of ulceration on the posterior aspect and evidence of recent bleeding. The gastric polyp was lifted with saline injection and poylpectomy was performed. The mass was retrieved and the margins were grossly inspected. The remainder of his hospital course was uneventful and he was discharged within 48 hours of the procedure. The pathology from the polyp revealed morphologic features of clear cell RCC with a clear margin of resection. When compared to stored kidney tissue from the 1995 resection the cytological characteristics of the gastric polyp closely matched the original tumor. A body CT scan was performed and revealed a small lesion in the inferior pole of the left kidney resembling metachronous RCC, as well as a concerning mass in the pancreatic tail. He was subsequently referred for evaluation by our oncology specialists who initiated chemotherapy with pazopanib (a selective tyrosine kinase inhibitor). Discussion: Renal cell carcinoma (RCC) can metastasize to a variety of locations including most frequently the lung, liver, bone and brain. Metastatic RCC to the stomach is rare with an estimated incidence of 0.2-3.1% of all gastric metastatic lesions. Moreover, the timeframe for recurrence of metastatic disease is typically significantly closer to the initial resection. There are reports of RCC metastasizing to the gastrointestinal (GI) tract several years after the primary tumor has been successfully resected. The estimated interval from the time of surgical resection of the primary RCC to noting the gastric metastasis was roughly 7 years in one series. In a larger series of 22 patients the average interval to gastric metastasis was 6.3 years. In our case, the time interval was over 18 years making it one of the latest presentations in the current literature. References: De Palma GD, et al. World J Gastroenteral. 2006. Tsutomu N, et al. Oncol Letters. 2012 Pollheimer MJ, et al. BJU Int. 2008.

892 Contained Gastric Ulcer Perforation Treated with Medical Management Charles Rives, MD, Aaysha Kapila, MD, Eric Carter, DO, Pranav Patel, MD, John Litchfield, DO, Mark Young, MD. East Tennessee State University, Johnson City, TN. Introduction: Contained gastric ulcer perforations (CGUP) are most commonly treated surgically. We present a case in which a CGUP was successfully treated solely with medical management. Case Report: A 48-year-old female taking non-steroidal anti-inflammatory drugs (NSAIDs) daily for migraines, presented with a 3 week history of worsening abdominal pain. The pain was mid-epigastric, radiated to her back, increased with food and was associated with nausea and vomiting. Vitals were stable, physical exam was benign except for mild tenderness to palpation in the mid-epigastric area and hypoactive bowel sounds. Comprehensive metabolic panel was unremarkable. The patient was mildly anemic with hemoglobin 9.8 g/dL, and MCV 84 fL with a history of recently menstruating. CT of abdomen and pelvis with contrast was significant for: diffuse gastric wall thickening, a large ulceration (2.8 x 3.6 cm) extending through the posterior aspect of the gastric body and stranding changes within the mesenteric fat adjacent to the ulceration. Maximum thickness of the adjacent gastric wall was 1.9 cm and there was no free air or fluid within the peritoneum. The patient was started on intravenous fluids, pantoprazole and kept NPO. On day 4 of hospitalization the patient’s pain had resolved and she tolerated a diet. The patient was discharged with oral sucralfate, pantoprazole twice a day and follow up with gastroenterology in 4 weeks. Discussion: The classic presentation of a gastric ulcer is intermittent mid-epigastric pain that is worsened by food. If the pain increases in severity, radiates to the back or presents with peritoneal signs, the suspicion for perforation dramatically increases. CT of the abdomen with contrast has increased capabilities of detecting evidence of a gastric perforation such as mesenteric fat stranding, bowel wall thickening or free air/contrast within the peritoneum. A CGUP is a perforated gastric ulcer with surrounding gut structures preventing the release of gastric contents into the peritoneum. The most common treatment of a CGUP is laparoscopic or open laparotomy repair of the defected gastric wall with post-operative medical management. However, as much as 50% of all gastric perforations will self-seal allowing certain hemodynamically stable patients to be managed non-operatively with a success rate as high as 82% and a morbidity and mortality rate of 0-8%. Medical management of CGUPs should include IV fluids, gastric acid suppression and gastric rest. Prophylactic antibiotics may be appropriate to prevent infection. Conclusion: Hemodynamically stable patients with CGUPs and minimal symptoms can be treated effectively with medical management alone.


893 When It’s Not Just the Baby: Krukenberg Tumor in Pregnancy Paul Co, MD, Ashutosh Gupta, MD, Bashar Attar, MD, PhD, FACG, Melchor Demetria, MD. Internal Medicine, John H Stroger Jr. Hospital of Cook County, Chicago, IL. Introduction: Gastric cancer in pregnancy is extremely rare and often advanced on presentation. A Krukenberg tumor refers to a malignancy in the ovary that has metastasized from a primary site, classically the gastrointestinal tract. Case Report: A 38-year-old female Gravida 4 at 22 weeks of gestation presented with several months of worsening epigastric pain, nausea and vomiting. Poor oral intake prompted hospital admission. Pertinent exam finding was a gravid abdomen, epigastric tenderness, and a tender mass from midline to her left flank. CA 125 was 846 U/mL. Abdominal ultrasound showed a possible pancreatic mass and a pelvic mass. MRI confirmed a large pelvic mass arising from the left adnexa, ascites and demonstrated edema of the mesentery and omentum, with no evidence of questioned pancreatic mass. A few days after admission, she had worsening abdominal pain and was found to be in active labor. She subsequently delivered a viable infant via vaginal delivery. This was followed by an exploratory laparotomy, omentectomy, and bilateral salpingo-oophorectomy which revealed a large mass originating from her left ovary, diffuse thickening of the lesser curvature of the stomach, straw colored ascites, and small nodularities within the omentum. Intraoperative frozen section showed signet cell adenocarcinoma consistent with Krukenberg tumor. Subsequent EGD showed linitis plastica while biopsy confirmed presence of invasive poorly differentiated adenocarcinoma. She was diagnosed as having stage IV gastric cancer and was planned for FOLFOX chemotherapy. Discussion: Gastric cancer during pregnancy is a diagnostic challenge because of its extremely rare probability as a cause of extremely common symptoms such as nausea and vomiting. It is often associated with a poor prognosis since the cancer is usually advanced at the time of diagnosis. GI endoscopy in pregnant patients is inherently risky because the fetus is particularly sensitive to maternal hypoxia and hypotension, either of which can lead to fetal demise. A Krukenberg tumor is an advanced presentation of gastric cancer and can be confused with other adnexal masses more commonly seen in pregnancy such as teratomas and corpus luteum cyts. Ultrasonography and MRI are the modalities of choice for imaging. CA 125 testing alone has low sensitivity and specificity but may be used in combination with other findings. The management remains a challenge because of the need for early treatment and the continuation of the pregnancy. A therapeutic plan should consider the gestational age and should involve a multidisciplinary team of specialists in perinatal obstetrics, and gastric cancer specialists.

894 A Mysterious Cause of Abdominal Pain Tarek Sawas, MD, Mubarak Sayyar, MD, Won Cho, MD, FACG. Georgetown University Medstar Washington Hospital Center, Washington, DC. Introduction: Median arcuate ligament syndrome (MALS) is a rare cause of abdominal pain that results from anatomic abnormality in the median arcuate ligament of the diaphragm. We present the first case of this syndrome in association with Lynch syndrome Case Report: 51-year-old African American female with a history of diabetes mellitus and family history of Lynch syndrome presented with one week of severe colicky, 10/10 epigastric pain that was aggravated by food. She denied nausea, blood with stool. physical examination was completely unremarkable. She denied taking NSAIDs. Extensive work up was done including esophagogastroduodenoscopy, CT abdomen, abdominal ultrasound, colonoscopy and a gastric emptying study. All these studies were normal. She was treated symptomatically with proton pump inhibitor and discharged. She continued to have symptoms and 1 month later she developed nausea, bilious vomiting and lost 20 lbs. Further workup was proceeded with magnetic resonance cholangiopancreatography which was negative. She had duplex ultrasound of the abdomen, which revealed 90% stenosis in the celiac artery with velocity of 570 cm/s. CT angiography of the abdomen was done and demonstrated acute angulation and narrowing of the proximal celiac axis with a “hooked” appearance that is characteristic of MALS. She was referred to surgery for celiac artery decompression. Discussion: MALS is a rare cause of abdominal pain 1/1000. Abdominal pain is not related to the blood flow obstruction, but rather to the damage of splanchnic celiac nerve plexus. The characteristic symptoms are the triad of abdominal pain, weight loss, and abdominal bruit. The diagnosis is made by excluding other common causes of abdominal pain and the characteristic finding on CT angiography. Treatment is mainly surgical decompression. The association between this syndrome and other genetic disorders has not been established. We described the first case of MALS in association with Lynch syndrome. Median arcuate ligament syndrome should be considered as a reason for chronic unexplained abdominal pain

895 An Uncommon Presentation With an Inevitable Outcome Jayakrishnan Krishnakurup, MBBS, MD, Venkata Gourineni, MBBS,MD, Shady Henien, MD, Nicholas Lillo, MD, Alan Nelson, MD. Bridgeport Hospital, Bridgeport, CT. Introduction: Seventy-two-year-old male was admitted with headache, neck pain, and nausea and vomiting of 10 days duration. He denied fever, any focal weakness, visual changes or photophobia. Physical exam was unremarkable. The labs were normal except for hb of 12.6 gm/dl. A non-contrast CT head revealed frontal sinusitis. By second day of hospitalization, he became bewildered with visual hallucinations. MRI brain was normal. EEG displayed intermittent mild diffuse background slowing suggestive of drowsiness and possibly a mild encephalopathy. On the third day of hospital stay he developed positive kernig sign. CSF analysis revealed increased leucocytes of 680 /cmm (94% neutrophils and 4% lymphocytes), CSF cultures, PCR for CMV and HSV, were negative. CSF cytology revealed signet ring cells positive for AE1/AE3. The serum levels of CA19/9, and CEA were 1396 and 664, respectively. CT chest and abdomen were unremarkable except for multiple enlarged lymph nodes along the celiac axis


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[894A] Figure 1. CT angiography demonstrates the hooking appearance of the celiac artery.

and left para-aortic region. A screening EGD revealed a large fungating non-circumferential mass at the gastroesophageal junction extending in to the gastric cardia. Biopsy of the mass exhibited moderately differentiated adenocarcinoma with signet ring cell features. Immuno histochemistry for human epidermal growth factor receptor 2 (HER2) displayed equivocal reactivity. Further FISH analysis of the tumor was not obtained due to rapid deterioration of his condition. The patient embraced hospice care. Discussion: Stomach cancer represents 1.3% of all new cancer cases in the USA. The incidence of leptomeningeal spread in gastric cancer is rare with an incidence of 0.14%-0.24%. Leptomeningeal carcinomatosis as the initial presentation of gastric cancer is scarce. A diagnosis of LMC is based on neoplastic cells in the CSF. Most common presenting symptoms are those of meningeal irritation. Poorly differentiated signet ring cell gastric carcinomas can often present with leptomeningeal involvement. The median survival in untreated cases are about 4 to 6 weeks. Aggressive chemotherapy may increase the survival time to 4 to 6 months. The prognostic role of HER2 overexpression in esophagogastric cancers remains unclear. Multiple studies have shown poorer survival and vice versa. HER-2 positivity is more commonly observed in intestinal cancer subtype and typify aggressive tumors with an increased depth of invasion, early lymph node involvement and distant metastasis. Trastuzumab inhibits proliferation of cells which overexpress HER2 protein. There are no predictive biomarkers to predict the response to trastuzumab and no standard second-line therapies for HER2 positive EG cancer after progression on trastuzumab.

896 Post-Transplant Lymphoproliferative Disorder With Diffuse Large B-Cell Lymphoma of the Stomach 14 Years Post-Orthotopic Heart Transplant Aaysha Kapila, MD,1 Lovely Chhabra, MD,2 Pranav Patel, MD,1 Mark Young, MD1. 1. East Tennessee State University, Johnson City, TN; 2. University of Connecticut, Hartford, CT. Introduction: Post-transplant lymphoproliferative disorders (PTLD) are fatal complications that develop post-transplant secondary to chronic immunosuppression. We herewith present a case of high grade Bcell lymphoma in a patient with cardiac transplantation. A 44-year-old African American male with medical history of orthotopic heart transplantation 14 years prior presented with left upper abdominal pain and 6 lbs unintentional weight loss in 2 weeks. Initial vital signs were unremarkable except for tachycardia (pulse=102/min). Physical examination was remarkable for a chronic abdominal wound with surrounding pink granulation tissue, peripheral induration without erythema or tenderness. Labs on presentation were remarkable only for known chronic anemia and chronic kidney disease. Computed tomography of the chest and abdomen demonstrated a central abdominal soft tissue mass measuring 5.9 cm x 5.8 cm with adjacent lymphadenopathy, and several left upper lobe nodules with the largest one measuring 2 cm in size even in the absence of symptoms.

916 Sequential Endoscopic Gastropexy and Esophageal Stent Placement for Treatment of Gastric Volvulus With Early Signs of Ischemia

[913A]

Figure 1. Excised malignant spot-stained gastric tissue.

914 Collagenous Gastritis: A Case Report and Clinical Review Karthik Garapati, MD,1 Mazyar Malakouti, MD,1 Charles Randall, MD2. 1. University of Texas Health Science Center at San Antonio, San Antonio, TX; 2. Gastroenterology Research of San Antonio, San Antonio, TX. Introduction: Collagenous gastritis (CG) is a rare, idiopathic disorder first described in 1989. It is characterized by gastric subepithelial collagen deposition greater than 10μm with associated lamina propria inflammation composed of lymphocytes, plasma cells, and eosinophils. We report a case of a 61-year-old man who presents to clinic with a 13-month history of nausea, early satiety, post-prandial pain, and a 36 lb weight loss. The physical exam was notable for mild, generalized abdominal tenderness. Laboratory studies including a celiac panel, Helicobacter pylori, and autoimmune panel were all normal. Esophagogastroduodenoscopy demonstrated diffuse friability of gastric and duodenal mucosa. Gastric histology demonstrated an increased chronic inflammatory infiltrate with collagen deposition. Chronic duodenitis was also seen with normal villi and without collagen deposition. Colonic samples showed no evidence of microscopic colitis or inflammatory bowel disease. The patient was treated with an indefinite course of pantoprazole 40 mg daily and sucralfate 1g QID for the first month. The patient’s nausea, vomiting and pain resolved within 2 months. However, the patient continued to have early satiety, with an electrogastrogram demonstrating bradygastria. He was successfully treated with 3-month course of domperidone. At the 3-year follow up, the patient’s weight was stable without additional GI symptoms. CG can present in children and young adults from the ages of 2 to 22, and in older adults from the ages 35 to 77 with a slight female predominance overall. Adult patients can present with abdominal pain, chronic diarrhea, malabsorptive symptoms, and protein losing enteropathy. They are also more likely to have associated autoimmune diseases and intestinal disease such as collagenous colitis. The most favored theory suggests that the pathognomonic collagen deposition is secondary to chronic inflammation. Due to its rather nonspecific presentation it is diagnosed by the histopathologic examination of gastric mucosal biopsies. The gross endoscopic findings include erythema, erosions, ulcerations and hemorrhages in the gastric body and fundus. The subepithelial collagen deposition is commonly highlighted with a Masson trichrome stain. Given these pathologic findings, anti-inflammatory and anti-secretory measures encompass the most common treatment approaches. Corticosteroids, proton pump inhibitors, histamine-2 blockers, and dietary restrictions have all been attempted with variable success. CG’s wide array of clinical presentations and association with common autoimmune conditions makes it clinically relevant for the gastroenterologist.

915 Antral Hyperplastic Polyp Causing Gastric Outlet Obstruction: Case Report and Review of Literature Prathab Devaraj, MD,1 Shashank Ponugoti, MD,2 Swati Pawa, MD1. 1. West Virgnia UniversityDepartment of Digestive Disease, Morgantown, WV; 2. West Virginia University- Department of Internal Medicine/Clinical and Translational Sciences (CTSI), Morgantown, WV. Introduction: The prevalence of gastric polyps ranges from 0.75 to 7%. They are usually asymptomatic with fundic gland polyps being the most common. The incidence of hyperplastic gastric polyps is decreasing due to increasing detection and eradication of Helicobacter pylori. We report a rare case of gastric outlet obstruction (GOO) due to a large prolapsing hyperplastic antral gastric polyp.


Ramen Sakhi, MD, Raja Thotakura, MD, MS, Dinuli Delpachitra, MD, Tariq Hammad, MD, Osama Alaradi, MD, Ali Nawras, MD, FACG. Internal Medicine, University of Toledo Medical Center, Toledo, OH. Introduction: Gastric volvulus could either be acute or chronic. The former is an emergency while the latter can be treated electively. Laparoscopic repair of the diaphragmatic hernia with gastropexy is the treatment of choice. We report a case of gastric volvulus managed with a combination of laparoscopic and endoscopic gastropexy along with esophageal stent placement in a patient with gastric volvulus and suspected gastroesophageal junction ischemia. The patient is an 86-year-old Caucasian female, who presented with complaints of intermittent epigastric pain, inability to tolerate oral intake and post-prandial emesis of one week duration. A CT scan of the chest and abdomen showed an organo-axial gastric volvulus with no transition of oral contrast past the diaphragmatic hiatus and gastric outlet obstruction. A nasogastric tube was placed for gastric decompression. Due to the concern for strangulation, she was taken to the operating room for endoscopic evaluation and laparoscopic reduction of the volvulus with hernia repair. During the intra-operative esophagogastroduodenoscopy, a small area of patchy discoloration of the esophageal mucosa near the hiatus was identified. In consideration of the mucosal findings and to avoid the risk of devitalizing the esophago-gastric junction by division of the short gastric arteries, it was decided to abandon definitive repair and instead to perform a gastropexy. The stomach was reduced back into the abdomen using laparoscopic approach. An endoscopic gastropexy was accomplished by the placement of a PEG tube. On post-operative day 1, the patient developed chest discomfort and imaging study showed significant dilatation of intrathoracic part of the stomach and severe narrowing of the diaphragmatic hiatus. A 23 x 155 mm, fully covered, self-expandable metallic stent was placed across the hiatus under endoscopic and fluoroscopic guidance. The patient did well after the procedure and was subsequently discharged home. This combined procedure of endoscopic gastropexy and esophageal stent placement can be used as a temporizing measure for surgery, such as in this patient, when there are signs of ischemia. The procedure is less invasive, safe and effective in maintaining the position of the stomach after laparoscopic reduction and gastropexy and decompressing the intra-thoracic part of the stomach.

917 Candida-Associated Peptic Ulcer Disease in the Setting of Acute Upper Gastrointestinal Bleeding: A Rare Entity? Karthik Penumetsa, MD, Swati Pawa, MD. West Virginia School of Medicine, Departement of Digestive Diseases, Morgantown, WV. Introduction: There remains very limited literature on Candida associated infection of the gastrointestinal tract outside the esophagus especially in relation to the stomach. Candida-associated gastric ulcer typically occurs in immunocompromised hosts or in patients who have had surgery for peptic ulcer disease but seldom in healthy individuals. Case Report: A 76-year-old male with history of kidney disease and hypertension was admitted for a diffuse rash covering most of his body. Biopsy was consistent with erythema multiforme. No obvious etiology or drug exposure was evident. Patient was noted to have melena and anemia with Hemoglobin of 6.2 and required transfusions. Upper endoscopy (UE) was performed and showed white plaques and brushings in the esophagus consistent with Candida. A large 1.5 cm ulcer with a blood clot was seen in the funds which was injected with epinephrine and hemo clipped. No active bleeding was seen. There were several, raised, ulcerated lesions with central dark spots with thick surrounding exudates averaging 5-6 mm in size involving the body and antrum. The biopsies from all these ulcers revealed chronic active gastritis with ulceration and Candida species identified by GMS special stain. However, no Helicobacter pylori or intestinal metaplasia or malignancy was identified. He was treated with IV fluconazole along with high dose omeprazole, but he continued to have refractory anemia with melena. Patient underwent an IR embolization of left gastric and splenic arteries, with control of bleeding. Repeat UE showed healing of previously noted ulcers. He was eventually discharged on hospice after suffering pulmonary complications secondary to his underlying pneumonia.


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Abstracts Discussion: Unlike the classical plaque like appearance of the esophageal candidiasis on endoscopy, candida involvement of the stomach is typically more ulcer like and is typically associated with a complicated course, such as abdominal pain, nausea, emesis or fevers. Our patient had significant Candida - associated ulcer bleeding which happens to be a rarely reported complication. The natural history of Candida gastric ulcer is yet to be elucidated and current literature shows mixed results as to whether fungal colonization or invasion of gastric ulcer has any effect on healing of the ulcer.

918 Acute Hemorrhage From Gastric Schwannoma: An Uncommon Presentation of a Rare Submucosal Neoplasm Gobind Sharma, MD,1 Farihah Perwez, MD,2 Benjamin Bluen, MD,2 Missale Solomon, MD,1 James Reynolds, MD1. 1. Gastroenterology, Drexel University College of Medicine, Philadelphia, PA; 2. Hahnemann University Hospital, Philadelphia, PA. Introduction: Submucosal tumors of the GI tract, especially the stomach, are often asymptomatic and found incidentally. Gastric Schwannoma is one of the less commonly found gastric neoplasms and accounts for only 0.2% of all submucosal GI lesions. Schwannoma is most commonly found in females in their fourth to fifth decade and can be misinterpreted on imaging as a result of their similarity to other submucosal lesions. It is important for the clinician to maintain a broad differential diagnosis of these rare submucosal neoplasms, especially in the setting of acute upper GI hemorrhage, as demonstrated by the uncharacteristic presentation of our patient. We present the case of an 82-year-old Vietnamese male who underwent EGD for hematemesis and anemia. Endoscopy revealed a 3 cm donut shaped mass in the distal gastric body with central depression that bled upon contact. He underwent CT of the abdomen which revealed an 8 cm mass arising from the body suggestive of GIST. The patient underwent open surgical enucleation of the lesion without any complication. Histopathology of the lesion was consistent with gastric schwannoma. He recovered without complication and was discharged home and did well without any symptoms at 6 month follow-up. This patient represents a rare case of overt upper GI hemorrhage in a patient with a previously asymptomatic and unknown gastric schwannoma. It highlights the importance of maintaining a high suspicion for less common gastrointestinal neoplasms and rare causes of overt hemorrhage. This case also highlights that radiologic findings of schwannoma may share similarities with other types of GI neoplasms. In a less acute situation, it would be prudent to discern the type of lesion prior to pursuing a treatment strategy. In our case, further studies would find that our schwannoma was distinguished from GIST by immunohistochemistry which was positive for neural antigen S100 and negative for other markers such as CD34, CD117/KIT Receptor Tyrosine Kinase, and DOG, which are detected in GIST.

919 Gastric Calciphylaxis: Endoscopy and Histopathology Manifestations Bashar Attar, MD, PhD, FACG, Warren Piette, MD, Jesse Jiang, MD, Alexander Sauper, MD. Cook County Health and Hospitals System and Rush University Medical Center, Chicago, IL. Introduction: Calciphylaxis is a poorly understood and highly morbid syndrome which calcium accumulates in the arteriols of the fat and skin tissues precipitating ischemia and subcutaneous necrosis. Patients usually have renal failure on dialysis or recently had a kidney transplant. Gastric calciphylaxis is very rare. We report a case of gastric calciphylaxis associated with gastric ulcer perforation. A 51-year-old female with history of hypertension, HIV infection (CD4:710), end-stage renal disease (ESRD) on hemodialysis x 5 years, bilateral breast pain with cutaneous ulcerations of unclear etiology over the breasts and perianal area; presented with melena and anemia. Urgent EGD showed two large deep ulcers each 1-2 cm in size in the gastric prepyloric region. The ulcers showed stigmata of recent bleeding and was treated endoscopically and received PPI drip. Histology from the initial EGD revealed fragments of normal gastric mucosa and necrotic tissue consistent with ulcer. Immunostain for H. pylori was negative. Patient underwent double mastectomy due to her extensive necrotic breast lesions which showed breast tissue necrosis with arterioles showing luminal narrowing and mural calcification consistent with calciphylaxis. Approximately 4 weeks after her initial EGD, she developed signs of peritonitis. Abdominal CT revealed intraperitoneal free air with curvilinear focus of gas suggesting perforated gastric ulcer. She underwent laparotomy and a Billroth II gastrectomy. Histopathology of the gastric antrum revealed a 2 cm ulcer and necrosis, acute and chronic inflammation with associated perforation through serosal surface. There was a prominent calcification focally seen in the muscularis propria. Focally polarizable and nonpolarizable (calcium) material deposition within lymphovascular spaces in subserosa, which causes vascular obstruction, associated with the perforation. Nonpolarizable material deposition diffusely present in the walls of small and occasionally medium-sized blood vessels in the submucosa and muscularis propria suggestive of calcium deposits. This was confirmed by the von Kossa stain for calcium, validating the diagnosis of gastric calciphylaxis. Furthermore, the immunohistochemical studies for CD68 and S-100 were positive. Similarly, skin lesions were confirmed to be cutaneous manifestations of calciphylaxis. Thus, gastric calciphylaxis is a pseudo-vasculitis syndrome that blocks small vessels by calcium deposits leading to an ischemic process that may lead to gastric ulcers and perforation. This entity should be distinguished from gastric mucosal calcinosis which calcium deposits involve the gastric mucosa and stoma. The optimal treatment for gastric calciphylaxis arteriolopathy is not known.

920 The Eye Can Only See What the Mind Is Prepared to Comprehend: An Uncommon Cause of Dyspnea Eseoghene Ayisire, MD, MPH, Ebube Nwaigwe, MD, FACG. St. Vincent Charity Medical Centre/Case Western Reserve University, Cleveland, OH. Introduction: Gastric volvulus is the rotation of the stomach along its long or short axis. If undetected sequelae may include gastric outlet obstruction, ischemia, gangrene and intra-abdominal sepsis. Case Report: 83-year-old Caucasian female, PMH of hypertension, hypothroidism, bipolar disorder, dementia and panic attacks. She presents with intermittent shortness of breath over the last 3 weeks and chest discomfort. A cardiac work up was done and this was essentially negative. ROS: negative for nausea, vomiting, abdominal pain or change in bowel habits. Surgical history: None. Physical exam at admission showed an elderly woman, not in any obvious respiratory or painful distress. T-36.7, HR 60, RR 20, BP 108/57. Chest: clear lung fields bilaterally. CVS : RRR, S1 S2 only. Abdomen: scaphoid, BS present. No hepatosplenomegaly. Extremeties: no pedal edema, no calf tenderness. Labs at admission were grossly within normal limits. TSH was also normal. Blood gas showed pH of 7.49, pCO2 33 and pO2 of 77. A CT thorax ruled out a PE but revealed a large hiatal hernia with stomach in an organoaxial rotation in the thorax. Discussion: The differential diagnoses of shortness of breath are myriad but a good clinical history and physical exam usually helps to narrow them. An unusual cause of dyspnea is seen in this case of gastric volvulus. It is a diagnosis which is potentially fatal; sequelae may include gastric outlet obstruction, ischemia, gangrene and intra-abdominal sepsis. Gastric volvulus in itself is a rare clinical entity with the incidence peaking after the 5th decade in 80% of case1. A triad was described by Borchadt in which there is severe epigastric pain, unproductive retching and an inability to pass an NGT1. In most cases, it is difficult to ascertain from history and physical, leaving the diagnosis to imaging modalities. Radiographic findings of spherical gastric dilatation, paucity of distal gas and diaphragmatic elevation are suggestive of acute volvulus, particularly in patients with predisposing factors2. Predisposing factors includes paraesophageal hernia or diaphragmatic eventration1. Treatment of gastric volvulus is usually surgical reduction. Conclusion: Gastric volvulus will typically present as Borchardt triad. Our case illustrates that gastric volovulus can be a differential diagnosis in the symptom complex of dyspnea and chest discomfort. References: [1] Harford WV, McArthur KE. Diverticula, hernias, volvulus, and rupture. Sleisenger MH, Fordtran JS, eds. Gastrointestinal Disease: Pathophysiology, Diagnosis, Management. 5th ed. Philadelphia, Pa: Saunders; 1993:481-3. [2] Oh SK, Han BK, Levin TL, et al. Gastric volvulus in children: the twists and turns of an unusual entity. Pediatr Radiol 2008; 38:297.

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Figure 1. Gastric schwannoma arising from gastric body.

921 Successful Control of Upper GI Bleeding by Endoscopic Removal of Eroded Vertical Banded Gastroplasty Sadra Azizi, MD, Shawn Chaudhary, MD, Xinjun Zhu, MD. Albany Medical Center, Albany, NY. Introduction: We herein report a case of a 53-year-old woman with morbid obesity who had a vertical band gastroplasty 25 years ago presenting with a 1 day history of significant melena as well



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as left sided abdominal pain and nausea. Her hemoglobin downtrended to 7.7 with continued active melena in the emergency room requiring blood transfusion. EGD revealed hematin in the stomach with an eroded gastric band in the cardia of the stomach with surrounding ulcerated and inflamed mucosa. The surgery service was subsequently consulted and felt that taking the patient to the OR would be too high risk given the patient’s multiple co-morbidities. A therapeutic endoscopy was later performed for removal of the eroded band and to allow for more adequate mucosal healing to occur. Using a T2 scope, the mesh was grasped with forceps and pulled taut while endoscissors were used to cut and remove the majority of material to allow the cardia to return to its normal physiological position. After cutting away the major portion of the eroded band, the small remnants of mesh material retracted into the submucosa and the cardia became less constricted. The patient subsequently did well with no further bleeding or need for blood products and was discharged home several days later. This case further demonstrates the viability of endoscopic treatment of eroded gastric bands, which has been previously outlined in the literature. Eroded bands remain a significant long term complication of vertical band gastroplasty. Appropriate management and treatment of complications related to vertical band gastroplasty continues to be important, particularly as many of these patients are now presenting with long term complications from vertical bands performed 10 to 20 years ago. Relief of obstruction and reduction of gastric band material to allow for better healing along with reduction of further complications such as recurrent bleeding is achievable via an endoscopic approach. As the frequency of long term complications rises, the role of endoscopic therapy will continue to play an important role in the management of these patients. Our case demonstrates a viable, relatively low risk therapeutic option for treatment of complications related to vertical band gastroplasty.

tonitis. Here we describe a case of gastrointestinal bleed due to gastritis, as well as jejunitis and ileitis in a patient with paper pica. A 30-year-old male with a past medical history significant for biliary atresia, orthotopic liver transplantation with chronic rejection, diabetes mellitus, end-stage renal disease and sexual abuse in childhood presented with weakness, exertional dyspnea and melena. Physical exam revealed pale mucous membranes and heme positive stool. Laboratory studies on admission were significant for a hemoglobin of 5.8 from a baseline of 9.4. A CT scan of the abdomen showed nonspecific jejunitis and ileitis. An esophagogastroduodenoscopy (EGD) performed at the time of admission revealed nodular, erosive gastritis and a moderate sized clot without evidence of an active gastric bleed. The patient received multiple transfusions in the setting of persistent anemia. A second EGD performed on hospital day twelve revealed a large clot in the gastric fundus and multiple areas of nodular gastritis with visible oozing. On hospital day 29, the patient had an episode of emesis that contained fragments of paper mixed with digested food products. During a psychiatric evaluation, the patient admitted to daily ingestion of toilet tissue and paper towels. He later reported that this behavior developed following a period of significant sexual abuse by his father throughout childhood and adolescence. Paper pica is a rare etiology of colonic ischemia, peritonitis and intestinal perforation. Of these rare reports, intestinal obstruction was the most common clinical presentation requiring surgical intervention with mixed pica being a more likely cause of peritonitis and intestinal perforation. To our knowledge, this is the first known case of gastrointestinal bleed resulting from paper pica gastritis. Patients with this disorder often conceal their maladaptive behaviors. A thorough history and careful observation may hasten diagnosis and treatment in these rare and complex patients.

923 922 Gastric Sarcoidosis: A Case Report A Case of Gastritis in a Patient With Paper Pica Constantine Fisher, MD,1 Marci Laudenslager, MD,2 Manish Thapar, MD,1 Kenneth Rothstein, MD1. 1. Hahnemann University Hospital, Philadelphia, PA; 2. Drexel University College of Medicine, Philadelphia, PA. Introduction: Pica is an eating disorder characterized by excessive and persistent consumption of non-nutritive products. Paper pica is a rare etiology of intestinal obstruction, perforation and peri-

[922A]

Figures.

[923A]

Figure 1.


Kathlynn Caguiat, MD, Meira Abramowitz, MD, Veronika Dubrovskaya, MD, Safek Reka, MD, Rafael Garcia, MD, Ning Neil Chen, MD. SUNY Downstate Medical Center, Brooklyn, NY. Introduction: Gastric sarcoidosis is a rare disease characterized by granulomatous gastritis causing an array of symptoms and findings, including dyspepsia, upper gastrointestinal bleeding, and ulcerations. Involvement of the gastrointestinal tract occurs in 0.1 to 0.9% of patients with sarcoidosis, and to date, there are only 25 reported cases in the literature with histological evidence.


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[923B]

Figure 2.

Case Report: A 35-year-old African American female with history of cutaneous sarcoidosis, not requiring maintenance therapy, presented with one year history of epigastric abdominal pain. Physical exam demonstrated mild lower extremity edema with annular macules and dark discoloration on the lower extremities. Helicobacter pylori stool antigen was negative. She was treated with pantoprazole 40 mg daily and returned eight weeks later with persistence of her symptoms. The patient underwent upper endoscopy, which revealed superficial gastric ulcers in the antrum. Biopsies were obtained revealing active and chronic inflammation with non-caseating granulomas. Immunohistochemical staining did not reveal evidence of Helicobacter pylori or acid fast bacilli, or any other organisms. The diagnosis of gastric sarcoidosis was made given patient’s history of sarcoidosis, the endoscopic finding of gastric ulcers and histologic findings of non-caseating granulomas without presence of infection. Discussion: Gastric sarcoidosis is a rare cause of gastric ulcerations. In the setting of a known diagnosis of sarcoidosis with histologic findings of non-caseating granulomas in the stomach, the diagnosis of gastric sarcoidosis may be carried out once infectious etiology is ruled out. Treatment for gastric sarcoidosis is not well described in literature. It may include initiation of steroids with or without immunomodulators. The treatment of gastric sarcoidosis should be a collaborative approach between the gastroenterologist and the rheumatologist.

924 Afferent Limb Syndrome Presenting as Pancreatitis Due to Obstructing Gastric Stump Carcinoma Vinod Kumar, MD,1 Shobha Shahani, MD,1 Wael Youssef, MD, MBA, FACG2. 1. University of Illinois at Urbana Champaign, Chamapign, IL; 2. Carle Foundation Hospital, Urbana, IL. Introduction: Afferent limb syndrome is a serious complication after Billroth type II gastrectomy. One of the important causes is malignancy compressing on the afferent limb which may lead to obstruction to biliary flow, causing pancreatitis. Case Report: A 69-year-old Caucasian male with a history of Billroth type II procedure for peptic ulcer disease, presented with sudden onset of abdominal pain, nausea and vomiting for one day. Patient was noted to be febrile and he had leukocytosis and elevated lipase. Contrast enhanced computed tomography of abdomen/pelvis, was consistent with acute pancreatitis, soft tissue thickening, concerning for malignancy and limb obstruction. Upper endoscopy and endoscopic ultrasound was done which showed a large fungating mass at the junction of gastro-jujenal anastomosis from billroth type II surgery, causing significant narrowing of the afferent limb. Biopsies confirmed poorly differentiated adenocarcinoma. Subsequently, patient was taken for total gastrectomy with esophageal-jujenal pouch formation but intra operatively it was noted that there was a massive distension of proximal jejunal loops which were traced and found it to be consistent with the afferent limb coming up to the stomach. The afferent limb was massively distended, almost to the point of undergoing ischemic changes and causing pancreatitis as the biliary and pancreatic secretions were being trapped within the afferent loop. A drainage catheter was placed for decompression of afferent limb with a distal feeding jujenostomy catheter. Post-operatively, patient was started on total parental nutrition and later discharged to an extended care facility to recover and to be started on neo-adjuvant chemotherapy and to return for complete resection of the mass at a later date.


Discussion: Patients who have undergone partial gastric resections are at an increased risk for the development of cancer in the gastric remnant. Anastomotic or suture line recurrence of gastric cancer after gastrectomy is reported to be 3% to 10%. The overall risk increases over time and is greater in patients with gastric ulcers as compared to duodenal and in men following partial gastrectomy with Billroth II reconstruction. Malignancy causing afferent limb syndrome is a very rare and can lead to bowel ischemia, pancreatitis and ascending infection. Other causes of afferent limb syndrome include strictures, adhesions, volvulus and enteroliths. Conclusion: Early identification and treatment is essential as it is life saving for the patient and prevents bowel ischemia, perforation and peritonitis. Also early identification of the cancer and resection can prevent metastasis and leads to increased survival.

925 Superior Mesenteric Vein Thrombosis Secondary to Intestinal Malrotation Following Roux-En-Y Gastric Bypass Presenting as Recurrent Episodes of Ascites Victor Velocci, MD,1 Ahmad Malas, MD,2 Michael Piper, MD, FACG2. 1. Internal Medicine, Providence Hospital, Southfield, MI; 2. Gastroenterology, Providence Hospital, Southfield, MI. Introduction: Superior mesenteric vein (SMV) thrombosis in association with Roux-En-Y gastric bypass (RYGB) is a phenomenon that typically occurs in the acute postoperative period. Patients present with symptoms of increasing abdominal pain requiring immediate intervention. We report an unusual case of chronic thrombosis of the SMV following RYGB secondary to intestinal malrotation, which presented as abdominal pain secondary to ascites. Case Report: The patient, a 41-year-old female with a medical history significant for RYGB 8 years prior, presented with complaints of abdominal distension and pain. The pain had started 2 weeks prior, was diffuse and achey and continued to increase in intensity. Physical examination was significant for moderate abdominal distension. Workup included an US guided paracentesis that produced 1 000 milliliters of straw colored fluid. Analysis revealed a SAAG of 1.5 with a low protein level, consistent with cirrhosis as the underlying etiology. The patient had a CT guided biopsy of the liver which showed chronic hepatitis, with grade 2 inflammation and stage 2 fibrosis. The ascites was attributed to her liver disease and portal hypertension, and appropriate diuretic therapy with furosemide and spironolactone was started. During the subsequent 12 months, and in spite stable liver disease on subsequent biopsy, the patient was admitted an additional 15 times. Three admissions for abdominal pain due to a recurrence of ascites and 12 for symptomatic severe anemia with obscure overt GIB. EGD performed during one of these admissions was significant for small non-bleeding esophageal varices grade 1-2. CT angiogram of the abdomen and pelvis demonstrated extensive mesenteric varices due to chronic occlusion of the superior mesenteric vein. It was now believed that the patient’s recurrent episodes of ascites and anemia were in part due to this chronic occlusion of her SMV, and caused by intestinal malrotation following her RYGB. Discussion: Both surgery and cirrhosis are independent risk factors for the formation of chronic SMV thrombosis. In addition to these two features, our patient also had intestinal malrotation associated with her RYGB, a condition which has been described in the pediatric literature as being responsible for


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chronic SMV thrombosis. Gastric varices formation is known to be caused by chronic SMV thrombosis and is responsible for up to 37.5% of the mortality amongst these patients. The development of ascites is less common and described mainly in case reports. We present a novel case of a patient with complaints of abdominal pain secondary to ascites caused by chronic SMV thrombosis, attributed in part to intestinal malrotation after RYGB.

926 A Stomach Through the Eyes of EBUS Bronchoscopy Tarek Sawas, MD,2 Shadi Al Halabi, MD MPH,1 Abdul Hamid Al Raiyes, MD,1 Thomas Gildea, MD1. 1. Cleveland Clinic, Cleveland, OH; 2. Georgetown University Medstar Washington Hospital Center, Washington, DC. Introduction: Hiatal hernias are frequently an incidental finding on an upper endoscopy, barium swallow, manometry study or abdominal/chest imaging. We present the first reported case of a sliding hiatal hernia as an incidental finding on EBUS bronchoscopy. Case Report: A 72-year-old man with a history of a pituitary macroadenoma was transferred to the medical ICU with altered mental status, hypotension and worsening of non-productive cough. Upon further workup, a computed tomography of the chest demonstrated mediastinal adenopathy in addition to migration of subdiaphragmatic stomach into the chest cavity (Figure 1). While navigating the airway with EBUS bronchoscopy, stomach tissue was identified at the medial wall of the left main bronchus consistent with a hiatal hernia (Figure 2). Discussion: A hiatal hernia is described by the protrusion of the gastroesophageal junction into the chest cavity. It can be seen in up to 80% of the general population. It is usually suspected in patient with gastroesophageal reflux disease and has been associated with Barrett’s esophagus. It is frequently an incidental finding on an upper endoscopy, barium swallow, manometry study or abdominal/chest imaging. Hiatal hernia has been recently reported as an extra-cardiac finding on echocardiographic exams. To the best of our knowledge this is the first reports of a sliding hiatal hernia as an incidental finding on EBUS bronchoscopy.

months. On physical exam he was febrile to 38.4 C, tachycardic, tachypneic, and had mild tenderness to palpation in the epigastric region. Significant laboratory work up revealed a normocytic hemoglobin of 11.5 gm/dL, total protein of 9.1, albumin of 2.7, and globulin of 6.4 gm/dL. Further work-up revealed paraprotenemia with elevated IgM levels to 5,880 mg/dL with normal IgA and IgG. Serum protein immunofixation revealed a monoclonal gammopathy of the IgM Kappa type at 895 mg/dl. Urine protein immunofixation found monoclonal-free kappa light chains. Computed tomography of the abdomen demonstrated marked thickening of the stomach with splenomegaly, left adrenal enlargement, and retroperitoneal adenopathy. The patient underwent an endoscopic evaluation and gastric biopsies which confirmed a small B cell lymphoma consistent with gastric MALT lymphoma. Cytogenetic analysis demonstrated a translocation (11:18), confirming the diagnosis. Interestingly, Helicobacter pylori stains were negative. A thorough literature review revealed several studies finding an association between monoclonal gammopathies and ‘extragastric’ MALT lymphoma. As such, up to one-third of patients with extragastric MALT lymphoma also have monoclonal gammopathy, though, IgM gammopathy is not exceedingly rare in extragastric MALT lymphoma, an elevated IgM level is extremely rare in gastric MALT lymphoma with only one Korean case report in the literature. The findings of monoclonal IgM Kappa gammopathy are most often associated with Waldenström’s macroglobulinemia (WM). It is important to distinguish the two as the treatment of WM differs greatly from the treatment of MALT lymphoma. Extensive literature review on this topic found that hypergammopathy is associated with a more difficult to treat extragastric MALT lymphoma as well as distant metastasis. Thus, it has been suggested that paraprotein analysis be done routinely in the staging of MALT lymphoma along with monitoring of IgM levels to monitor therapeutic response. It is not known if this therapeutic response can be found in gastric MALT lymphoma. Our patient will be followed with serial IgM levels to see if the same response to treatment occurs. We highlight in this case report the rare finding of IgM kappa gammopathy and gastric MALT lymphoma, which has not been extensively described in the literature.

928 Severe Hyponatremia Causes Intractable Nausea and Vomiting Stacey Wells, MD,1 Sarah Khan, MD,2 James Morris, MD,3 Neeraj Singh, MD4. 1. Internal Medicine, LSU HSC Shreveport, Shreveport, LA; 2. LSU HSC Shreveport, Shreveport, LA; 3. LSU HSC Shreveport, Shreveport, LA; 4. LSU HSC Shreveport, Shreveport, LA.

927 Gastric Mucosa-Associated Lymphoid Tissue (MALT Lymphoma) and Immunoglobulin IgM Kappa Gammopathy: Is There an Association? Ibrahim Habib, MD, Sarosh Bukhari, DO, Dean Silas, MD, Hymie Kavin, MD. Advocate Lutheran General Hospital, Mount Prospect, IL. Introduction: A 58-year-old man with no significant history presented with progressive dyspnea and weight loss over the past 6 months. He also complained of intermittent nose bleeds and diarrhea for 2

Introduction: Intractable nausea and vomiting is a common cause of hyponatremia. We present a case where a seemingly simple diagnosis of hyponatremia, nausea and vomiting proved to be very complex. A 62-year-old man presented to the emergency room for intractable nausea, vomiting, altered mental status and falls. The patient’s medical history included alcohol abuse, chronic hyponatremia, chronic pancreatitis, chronic hepatitis C, coronary artery disease, hypertension, chronic kidney disease and diabetes mellitus. He had been discharged from the hospital weeks prior; after discharge, he continued alcohol binges, until relentless nausea and vomiting led to decreased oral intake, altered mental status for 2 weeks and slurred speech for 4 days prior to presentation. Blood pressure was 181/107.

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Figure 1. CT scan demonstrating hiatal hernia.

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Figure 2. Endobronchial ultrasound (EBUS) bronchoscopy revealing contour of a stomach at the medial wall of the left main bronchus.



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Abstracts Laboratory analysis showed serum sodium of 112 mmol/L (baseline 131 mmol/L), hypochloremic metabolic alkalosis, and lipase of 517 U/L. Creatinine was 1.7 mg/dL (baseline 1.1 mg/dL). Serum osmolality was 252 mOsm/kg (reference range 270-290 mOsm/kg) and urine sodium was less than 19 mmol. However urine osmolality returned elevated at 483 mOsm/kg. Urine toxicology revealed no ethyl alcohol. It was postulated that volume depletion secondary to nausea and vomiting from alcoholinduced pancreatitis caused severe hyponatremia. In the ER, 500 ml of normal saline was given, with a serum sodium increase to 113. He was transferred to the step-down unit on slow infusion of hypertonic 3% saline. After 2 days, serum sodium trended upward. Nausea and vomiting finally subsided. However, serum osmolality did not exceed 270 mOsm/kg and urine sodium and osmolality unexpectedly trended upward, indicating a persistent release of anti-diuretic hormone. A diagnosis of syndrome of inappropriate anti-diuretic hormone secretion (SIADH) was made. However, an etiology was not yet known. Chest X-ray and review of medications were nonrevealing. HIV test was negative. Finally, MRI of the brain showed a remote CVA in the left parietal lobe, a likely cause of chronic SIADH, hyponatremia and thus, patient’s intractable nausea and vomiting. Severe hyponatremia can cause neurologic and gastrointestinal sequelae. GI symptoms usually present when serum sodium falls less than 115 mmol/L and will cease once sodium increases toward the normal range. This case is an example of why recognizing the complex diagnostic algorithm of hyponatremia is important for all physicians, even the gastroenterologist.

929 Gastric Kappa-Restricted Plasma-Cell Neoplasm: Diagnosed on Routine Endoscopic Evaluation Rizwan Jafri, DO, Abby Sapp, DO, Mustafa Nawaz, DO, Alex Yarbrough, DO, FACG. Franciscan St. James Hospital, Olympia Fields, IL. Introduction: Extramedullary plasmacytoma is a solitary plasma cell neoplasm that occurs outside of the bone marrow and rarely involves the gastrointestinal tract. Methods: The patient was a 68-year-old male with past medical history remarkable for Barrett’s esophagus (diagnosed 11 years ago), hepatocellular carcinoma, GERD, prostate cancer, and lupus who presented for routine EGD screening. His chronic GERD was being managed with esomeprazole 40 mg daily. He denied weight loss, fevers, chills, lymphadenopathy, night sweats, abdominal pain, dysphagia, odynophagia, nausea, vomiting, or appetite changes. EGD with gastric biopsy revealed kapparestricted plasma cell neoplasm with associated amyloidosis. GE junction biopsy revealed ulcerative chronic active gastritis suggestive of early Barrett’s. In situ hybridization demonstrated marked predominance of kappa-positive plasma cells and few lambda-positive plasma cells. Immunofixation showed IgG kappa peak. IgM, free kappa, and lambda light chain, and β-2 microglobulin were all elevated. Urine protein electrophoresis demonstrated peak in the gamma region but negative immunofixation. Serum protein electrophoresis revealed M-spike. CBC did not reveal anemia. CMP was remarkable for creatinine of 1.3. Bone marrow biopsy revealed 2 mg/dl, and bone lesions. These findings were negative in our patient. Bone marrow biopsy revealed a small kappa predominant B-lymphocyte and plasma cell populations but was less than 1% of the total population. Solitary plasmacytoma show light chain restriction with either kappa or lambda but not both. Patients typically report symptoms related to the mass location. Our patient denied any active symptoms; however, he was actively taking omeprazole.

930 Unusual Case of Gastric Outlet Obstruction Amrit Banwait,1 Kuldip Banwait, MD, MBA2. 1. Amarillo High School, Amarillo, TX; 2. Panhandle Gastroenterology, Amarillo, TX. Introduction: To increase the awareness how duodenal ulcer with bleeding can present with gastric outlet obstruction. Methods: An 80-year-old man with a history of coronary artery disease, hypertension, arthritis on Plavix and aspirin who presented to the ER because of abdominal pain and vomiting. The abdominal pain has been going on last few weeks and the vomiting started 1 day before the admission. CT scan of the abdomen showed large amount of fluid in the stomach. Nasogastric suction tube was put with suction of large amount of fluid. Results: Upper endoscopy was performed which showed the stomach was distended with still large amount of fluid. Approximately 3 litres of dark fluid was suctioned out. There was a large blood clot at the pyloric channel. The patient was kept NPO with pantoprazole drip and NG suction. Repeat upper endoscopy 3 days later showed a large ulcer in the duodenal bulb. There was a large blood clot covering the ulcer. No attempt was made to dislodge the clot. The patient was prescribed Pantprazole and repeat upper endoscopy 6 weeks later showed complete healing of the ulcer. Conclusion: Blood clot from a duodenal ulcer is a rare cause of gastric outlet obstruction. We have to keep this in mind whenever a patient presents with abdominal pain, nausea and vomiting and evidence suggests gastric outlet obstruction.

[930A]

Figure 1. Pyloric channel blood clot.

931 Mechanically Engineered Bleeding From Gastrointestinal Tract Sabeen Zeb, MD. Internal Medicine, UIUC, Champaign, IL. Introduction: Melena is a very common presentation of upper gastrointestinal bleeding, seen very commonly in day to day practice and hospital admissions. The common causes usually seen are due to, gastric and/or duodenal ulcers, esophagogastric varices with or without portal hypertensive gastropathy. erosive gastritis or duodenitis, Mallory-Weiss syndrome, agiodysplasia, mass lesions (polyps/cancers), medication induced. A 55-year-old male, with past history of coronary artery disease status post coronary artery bypass graft, systolic and diastolic heart failure status post left ventricular assist device (LVAD), was admitted due to melena, without any other symptom. On admission hemoglobin was stable. There was neither history of use of no steroidal anti-inflammatory drugs use nor any dyspeptic symptoms. Upper gastrointestinal endoscopy was scheduled and that showed two bleeding points suggestive of arterio venous malformations (AVM) in the stomach and argon ablation was done. This was followed by video capsule endoscopy to look for further bleeding points. Meanwhile literature was reviewed and it has been documented that LVAD is associated with increased risk of AVM due to increase flow and resultant bleeding. The cause of bleeding is due to sheer forces on the blood as it gets pushed through the LVAD propellers, breaking up the globules of von Willebrand factor into fragments resulting in a coagulopathic state. Another important laboratory finding is the fact that INR in LVAD patients with bleeding was close to normal INR. In conclusion patients presenting with melena, especially with history of cardiac device, AVM due to device and resulting coagulopathic state should also be a consideration in the work up.

CLINICAL VIGNETTES/CASE REPORTS PANCREATIC/BILIARY

932 A New Complication of Biliary Stents Chang-Ho Yoon, BA, MBBCh,1 Jack Beadle, BSc, MBBS,2 Cassandra McDonald, BSc, MBBCh,2 Sohail Shariq, MBBS,2 Arabinda Pal, MBBS,2 Mariasoosai Pathmarajah, MBBS2. 1. Hammersmith Hospital, Imperial College NHS Trust, London, United Kingdom; 2. Ealing Hospital NHS Trust, London, United Kingdom. Introduction: This is the first reported case of a uterocolic fistula as a complication of biliary stent migration. The patient’s vague symptoms were disproportionate to the gravity of the iatrogenic



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pathology, and this vignette serves to highlight the importance of having a low index of clinical suspicion. Other educational points pertain to the choice of the biliary stent subtype, and to the issue of patient consent.

933 Drainage of a Pancreatic Pseudocyst Via a Spontaneous Cyst Duodenostomy: A Case Report Lilly Sadri, MD, Amar Thosani, MD, Satish Nagula, MD, FACG, Jonathan Buscaglia, MD, FACG. Stony Brook University Hospital, Stony Brook, NY. Introduction: Pseudocyst formation is a common complication of pancreatitis occurring in approximately 30-40% of chronic cases. Endoscopic or surgical drainage procedures are reserved for a cyst with mature walls and symptoms of abdominal pain, early satiety, or infection. We present a case of a 51-year-old woman with a history of necrotizing gallstone pancreatitis who presented 11 weeks later with a large pseudocyst complicated by severe abdominal pain and fevers. In the interim between CT scan and attempted endoscopic drainage of the pseudocyst, a spontaneous and acute fistula developed between the cyst cavity and the duodenum. The large cyst-duodenostomy seen on endoscopy allowed for complete drainage, thus precluding the need for endoscopic intervention and allowing for resolution of sepsis. Repeat endoscopy 3 months later confirmed complete closure of the fistula and resolution of the cyst cavity.

[932A] Figure 1. A parasagittal section of the CT abdomen illustrating the migrated biliary stent as a linear, high-attenuation entity involving both the colon and the uterus lying posterior to it.

[932B] stent.

[933A]

Figure 1. CT showing large pseudocyst.

[933B]

Figure 2. Pseudocyst after spontaneous drainage.

Figure 2. An axial section of the CT abdomen illustrating the same migrated



| OCTOBER 2014

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Abstracts

[934A]

Figure 1. MRCP and ERCP images.

934 Ominous Yet Benign Double Duct Sign in a Patient on Long-term Methadone Maintenance Virendra Tewari, MD,1 Deepali Tewari, MD,2 Raveendra Chigurupati, MD,3 Ayyappa Rangaraju, MD,3 Saurabh Dwivedi, MBBS3. 1. SUNY Downstate Medical Center, Brooklyn, NY; 2. NY Medical College, Valhalla, NY; 3. Interfaith Medical Center, Brooklyn, NY. Introduction: A 67-year-old African American male with hypertension, COPD, hepatitis C, latent tuberculosis, ex-intravenous drug abuser on methadone (30 mg daily, quit 20 years ago) came with RUQ abdominal pain and intermittent fever for 7 days. ROS was positive for constipation and laxative use. He was an ex-smoker and drinks 30 mL of vodka every other day. His vitals were: temp 100.1 F, BP 140/90, HR 84, RR 18, pulse O2 98%. Abdomen has significant RUQ tenderness. The rest of the exam was normal. Significant labs were Hb 10.4, creatinine 1.8, albumin 3.1, and total bilirubin 1.3. The rest of LFT, amylase, and lipase were normal. UA had 100 hpf RBC. Abdominal CT and sonogram showed dilated CBD 1.6 cm and PD 7.3 mm, distended GB with multiple stones, thickened wall and pericholecystic fat infiltration, right renal calculus and left ureteral calculus, and hydronephrosis. He was admitted with diagnosis of acute calculous cholecystitis with possible choledocholithiasis, and left ureter calculus with hydronephrosis. HIDA scan confirmed cystic duct obstruction. MRCP did not show any intraductal stone. His CA 19-9 turned as 417 (ref 0-35). Subsequently, he underwent 4 ERCPs (procedures performed were sphincterotomy and extension in first, second, and third balloon swipes in all, stent placement in second and fourth, stent removal in third) and 1 EUS examination at 2 institutes. None of them showed intraductal stone or other suspicious lesions. Biliary brushing from first and third ERCP were negative for malignant cells. Meanwhile, cholecystitis was managed conservatively with IV antibiotics. Repeat abdominal CT showed worsened cholecystitis with ascites. Though his CA 19-9 trended down significantly to 71, the ampullary biopsy obtained in third ERCP showed atypical cells. Modified Whipple surgery was performed for suspicion of malignancy, but histopathology examination of the resected surgical specimen found negative for malignancy. Six months post surgery, he is doing well and is pain free. Urologist has assessed his left kidney to be nonfunctional, which would not benefit from release of obstruction. In conclusion, apparently our patient had biliary and pancreatic ductal dilatation secondary to long-term opioid abuse and methadone maintenance treatment. He needed cholecystectomy and cautious follow-up only.

[935A] Figure 1. CT scan revealing a 3.9-cm solid pancreatic tail mass and metastatic-appearing liver lesion.

935 Pancreatic Tail and Liver Metastases Related to Recurrent Breast Cancer

936

Joseph Yarze, MD, FACG. Gastroenterology Associates of Northern New York, Glens Falls, NY.

“Migrating” Cholecystectomy Clip Within a Choledocholith

Introduction: To describe a case of pancreatic tail and liver metastases related to recurrent adenocarcinoma of the breast. Case Report: A 71-year-old female presented in March 2013 with a 2-month history of dull, intermittent LUQ pain that had no precipitating, exacerbating, or mitigating factors, and a few-pound weight loss. Her past medical history was significant for prior adenocarcinoma of the right breast [ER (+), PR (-)], which was diagnosed in 2005. She was initially treated with modified radical mastectomy and a subsequent 5-year course of adjuvant tamoxifen. Prior to GI consultation, an abdominal CT scan was normal, aside from a suggestion of left colon thickening. Colonoscopy was normal to the cecum, with ileal intubation. EGD was performed due to dyspepsia, and it was normal, including random sb biopsies. Due to the persistence of pain, a repeat abdominal CT scan was pursued in August 2013, and it now revealed a 3.9-cm solid pancreatic tail mass and numerous metastatic-appearing bilobar liver lesions (Figure 1). Liver biopsy revealed adenocarcinoma. A serum Ca 19-9 was 2 (N=0-37 U/mL). A serum 27.29 was 209.2 (N=0-38.6 U/mL), and it had previously been normal on numerous occasions. Immunostaining of the liver biopsy tissue revealed that it was ER (+), PR (-), and there was expression of GATA3. In concert, these clinical, pathologic, and serologic findings were believed to be most consistent with recurrent breast cancer. The patient was initially treated with systemic chemotherapy (paclitaxel) in association with an aromatase inhibitor. Conclusion: Recurrent breast cancer can often present in an unusual fashion, as in this patient, who, 8 years after initial diagnosis, developed metastatic disease to the pancreatic tail and liver.

Joseph Yarze, MD, FACG. Gastroenterology Associates of Northern New York, Glens Falls, NY.


Introduction: To describe a case of a “migrating” cholecystectomy clip, which was found to be within a choledocholith. Case Report: A 68-year-old male with a history of afib and diabetes melitus presented with transient RUQ pain, fever, and rigors. He had undergone laparoscopic cholecystectomy 12 years previously for treatment of gangrenous cholecystitis. Upon hospital admission, physical exam revealed RUQ tenderness and bloodwork revealed peripheral leukocytosis. The LFTs were abnormal, with serum total bilirubin 4.0 (N=0.2-1 mg/dL), AST 439 (N=12-32 U/L), ALT 579 (N=20-65 U/L). The serum alkaline phosphatase was normal. RUQ sono revealed the patient to be status post cholecystectomy, and there was no biliary dilation or liver abnormality. Abdominal CT revealed a 2-cm cystic-appearing lesion and numerous clips in the gallbladder (GB) fossa region. There also appeared to be a vertically oriented clip in the CBD. Interestingly, an abdominal radiograph performed prior to an UGI series 2 months previously revealed only a solitary cluster of clips in the RUQ region. The patient was diagnosed as having clinical cholangitis. He was started on broad-spectrum antibiotics and ERCP was performed. At ERCP, biliary cannulation revealed a 5-mm filling defect within a non-dilated CBD. There was a vertically oriented clip within this CBD filling defect (Figure 1). There was also a large GB fundus remnant with numerous clips in the vicinity. Another filling defect (which had a clip in its center) was seen in the GB remnant. The intrahepatic biliary tree was normal. Biliary sphincterotomy was performed, and the small CBD stone (with clip) and purulent bile were removed with a balloon. The patient recovered uneventfully.


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Conclusion: Surgical clips can act as a nidus for biliary stone formation. Given the number of RUQ surgical clips that were visualized and the large gallbladder fundus remnant noted, it was suspected that there was difficulty at the time of prior cholecystectomy. It is hypothesized that some of the surgical clips may have migrated into the biliary tree postoperatively, after which they became nidi for gallstone formation.

[937B]

[936A]

Figure 1. Vertically oriented clip within a choledocholith.

937 Metastatic Renal Cell Carcinoma to the Distal Common Bile Duct Presenting as Jaundice Hina Omar, MD, Catherine Ly, DO, Baseer Qazi, MD, Kenneth Chi, MD. Lutheran General Hospital, Park Ridge, IL. Introduction: We present a case of renal cell carcinoma with intraductal metastasis of the distal common bile duct. A 69-year-old male was admitted with 2 weeks of pruritus, dark urine, and clay-colored stools. Physical examination revealed scleral icterus. His abdomen was soft, non-tender,

Figure 2.

non-distended without organomegaly or ascites. The total serum bilirubin was 19.8 mg/dL (conjugated bilirubin was 14 mg/dL), alkaline phosphatase at 855 U/L, and a serum aspartate aminotransferase and alanine aminotransferase at 446 and 313, respectively. Serum lipase was 538 U/L as well as tumor marker CA 19-9 at 45 U/mL. Computed tomography scan (Figure 1) of the abdomen and pelvis revealed a left renal mass, left aortic lymphadenopathy, and suspected metastatic pulmonary nodules. Intra- and extrahepatic biliary dilation with gallbladder distension was seen secondary to distal common bile duct obstruction. Endoscopic retrograde cholangiopancreatography revealed filling defects in the distal common bile duct. Sphincterotomy was followed by multiple balloon sweeps removing 2 small calculi. Repeat cholangiogram (Figure 2) revealed a persistent filling defect in the distal common bile duct. A 10 x 60-mm covered metal biliary stent was placed and intraductal biopsy showed a clear cell carcinoma, consistent with renal origin. There are few reported cases in the literature of renal cell carcinoma with intraductal metastasis to the distal common bile duct without liver involvement. Renal cell carcinoma is often characterized by the presence of metachronous metastases to unusual sites. However, metastatic common bile duct tumors are extremely rare. This case illustrates the importance of considering metastatic renal cell cancer as a cause for obstructive jaundice in a patient with a renal mass or a history of renal cell cancer.

938 Noncommunicating Mucinous Biliary Cystadenoma: A Rare Cause of Jaundice Alicia Alvarez, MD, Kanwarpreet Singh Tandon, MD, Luis Lara, MD, FACG. Cleveland Clinic Florida, Weston, FL.

[937A]

Figure 1.


Introduction: Biliary cystadenomas (BCA) represent a rare cystic biliary neoplasm with the potential for malignant transformation. A limited number of cases of BCA have been reported worldwide. Two types have been described: mucinous and serous. BCA with ovarian-like stroma is a characteristic of mucinous cystadenomas and mainly affects women. Their clinical presentation is non-specific, including abdominal pain and fullness, nausea, increased abdominal girth, and, rarely, a palpable mass. We report a rare case of noncommunicating mucinous BCA presenting as painless jaundice. A 58-year-old healthy female presented with jaundice, pruritus, elevated liver enzymes, and dilated bile duct on abdominal US. MRI showed intrahepatic duct dilation and a cystic dilation of the common hepatic duct. ERCP revealed a stricture at the common hepatic duct near the bifurcation, cholangioscopy, and directed biopsies were unremarkable. Placement of a biliary stent resulted in a significant clinical improvement and resolution of lab abnormalities. The patient underwent endoscopic ultrasound, which showed an exophytic cyst compressing the common hepatic duct. Ten cc of mucinous fluid was aspirated with FNA. MRI showed a decreased size of the cystic lesion at the porta hepatis. ERCP was repeated to exchange the biliary stent. Cholangiogram showed luminal narrowing at the left hepatic duct take off with a fixed, round opacification occluding 75% of the lumen, and proximal to this was a second stricture where the lumen narrowed up to 95%. Due to the persistence of biliary obstruction, a laparoscopic common bile duct excision with cholecystectomy and choledochoduodenostomy was performed. A mass adherent to the anterior wall of common bile duct was removed. Histology showed a polycystic mucinous cystadenoma with ovarian type stroma and no dysplasia. The diagnosis of cystadenoma is rare, even more so when not communicating with the bile duct. It requires a high degree of suspicion and a multi-disciplinary approach to consider the diagnosis. Due to malignant potential and recurrence, they should be excised. Consider this unusual diagnosis in females with painless jaundice, elevated LFTs, and solitary cystic lesion.


| OCTOBER 2014

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Abstracts

[938A]

Figure 1.

[938B]

Figure 2. H&E; peroxidase stains.

939 Bouveret’s Sydrome: Not Your Garden Variety Gallstone Ileus Mohammad Ali, MD, Prateek Chapalamadugu, MD, Jennifer Slane, DO, Jarred Marshak, MD, Sabrina Mahboob, MD, David Friedel, MD, Stavros Stavropoulos, MD. Winthrop University Hospital, Mineola, NY. Case 1: An 81-year-old woman presented to the ER with 2 days of coffee-ground emesis associated with diarrhea, decreased appetite, and early satiety. Computed tomography (CT) scan revealed air in a contracted gallbladder and biliary tree with a gallstone distally in the gastric antrum measuring 1.6 x 1.7 x 1.7 cm. These findings indicated a biliary-enteric fistula, which lead to a partial obstruction. The gallstone was retrieved endoscopically after being broken into smaller fragments using a basket and

mechanical lithotripsy. Post-procedural recovery was uncomplicated, and the patient was subsequently discharged. Case 2: An 87-year-old woman presented complaining of 3 days of nausea, vomiting, and right upper quadrant abdominal pain. CT of the abdomen showed the presence of a lamellated radiopaque density in the third portion of the duodenum, implying a cholecystoduodenal fistula. EGD was performed and exposed an obstructing 4-cm stone in the duodenum. Electrohydraulic lithotripsy was effectively used to break the stone into smaller fragments before retrieval. The patient tolerated the procedure well, without complications. Discussion: Bouveret’s Syndrome is a form of gastric outlet obstruction caused by a gallstone in the distal antrum or proximal duodenum. It is more common in elderly women with a mean age of 74 years. Prominent signs and symptoms include nausea/vomiting, abdominal pain, hematemesis, abdominal

[939A] Figure 1. Abdominal CT images showing gallstone in gastric antrum.



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[939B]

Figure 2. (Left) Basket being used to perform mechanical lithotripsy. (Right) Gallstone fragments after removal.

tenderness, dehydration, and abdominal distention. Abdominal ultrasound and CT are the preferred diagnostic modalities. Although Bouveret’s is an uncommon variant of gallstone ileus, there is high morbidity and mortality associated with it. The purpose of this case series is to promote early recognition and illustrate how innovative endoscopic techniques provide useful treatment alternatives with high success rates, low morbidity, and negligible mortality.

940 SpyGlass Retrieval of SEMS Proximal to CBD Stricture Michael Richins, DO, MBA. University of North Texas Health Science Center, Fort Worth, TX. Introduction: A 52-year-old woman presented for an endoscopic retrograde cholangiopancreatography (ERCP) with stent exchange. She had a history of idiopathic chronic pancreatitis and had undergone 7 ERCPs for plastic stent placement and retrieval. The decision was made to use a covered self-expanding metal stent (SEMS) for the benign stricture, to avoid excessive repeat ERCP for plastic stent exchanges. After removing her plastic stent, a fully covered SEMS 10 x 40 mm was advanced to the site of the lesion. Due to miscommunication, it was deployed proximal to the stricture (Figure 1). Using balloon catheters, attempts were made unsuccessfully to drag the stent distally. At this point, the SpyGlass catheter was inserted, which allowed the distal aspect of the stent to be visualized (Figure 2). Despite poor visual acuity inside the CBD, the stent was grasped using a SpyByte forcep and pulled distally across the stricture. Other than mild stretching of a rim loop (Figure 3), it was intact. Normal bile flow was noted through the stent, and confirmed on fluoroscopy (Figure 4). This case illustrates an additional option to surgical management for patients who had a stent deployed proximal to a stricture inside the CBD.

[940A]

Figure 1.


[940B]

Figure 2.

[940C]

Figure 3.


| OCTOBER 2014

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Abstracts 942 Pancreaticoureteral Fistula: A Rare Complication of Pancreatitis Hiren Patel, MD,1 Nhat Nguyen, MD,2 Nihar Shah, MD,2 Sohail Shaikh, MD,1 Walid Baddoura, MD2. 1. St. Joseph’s Regional Medical Center, Paterson, NJ; 2. Seton Hall University School of Health and Medical Sciences, South Orange, NJ.

[940D]

Introduction: Pancreatitis is an inflammatory condition that can cause progressive and permanent destruction of the pancreas, which can lead to exocrine and endocrine insufficiency. There are many other complications associated with pancreatitis including formation of pseudocysts, pancreatic ascites, pleural effusions, splenic or portal vein thrombosis, pseudoaneurysm of splenic artery, and pancreatic fistulas. This case report describes an uncommon formation of a pancreaticoureteral fistula as a result of pancreatitis. Case Report: A 69-year-old Hispanic female with past medical history significant for recurrent episodes of pancreatitis with pseudocyst formation presented to emergency department with a chief complaint of sharp, severe, constant abdominal pain associated with nausea and a few episodes of non-bloody, non-bilious vomiting. Her last episode of acute pancreatitis was 2 months ago. Vital signs were normal. Physical examination revealed mild tenderness in the left upper and left lower quadrant without any guarding or rigidity. A computed topography (CT) scan of abdomen was performed which showed an abnormal pancreatic duct in the body and tail of the pancreas with complex multiloculated pseudocyst within the body and tail of the pancreas, extending anteriorly into the lesser sac to the stomach, posteriorly and medially extending into the level of the left kidney with possible fistula formation with mild left-sided hydronephrosis. To evaluate the presence of the fistula, the patient underwent cystoscopy with a left retrograde pyelogram which confirmed the presence of a fistula connecting the left renal pelvis to the pancreatic duct. A ureteral stent was placed at that time to facilitate closure of the fistula. Despite ureteral stent placement, the patient’s symptom did not improve so she underwent an endoscopic retrograde cholangiopancreatography (ERCP) with pancreatic duct stent placement. The patient remained symptomatic and ultimately underwent pancreatic cyst gastrostomy. Post-procedure, the patient improved and a repeat left retrograde pyelogram showed resolution of the pancreaticoureteral fistula. Conclusion: Pancreatic fistulas are rare complications of pancreatitis. Diagnosis can be made by imaging modalities such a CT, MRCP, ERCP, fistulography, etc. Treatment is conservative medical management; however, patients may need endoscopic or surgical intervention. Keep this rare complication in mind when evaluating a patient presenting with pancreatitis and urinary complaints.

Figure 4.

943

941

Small-Cell Neuroendocrine Carcinoma of the Gallbladder

Successful Use of Budesonide in the Treatment of IgG4 Cholangiopathy Carmi Punzalan, MD, MS, Curtis Barry, MD. Gastroenterology, UMass Medical Center, Worcester, MA.

Hiren Patel, MD,1 Abhishek Kumar, MD,2 Michael Maroules, MD2. 1. St. Joseph’s Regional Medical Center, Paterson, NJ; 2. Seton Hall University School of Health and Medical Sciences, South Orange, NJ.

Introduction: IgG4 cholangiopathy is an autoimmune diffuse sclerosing cholangitis typically associated with autoimmune pancreatitis. The disorder presents as obstructive jaundice and responds dramatically to steroids. Prednisone is the usual initial treatment for this disease. Steroid-sparing immunomodulators such as azathioprine can also be used. Case Report: A 66-year-old gentleman with diabetes initially presented with jaundice and abdominal pain in March 2013. ERCP demonstrated severe, malignant-appearing biliary stricture in the distal common bile duct (CBD). FNA was nondiagnostic, and brushings were negative for malignant cells. Endoscopic ultrasound demonstrated a thickened distal bile duct with suggestion of a small, 14-mm mass adjacent to the CBD. Subsequently, he underwent a Whipple procedure. Pathology demonstrated lymphoplasmacytic sclerosing, or autoimmune, pancreatitis. IgG4 was elevated at 133 mg/dL. He presented several weeks later with jaundice and pruritis and was found to have increase in his LFTs with a total bilirubin of 6.3. Repeat ERCP demonstrated multiple hepatic strictures, which were dilated and stented. Given his history and the ERCP findings, he was diagnosed with autoimmune cholangiopathy. He was started on prednisone 40 mg daily. Two months later, repeat ERCP demonstrated mild diffuse intrahepatic duct irregularities significantly improved from prior procedure. Stents were removed. LFTs normalized and he was started on azathioprine. LFTs increased whenever prednisone was discontinued. Blood sugars significantly increased on prednisone. Prednisone was then stopped, and he was started on budesonide 9 mg daily. Azathioprine 150 mg daily was continued. LFTs improved and have remained normal. Discussion: To our knowledge, this is the first case reported of the successful use of budesonide in the treatment of IgG4 cholangiopathy. Budesonide is a synthetic steroid with high first pass in the liver, which decreases its systemic effect. The successful use of budesonide in autoimmune hepatitis use has been extensively reported. A large study would be useful to evaluate the efficacy and safety of budesonide on the treatment of IgG4 cholangiopathy.

Introduction: Neuroendocrine carcinoma of the gall bladder is very rare. According to the reports of Modlin et al, it accounts for 0.2% of all the gastrointestinal carcinoids. It was first described by Albores-Saavedra et al in 1981. We present a case of small-cell neuroendocrine carcinoma of the gallbladder. Case Report: A 53-year-old Hispanic male with past medical history of hypertension presented to ER with 2 weeks’ history of constant right upper quadrant abdominal pain. The pain was associated with nausea, aggravated by meal intake, and no alleviating factors. The patient denied any fever, chills, jaundice, pruritus, changes in appetite or weight, and other bowel or bladder problems. The patient quit smoking 1 year ago and had history of 10 packs a year. He denied any alcohol or illicit drug use. There was no family history of any cancers. Vitals were within normal limits. Only positive physical exam finding was mild tenderness present on deep palpation in the right upper quadrant. Laboratory studies including liver functions tests were normal. Ultrasound of the abdomen showed large gallbladder polyp. MRCP revealed focal areas of polypoid wall thickening of the gallbladder measuring 1.1 x 6.6 mm and the second area of the contralateral side measuring 1.6 x 1.1 cm with luminal narrowing of the gallbladder and normal common bile duct. The patient underwent diagnostic laparoscopy with intraoperative ultrasound, showing 2 masses in GB with 1 small nodule noted in segment 4 and mass noted in segment 1 of the liver with thickened omentum. Biopsy was sent taken from omentum revealed poorly differentiated neuroendocrine carcinoma. Tumor cells were positive for ck7, synaptophysin, and chromogranin while negative for CK 20 and CA 19-9, which were consistent with small cell neuroendocrine carcinoma. Conclusions: Around 7,000 new cases of GB carcinoma are diagnosed each year, but incidence of neuroendocrine carcinoma of the gallbladder is very low, approximately 0.5% of all gallbladder cancers. Median age of diagnosis is 67 years. Up to 65% of the cancers are metastatic at the time of diagnosis.

[941]

Table 1. LFT Response to Treatment

Date

3/2

3/4

3/28

5/13

Event

Initial Admission

Post-ERCP

Post-Whipple

Readmissions

6/6 Post-ERCP and initiation of prednisone

10/30

11/20

12/26

2/25

Prednisone & AZA

AZA

Budesonide & AZA

Budesonide & AZA 0.5

Total Bilirbuin mg/dL

9.8

4.3

1.4

6.3

1.1

0.8

1.0

0.6

Alkaline Phosphotase U/L

446

309

53

855

198

121

360

124

81

AST U/L

206

140

67

135

17

24

53

22

22

ALT UL

437

351

62

361

144

26

65

31

25

AZA: azathioprine.



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The pathogenesis of acute pancreatitis in bulimia is likely multi-factorial, including the following: 1) thickened pancreatic secretions due to dehydration may reduce ductal flow, which is exacerbated by the increased enzymatic production with binge eating, 2) acinar cell atrophy, epithelial metaplasia, and increased zymogen granule release putatively from chronic malnutrition, 3) pancreatic cell damage and ductal disruption due to increased levels of pro-inflammatory cytokines (IL 1, IL 6 and TNF alpha), and 4.) depleted antioxidants. Additionally, retrograde pressure or reflux of duodenal contents into the pancreatic duct can occur with visceroptosis (gastrointestinal ileus and dilatation) seen after rapid weight loss and refeeding after starvation, leading to restricted flow of pancreatic secretions as well as impaired pancreatic capillary perfusion. Anorexia is not uncommonly seen together with bulimia. This condition has also been reported in conjunction with acute pancreatitis in about 15 cases in the literature. In summary, an underlying eating disorder, occult or known, should be considered as a possible etiology for acute pancreatitis in patients who do not have other more common risk factors.

946 Gastrostomy Tube Migration Causing Acute Pancreatitis Feng Li, MD,1 Mohamed Naem, MD,2 Cheng Zhang, MD, PhD,2 Somashekar Krishna, MD, MPH2. 1. Department of Internal Medicine, Ohio State University Wexner Medical Center, Columbus, OH; 2. Division of Gastroenterology, Hepatology and Nutrition, Department of Internal Medicine, Ohio State University Wexner Medical Center, Columbus, OH.

[943A] Figure 1. Hematoxylin and eosin section showing tumor cells consistent with small cell carcinoma.

944 A Rare Case of Multiple Pancreatic Metastases in a Patient With Renal Cell Carcinoma Syed Amer, MBBS, Vishnu Teja Kommineni, MD, Wajeeh Salah, MD, Cuong Nguyen, MD, Rahul Pannala, MD. Mayo Clinic, Phoenix, AZ. Introduction: A 76-year-old male was seen at another institution for nonspecific abdominal pain. Patient was status post right nephrectomy in 2006 for a 6-cm, clear cell, Fuhrman grade 2, pT1, N0, M0 renal cell carcinoma (RCC). He also had Gleason score of 8, T2 prostate cancer, with completion of neoadjuvant androgen deprivation and radiation therapy in 2013. His CT abdomen showed multiple enhancing nodules throughout the pancreas, thought to be consistent with chronic pancreatitis, due of his well-established history of heavy alcohol intake. Patient subsequently sought a second opinion at our institution. MRI and EUS showed multiple large hypervascular masses throughout the pancreas. EUS-guided FNA of the pancreatic tail mass was positive for adenocarcinoma, consistent with primary renal cell carcinoma. The patient declined treatment and eventually decided to pursue palliative care. A relatively uncommon malignancy, approximately 65,100 new cases of RCC were diagnosed in 2013, accounting for only 4% of all newly diagnosed cancers. SEER Registry data up to 2008 showed that 17% of RCC were metastatic. The most common sites of RCC metastases are the lung, bone, liver, brain, and adrenal tissue. Pancreas is a less common site, and the RCC mets are usually solitary. Vascular invasion is 5 times more likely than lymph nodes positivity, suggesting hematogenous spread as the possible metastatic route. On the other hand, metastases to the pancreas are also rare, accounting for 2-5% of all pancreatic malignancies. Radiologic findings that arouse suspicion for metastatic disease to the pancreas rather than a primary neoplasm include hypervascularity of lesions, absence of lymphadenopathy, and multicentricity. Differential diagnosis of a pancreatic mass includes lymphoma (minimal enhancement on CT), autoimmune pancreatitis (diffuse enlargement with loss of definition of pancreatic clefts and minimal peripancreatic fat stranding), and pancreatic ductal adenocarcinoma (poorly defined mass with surrounding desmoplastic reaction) and neuroendocrine tumors (well-circumscribed hypervascular masses). Synchronous presentation of primary RCC and pancreatic metastasis is rare, occurring in about 10%. The usual interval between nephrectomy to pancreatic recurrence is about 11 years, with no relationship between synchronous disease and survival.

Introduction: Percutaneous gastrostomy is the preferred method for long-term feeding for patients who cannot be fed orally. We present a case of acute pancreatitis caused by migration of the gastrostomy tube balloon into the duodenum causing obstructive pancreatitis. Case Report: A 52-year-old female with history of cerebral palsy presented to the emergency department with vomiting. The patient had a percutaneous endoscopic gastrostomy (PEG) tube placed 10 years ago due to dysphagia. Initial laboratory evaluation was significant for an elevated white cell count 15,200/uL, lipase 2238 U/L, ALT 78 U/L, AST 126 U/L. Bilirubin, calcium, and triglycerides were normal. Right upper quadrant ultrasound showed dilated common bile duct (CBD) 10-12 mm in diameter without evidence of calculus. CT abdomen/pelvis with IV contrast showed intrahepatic and extrahepatic biliary ductal dilatation with smooth tapering of the CBD up to the ampulla and PEG balloon within the duodenum near the ampulla (Figure 1). The balloon was deflated and the tube was withdrawn, resulting in improvement of laboratory values with normalization of transaminases and lipase over the next few days. A follow-up endoscopic ultrasound was performed in order to further eliminate other possible etiologies. The EUS showed reduction in CBD diameter to 6 mm without significant pathology in the entire pancreas or examined biliary tree. The patient continued to improve clinically and was discharged after 6 days. Discussion: This case illustrates an uncommon cause of acute pancreatitis. When a patient with a gastrostomy tube is diagnosed with acute pancreatitis or obstructive jaundice, gastrostomy malposition should be included in the differential, as early diagnosis and correction of obstruction can result in rapid biochemical and clinical improvement.

945 Bulimia: A Rare Cause of Recurrent Acute Pancreatitis Syed Amer, MBBS, Andrew Walker, PSM, MS, PAC, Cuong Nguyen, MD. Mayo Clinic, Phoenix, AZ. Case Report: A 30-year-old healthy, non-alcoholic woman was admitted with the third episode of acute pancreatitis in the preceding 5 months. She had no history of blunt trauma to the abdomen. The patient was only on PPI for GERD. An EGD, abdominal US, MRCP, and HIDA scan were normal at another hospital. On admission, her lipase was elevated at 250 (>4 x NL). Her abdominal CT scan showed a diffusely edematous pancreas with peri-pancreatic inflammation and fluid, consistent with acute pancreatitis. The CBC, BMP, lipids, IgG4, ANA, cocci titers, and HIV serology were within normal limits. Patient improved on conservative treatment. Further investigation revealed that the patient was under a psychiatrist’s care for a history for bulimia. In fact, she had been engaging in episodes of prolonged fasting followed by binging and self-induced vomiting. After extensive counseling, the patient was discharged with follow-up arranged with her psychiatrist. Discussion: Acute pancreatitis in the setting of bulimia is rare. Up to this date, fewer than 10 cases have been reported, whereas 25-60% of bulimic patients can have hyperamylasemia without radiographic evidence of acute pancreatitis. In the latter group, the non-pancreatic fraction of amylase is frequently elevated, suggesting a contributory role of observed parotid enlargement in bulimics.


[946A]

Figure 1.


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Abstracts 947 Intraductal Papillary Mucinous Neoplasm of the Pancreas in a Patient with Muir-Torre Syndrome Alicia Alvarez, MD, Kanwarpreet Singh Tandon, MD, Brenda Jimenez, MD, Luis Lara, MD, FACG, Andrew Ukleja, MD, FACG. Cleveland Clinic Florida, Weston, FL. Introduction: Intraductal papillary mucinous neoplasm (IPMN) of the pancreas is a potentially malignant cancer. We describe a rare patient with Muir-Torre syndrome (MTS) with a confirmed germline mutation of mismatch repair genes, who was found to have IPMN of the pancreas, a previously unrecognized association with the diagnosis of MTS. A 76-year-old Caucasian male with multiple malignancies (11): 3 colorectal, 3 bladder, 1 stomach, 1 duodenal, and 3 sebaceous and squamous cell cancers of the skin status-post total colectomy, partial gastrectomy, duodenectomy, and skin resections presented to the clinic with diarrhea, weight loss, and history of recurrent pancreatitis. The patient’s family history was significant for colon cancer in his mother, nephew, and niece, and stomach and colon cancers in half-brothers. The patient’s physical examination was unremarkable except for abdominal scars. CT scan showed dilation of main pancreatic duct and multiple cystic lesions in the body and tail of pancreas. MRI/MRCP showed the same findings consistent with main and side branch IPMN. EUS was technically not possible due to altered anatomy. Due to the extent of the disease, history of pancreatitis, and malignant potential, a distal pancreatectomy with splenectomy was performed. Pathology was consistent with IPMN with moderate dysplasia. Surgical margins were clear of disease. The tumor cells showed loss of expression of MLH1 and PMS2, suggesting microsatellite instability and retained expression of MSH2 and MSH6 compatible with the patient’s history of MTS. MTS described as a variant of Lynch syndrome (HNPCC), is a rare genodermatosis clinically characterized by at least 1 sebaceous tumor and 1 visceral (gastrointestinal or genitourinary) malignancy. It is an autosomal dominant disease associated with microsatellite instability and mutations of MLH-1, MSH-2, and MSH-6 DNA mismatch repair genes. Both MTS and HNPCC have been associated with pancreatic, bile duct, and ampullary adenocarcinomas, but IPMN has not been previously described with MTS and could be a precursor lesion for adenocarcinoma. Poor prognosis of pancreatic cancer makes early identification of high-risk individuals necessary. It is important to identify patients with familial cancer syndromes (FCS) in order to recommend appropriate screening interval and modality. IPMN can be diagnosed with non-invasive radiological studies or ERCP. In those patients with IPMN and FCS, treatment with pancreatic resection prevents progression to invasive cancer. Further studies are necessary to determine the prevalence of IPMN in MTS families.

948 From the Toe to the Pancreas? A Case Report of Metastatic Melanoma Presenting as an Obstructive Pancreatic Mass in an African American Male Cortni Tyson, MD. Howard University Hospital, Washington, DC. Case Report: A 77-year-old African-American male with dementia, hypertension, and history of recurrent melanoma presented to the hospital with chest pain for 1 day and mild unquantifiable weight loss over the last 2 months. He denied any abdominal pain, nausea, vomiting, diarrhea, or constipation. Cardiac evaluation was negative. Previously, he underwent a left halux amputation secondary to stage IIIc melanoma in 2006, with a recurrence to the left thigh in 2009, requiring excision. There was no family history of cancer. Social history was significant for less than 10-packs yearly history of tobacco use, no alcohol or drug use. On physical exam, vitals were normal, sclera icterus and jaundice were present, but no palpable abdominal masses noted on abdominal exam. Laboratory investigations revealed mild anemia with hemoglobin of 11.2, platelets 111, total bilirubin 11.6, AST 156, ALT 160, and alkaline phosphatase of 500. CT scan showed a pancreatic mass involving the neck, body, and uncinate process with regions of obliteration of the superior mesenteric vein and portal vein, and few small retroperitoneal soft tissue densities. Intrahepatic and extrahepatic ductal dilation were present. CT scan 21 months earlier was normal. ERCP was performed and demonstrated a single solitary mass in the head of the pancreas and pancreatic duct dilated to 3 mm in body. Preliminary cytopathology showed malignant cells, and biopsy showed characteristics suggestive of metastatic melanoma. Discussion: Melanoma represents 3% of all skin cancers, but 65% of deaths. Overall lifetime risk for African Americans is near 1/1000. Greater than 80% of melanoma is diagnosed at early stage; however, African Americans have overall lower 5-year survival, 78%, even when diagnosed at an early stage. They present with lesions in unconventional areas such as the soles of feet and mucosal membranes, and lesions are often misdiagnosed being mistaken for warts, ulcers, and calluses. Risk factors for non-whites have not been vigorously studied. The pancreas has been noted to be a site for metastasis in 40% of those with all types of malignancy, and is seen in 50% of patients with disseminated melanoma. Less than 1-2% present as a solitary metastatic melanoma lesion in the pancreas. The 5-year survival rate of metastatic melanoma with a solitary metastasis is 12%, which decreases to 0% when multiple metastases are present with an average survival of 4 months from diagnosis. Treatment with ipilimumab has been seen to increase survival to an average of 10 months with 1 year survival in 46%. Our patient was started on this treatment, but was lost to follow-up. This case demonstrates an obstructive pancreatic mass arising from an unusual source.

rejection, and coronary artery disease with stent placement 2 weeks prior to admission presented to Robert Wood Johnson University Hospital with multiple syncopal episodes and hematemesis. He denied melena and hematochezia. Vitals were notable for a blood pressure of 82/43 mm Hg and pulse of 95 bpm. The hemoglobin level was 8.1g/dL from an unknown baseline. He was resuscitated with intravenous fluids and 1 unit of red blood cells. An esophagogastroduodenoscopy showed a normal esophagus, stomach, and duodenum without evidence of bleeding. Later that night, the patient had maroon-colored stools and became acutely hypotensive and tachycardic. Repeat hemoglobin was 5.2 g/dL despite being transfused 1 unit of red blood cells earlier that day. The patient then suffered a pulseless electrical activity arrest and died. An autopsy was performed, which showed a massive gastrointestinal bleed with blood clots present throughout the stomach, small intestine, and large intestine. The transplanted pancreas was necrotic and hemorrhagic. It also revealed a fistula through the duodenal cuff into the jejunal anastomosis containing clotted blood, which was deemed to be the culprit of the bleeding. Cases of gastrointestinal bleeding related to failed pancreatic transplants are rare, but should be considered in patients with a history of a pancreatic transplant given the potential for massive bleeding. It is known that a reduction of the blood flow at the duodenal graft can lead to anastomotic leakage and hemorrhage in the immediate postoperative period. One study indicated that 11% of the patients studied experienced anastomotic hemorrhage between the jejunum and duodenal stump. Outside of the immediate post-operative period, causes of massive gastrointestinal bleeding after rejection of the transplant include donor artery pseudoaneurysm formation and rupture with subsequent extravasation of blood through the small-bowel fistula. This diagnosis is made with arterial angiography as opposed to endoscopy. Two case reports highlight the timely use of angiography to successfully localize the pseudoaneurysm with subsequent embolization and/or transplant pancreatectomy. Therefore, in patients status post pancreatic transplants who present with gastrointestinal bleeding, physicians should consider the pancreatic transplant as the cause of the bleeding and have a low threshold for obtaining arterial angiography.

950 Sickle Cell Intrahepatic Cholestasis: Reversal of Liver Function Without Exchange Transfusion: A Case Report and Review Literature Nattamol Hosiriluck, MD, Supannee Rassameehiran, MD, Erwin Argueta, MD, Lukman Tijani, MD. Texas Tech Health Science Center, Lubbock, TX. Introduction: Sickle cell intrahepatic cholestasis (SCIC) is a rare but potentially fatal complication of sickle cell disease. It is characterized by abdominal pain, hepatomegaly, and extreme hyperbilirubinemia with variable transaminase levels. Its clinical course ranges from benign hyperbilirubinemia to fulminant hepatic failure. In severe cases, renal failure and coagulopathy can be found. The only effective management for severe SCIC is early exchange transfusion to reverse liver function. A 48year-old man with sickle cell anemia presented with jaundice, abdominal pain, fatigue, and fever for 1-week duration. Physical examination showed mild epigastric and right upper quadrant tenderness with palpable liver. Blood analysis was significant for a total bilirubin of 48.9 mg/dL and increase in creatinine to 3.3 mg/dL from a baseline 0.8 mg/dL, albumin and coagulation were normal. Hemoglobin electrophoresis showed hemoglobin S of 88.6%. Hepatitis serology was nonreactive. Ultrasound and MRCP ruled out obstruction. The patient refused exchange transfusion but accepted intermittent blood transfusions. His bilirubin rose to a maximum level of 78.9 mg/dL. His kidney function gradually improved with fluid and returned to baseline. Bilirubin trended down to 56.5 mg/dL before discharge. Outpatient follow-up showed normal bilirubin in 2 months with conservative management. Studies showed that SCIC has an overall mortality rate of over 50%. Diagnosis of SCIC is established by ruling out other causes of hyperbilirubinemia. The only known effective management is exchange

[950]

Table 1. Outcome of 24 Case Reports of Patients Over 18 Years of Age With SCIC Died

Survived

Mortality(%)

Exchanged Transfusion

3

9

25

Simple Transfusion

10

2

83

949 An Atypical Case of Fatal Gastrointestinal Bleeding Hannah Xu, BSE,1 Vanessa Mewani, MD, MS,2 Matthew Czaja, MD2. 1. Robert Wood Johnson Medical School, Piscataway, NJ; 2. Robert Wood Johnson University Hospital, New Brunswick, NJ. Introduction: A 48-year-old male with a history of type I diabetes mellitus, diabetic nephropathy status post deceased donor renal transplant in 2011, pancreatic transplant in 2012 complicated by


[950A] Figure 1.


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transfusion to lower hemoglobin S level to less than 30%. Overall cases report in adult population to date confirmed that exchange transfusion reduced mortality rate from 83% to 25%. There were only 2 case reports of adult patient survived SCIC without exchange transfusion. Our case was the third known case report of severe type SCIC in adult that had a favorable outcome with supportive treatment. However, there will be a prolonged return of bilirubin to baseline in as opposed to aggressive management.

952  Please see page S659 for OUTCOMES RESEARCH  STOMACH.

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953

Recurrent Acute Pancreatitis Following Roux-en-Y Gastric Bypass (RYGB): The Afferent Loop Syndrome

Pancreatic Schwannoma Masquerading as a Mucinous Cystic Neoplasm

Feng Li, MD,1 Jonathan Congeni, MD,2 Somashekar Krishna, MD, MPH2. 1. Department of Internal Medicine, Ohio State University Wexner Medical Center, Columbus, OH; 2. Division of Gastroenterology, Hepatology and Nutrition, Department of Internal Medicine, Ohio State University Wexner Medical Center, Columbus, OH. Introduction: Creation of a surgical gastrojejunostomy leaves a segment of small intestine (usually containing duodendum and proximal jejunum) proximal to the anastomosis called the afferent loop. Mechanical obstruction of the proximal limb leads to afferent loop syndrome. In this case, we describe a case of acute pancreatitis caused by afferent loop syndrome. Case Report: A 75-year-old male presented to the emergency department with nausea, vomiting, and abdominal pain. Past medical history was significant for gastroparesis, for which he underwent subtotal gastrectomy with a roux-en-Y gastric bypass (RYGB) in 2011. Since gastric bypass, the patient experienced 3 episodes of acute pancreatitis, all requiring inpatient management. On initial evaluation, his abdomen was tender and distended with a palpable right-sided abdominal mass. Laboratory evaluation showed lipase >6000 U/L, ALT 566 U/L, AST 738 U/L, total bilirubin 1.4 mg/dL, direct bilirubin 1 mg/dL, alkaline phosphatase 95 U/L, white blood cell count 13.4 k/uL. CT abdomen/pelvis with IV and oral contrast showed homogenous enhancement of pancreas with diffuse peripancreatic fat stranding. There was marked dilatation of the biliopancreatic duodenal limb up to 10 cm with transition in the distal duodenum (see image). He was diagnosed with afferent loop syndrome and “secondary” acute pancreatitis due to mechanical pressure-obstruction of the major papilla. The patient subsequently underwent exploratory laparotomy with lysis of adhesions, and duodenojejunostomy. Following this, the patient improved symptomatically with normalization in lipase and transaminases. No other cause of acute pancreatitis was identified. There have been no further episodes of acute pancreatitis at follow-up (4 months post-op). Discussion: Acute pancreatitis due to afferent loop syndrome is rare following RYGB. However, prompt diagnosis is crucial since relief from mechanical obstruction by surgery facilitates resolution of acute pancreatitis and is thus the treatment of choice.

Jessica Barrett, DO, Jeffrey Archer, MD, Thomas Robertson, MD, John Matyas, MD, David Lo, MD. Riverside Methodist Hospital, Columbus, OH. Introduction: Pancreatic schwannoma is a rare neoplasm with fewer than 50 cases reported in the literature. Due to its rarity, pancreatic schwannomas can be confused with other more common cystic lesions. We present a case of a pancreatic schwannoma initially diagnosed as a mucinous cystic neoplasm. A 58-year-old female presented with an incidental finding of a pancreatic cyst on computed tomography (CT). The patient was otherwise asymptomatic, without weight loss, abdominal pain, or jaundice. She denied any personal history of pancreatitis. On physical examination, her abdomen was completely benign without any palpable mass. Endoscopic ultrasound (EUS) showed a 3 x 3-cm multiseptated cyst in the pancreatic head. Fine-needle aspiration (FNA) demonstrated benign epithelial cells and possible mucin-like material. Cyst fluid CEA level was 1.4 U/L, and amylase level was 334 ng/ mL. Given these equivocal results, a repeat EUS-FNA was performed 6 months later, revealing interval enlargement and wall thickening of the cyst. Cyst fluid CEA and amylase levels, as well as cytology, were similar to prior results. Molecular analysis (RedPath Integrated Pathology, Inc, Pittsburgh, PA) of the cyst fluid demonstrated moderate DNA quality, poor DNA quantity, and no evidence of KRAS point mutation or loss of heterozygosity. Given that the cytologic and EUS findings were concerning for a mucinous cystic neoplasm, the patient then underwent a pylorus-sparing pancreaticoduodenectomy. Pathology revealed a non-malignant spindle cell neoplasm, positive for S-100 and negative for CD-34 and CD-117, consistent with a pancreatic schwannoma. All margins and resected lymph nodes were free of neoplasm. The patient’s postoperative course was uneventful. Follow-up CT 3 months after her resection revealed no evidence of residual or recurrent disease. Although exceedingly rare, pancreatic schwannoma should be considered in the differential diagnosis for pancreatic cysts. These lesions are typically found incidentally on cross-sectional imaging and are mostly located in the head of the pancreas. Patients can occasionally present with abdominal pain. Diagnosis can be made by EUS-FNA and intraoperative biopsy, but it may be difficult to obtain a definitive preoperative diagnosis. Molecular analysis may be a useful adjunct in the preoperative evaluation. In our patient, the molecular profile appeared benign, which did correlate with the final surgical pathology. To our knowledge, this is the first report of molecular analysis of cyst fluid in a pancreatic schwannoma. Surgical resection can be performed if patients are symptomatic. The vast majority of reported cases are benign, and patients who undergo resection have an excellent prognosis.

954 Massive Intraperitoneal Hemorrhage Due to Perforated Cholecystitis Hajime Hirose, MD, Satoru Miyazaki, MD. Kinan Hospital, Tanabe, Japan. Introduction: Hemorrhage cholecystitis with gallbladder perforation is an extremely rare but serious associated complication of acute cholecystits. Accurate diagnosis using computed tomography is essential role for urgent surgical treatment.

[951A]

Figure 1.

[954A]


Figure 1. CT abdomen showing high density fluid in subhepatic space.


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Abstracts Case Report: A 75-year-old male patient who was hospitalized with steroid pulse therapy for nephrotic syndrome complained of right back pain. He was on anticoagulation therapy with warfarin 2.5 mg and aspirin 100 mg for aortic valve replacement. Laboratory findings: WBC of 18,700, AST of 36 IU/L, ALT of 121 IU/L, PT-INR of 2.86. CT showed gallbladder was distended with small stone on the neck of gall bladder. Ascites had been seen since admission due to nephrotic syndrome. He started to be treated with a course of antibiotics as acute cholecystitis under the patient’s comorbidities. Twelve hours later, he became hemodynamically unstable and life-threatening shock. Laboratory data revealed acute anemia Hb of 9.9 g/dL, which was 15.8 g/dL 12 hours ago. Again, CT showed that high-density fluid appeared around liver and gallbladder. Active intraperitoneal bleeding due to gallbladder perforation was suspected and he underwent urgent laparotomy. Surgical findings: 2 liters of fresh blood and clots were evacuated from subhepatic space. The bleeding point was not from obvious vessels, but from the mucosa of perforated gallbladder. A cholecystectomy and 1.2 liters of transfusion were performed. He recovered and was discharged 25 days after surgery. Discussion: Spontaneous intraperitoneal bleeding of gallbladder perforation was a few reported as a complication of anticoagulant therapy or steroid therapy. If acute cholecystitis occurs in such patients, we should allow for the bleeding in the gallbladder.

955 Gastroduodenal Signet-Ring Cell Carcinoma Presenting as IgG4-Related Sclerosing Cholangitis: Not Everything That Glitters Is Gold Tossapol Kerdsirichairat, MD, Juan Manivel, MD. University of Minnesota, Minneapolis, MN. Introduction: IgG4-related sclerosing cholangitis (IgG4-SC) is a new entity of cholangiopathy and IgG4-related disease, described as dense infiltration of IgG4-positive plasma cells and extensive fibrosis in the bile duct wall. We presented a case of signet-ring cell carcinoma of the duodenum with initial presentation of IgG4-SC. A 75-year-old male presented with gradual-onset painless jaundice and right upper quadrant pain for 3 weeks. He was afebrile, with mild right upper quadrant tenderness, without Murphy’s sign. Labs were pertinent for AST of 142 U/L, ALT of 142 U/L, alkaline phosphatase of 461 U/L, and direct/total bilirubin of 3.5/9.3 mg/dL. MRCP showed intrahepatic biliary dilatation with right hepatic duct strictures and non-visualization of the proximal common hepatic and central common bile ducts, replaced with vague enhancement. Further investigations were significant for negative CA 19-9, CA-125 of 125 U/mL (0-30), and normal gamma immunoglobulin subclasses. EUS showed marked thickening of the extrahepatic bile duct up to the hilum without definite mass lesion. He underwent ERCP for biliary sphincterotomy and biliary stenting. Biopsies of the ampulla and the bile duct showed frequent IgG4-positive plasma cells (30 cells/highpower field). Steroid was initiated for possible IgG4-SC. At 10 days after the index ERCP, he had worsening nausea and vomiting without worsening labs. ERCP for biliary stent exchange showed narrowing of the duodenal bulb and the proximal second portion of the duodenum. Biopsies of the duodenum and the bile duct showed nonspecific inflammatory changes without evidence of malignancy. Over a 4-week follow-up after the index ERCP, he developed worsening clinical gastric outlet obstruction. Repeat ERCP/EUS revealed thickening of the pre-pyloric antrum and proximal duodenum without obvious mass, and diffuse sclerosis of the bile duct, especially the right hepatic duct, and markedly dilated left duct. Duodenal biopsies eventually revealed poorly differentiated signet-ring cell carcinoma. At 2 months, he developed new-onset symptomatic pleural effusion and ascites. Cytology analysis of the fluids showed adenocarcinoma. He died under hospice care at 2 months after initial presentation. IgG4-SC is a new challenging disease that clinicians should consider in the differential diagnosis of cholangiopathy (e.g., cholangiocarcinoma and primary sclerosing cholangitis). This case represents an example of signet-ring cell carcinoma of the stomach and duodenum that presented as IgG4-SC. These could represent separate concurrent disease processes; the latter could result from immune dysregulation secondary to occult malignancy, or represent a nonspecific change.

should raise concern for possible IgG4RD. Pancreatic masses from the disease are often associated with obstructive jaundice, as most of them are found at the head of the pancreas. Less common locations include the body and the tail. Clinical setting and correlation with histopathological findings are essential, regardless of the actual serum or tissue IgG4 concentration. About 30% of patients may present with normal serum IgG4 concentrations, but if high suspicion is present, treatment with glucocorticoids is warranted.

957 A Rare Case of Gastrointestinal Bleeding From Choledochoduodenal Fistula William Hsueh, MD, Dennis Nguyen, MD, Mitesh Patel, MD. Medstar Washington Hospital Center, Washington, DC. Introduction: Choledochoduodenal fistulas (CDF) are a rare entity with potentially devastating complications. CDFs usually form secondary to long-standing duodenal ulcers or cholelithiasis. Symptoms vary depending on etiology but can include abdominal pain, fever, jaundice, vomiting, and hematemesis. We present a case of CDF in an 85-year-old bedridden woman who presented from a nursing home with an episode of hematemesis and melena. The PMH was significant for hypothyroidism, dementia, appendectomy, and cholecystectomy. There was no history of GI bleed, EGDs, NSAID, or anti-coagulation use. The patient denied fever, abdominal pain, nausea, diarrhea, or constipation. Physical exam was significant for scant melena. Labs showed WBC 13.7, H/H 8.7/25.5, PLT 284, INR 1.3, BUN/Cr 50/1.8, AST 23, ALT 16, ALP 69, T. Bili 0.4. The patient underwent an EGD which revealed an approximately 2-cm non-bleeding cratered ulcer in the apex of the duodenal bulb without stigmata of bleeding. There were four 2-3-mm slits within the ulcer which were returning bubbles and bilious fluid. A CT scan showed duodenal wall thickening and pneumobilia, with multiple locules of air tracking into the common hepatic duct and porta hepatis. The patient’s hospital course was complicated by hypotension requiring norepinephrine, afib with RVR, and emergent intubation during which she was noted to have copious bright red blood refluxing into the pharynx. The patient required massive transfusion protocol and was considered for surgery but was deemed not a candidate. The patient was taken to IR for suspected massive GI bleed likely from fistulization of the gastroduodenal artery (GDA). Coil embolization of the GDA was performed with preliminary hemostasis achieved. However, the patient developed recurrent melena so discussions of goals of care were initiated and comfort care was pursued. The patient passed away 10 days after embolization. CDF, while relatively uncommon, can have serious complications such as massive GI bleed as found in our patient. While symptoms may be vague, clinicians should suspect CDF in cases of spontaneous pneumobilia on imaging. Diagnosis is multimodal and includes EGD, ERCP, CT, US, x-ray, and MRI. Treatment varies depending on the size of the orifice, underlying etiology, and patient characteristics.

956 A Mass in the Junction of the Body and Tail of the Pancreas Eduardo Rodriguez, MD, Aaron Garza Romero, MD, Frederick Williams, MD. Internal Medicine, University of Miami Miller School of Medicine, Palm Beach Regional Campus, West Palm Beach, FL. Introduction: IgG4-related disease (IgG4RD) is a newly described inflammatory and fibrotic condition characterized by protuberant lesions, lymphoplasmacytic infiltrate that contains IgG4 positive plasma cells, and elevated serum IgG4 concentrations. The following case describes a case of IgG4RD with negative serology and a mass located at the junction of the body and tail of the pancreas. A 55-year-old female patient with significant history of lupus nephritis and hypertension, on daily orally lisinopril 40 mg and hydroxychloroquine 200 mg, presented complaining of 5 months of unintentional weight loss (20 lbs) and abdominal pain described as intermittent, 6/10 in intensity, non-radiated, and associated with nausea and anorexia. On physical exam, the patient was in no acute distress and vitals signs were within normal limit. Abdomen had bowel sounds in the 4 quadrants; it was soft, non-distended, non-tender, and with no organomegaly. Left axillary exam revealed a small, rubbery lymph node in deep tissue. Hemoglobin, white count, liver function test, amylase, anti-smooth muscle antibody, anti-mitochondrial antibody, Ca 19-9, complement C3, and C4, as well as IgG4, were all within normal limits. CT of the abdomen showed a 3-cm mass at the junction of the body and tail of the pancreas. Endoscopic ultrasound described it as a mass encasing the splenic artery without vascularity on doppler. Biopsy results demonstrated lymphoplasmacytic infiltrate with negative markers for IgG4 and no malignancy cells. Bone marrow and left axillary lymph node biopsy flow cytometry were negative for malignancy. PET scan showed pancreas, bone marrow, spleen, and lymphadenopathy with hypermetabolic uptake. The patient was started on prednisone 40 mg orally for possible autoimmune infiltrative disease. After 6 months, she reported almost complete resolution of symptoms, and follow-up PET scan showed marked interval improvement. Prednisone was tapered and had no relapse. She has been following as outpatient since then, asymptomatic. Differential diagnosis for tumefactive masses and lymphoplasmacytic infiltrates


[957A]

Figure 1.

958 EUS-Guided Pancreatic Intervention For Treatment Of Pancreaticocutaneous Fistulas Abdul Haseeb, MD, Larissa Fujii, MD, Barham Abu Dayyeh, MD, Michael Levy, MD, Randall Pearson, MD, FACG, Suresh Chari, MD, FACG, Jonathan Clain, MD, FACG, Michael Farnell, MD, Ferga Gleeson, MBChB, FACG, Michael Kendrick, MD, Bret Peterson, MD, Mark Truty, MD, Santhi Swaroop Vege, MD, FACG, Mark Topazian, MD, FACG. Mayo Clinic, Rochester, MN. Introduction: To evaluate experience with endoscopic ultrasound (EUS)-guided treatment of pancreaticocutaneous fistulas (PCFs) at a tertiary referral center. Methods: Retrospective review of patients who underwent EUS-guided management of PCFs. Demographic, clinical, imaging, procedural, and outcome variables were abstracted. Results: Four patients (3 female, age range 30-71 years) presented with PCFs. In all cases the fistula was due to an obstructed and leaking pancreatic duct in tail: 3 developed PCFs after Whipple procedure for malignancy (n=2) or an inflammatory mass (n=1), and the fourth developed a PCF following percutaneous drainage of a pancreatic fluid collection in the setting of severe acute pan-


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Abstracts

creatitis with disconnected pancreatic duct syndrome. Mean duration of the fistula was 189 days (range: 80-233). PCFs persisted despite trials of nil by mouth with TPN (n=1), octreotide therapy (n=2), and failed attempts at ERCP (n=4). The mean output was 350 cc/day (range: 200-500 cc), and mean amylase concentration was 15,866 U/L. Patients underwent EUS-guided transmural puncture of the pancreatic duct (n=2), fistula track (n=1), or both (n=1), with placement of 1 or 2 plastic transmural stents providing internal drainage to the stomach (n=3) or duodenum (n=1). Patients underwent a mean of 1.75 endoscopic procedures (range: 1-2), with placement of additional stents in the transmural track during the second procedure, as well as transmural drainage of an additional site of pancreatic duct leakage in 1 patient. Drainage from PCFs ceased after the first endoscopic intervention in 3 patients and after the second procedure in the fourth patient, and all percutaneous drains were removed. Stents were left in place indefinitely. One patient was lost to follow-up; mean follow-up for the remainder was 226 days (range: 170-410). In all 3 cases there has been no recurrence of PCFs, and no patient developed symptoms of pancreatitis, pancreatic fluid collections, or hyperglycemia requiring medical therapy. Weight stabilized or increased in all, and PCF-related pain resolved. Follow-up CT or MR performed in all patients after PCF drain removal showed no pancreatitis or fluid collections. Conclusion: EUS-guided pancreatic duct intervention may successfully treat pancreaticocutaneous fistulas, allowing removal of percutaneous drains. EUS-guided therapy is an attractive alternative for patients who might otherwise require pancreatic tail resection or completion pancreatectomy to achieve resolution of a PCF.

diffuse strictures throughout the intrahepatic and extrahepatic bile ducts and a severe stricture of the common hepatic duct. A sphincterotomy was performed however the strictures were not amenable to dilation or stenting. Extensive laboratory workup of underlying hepatobiliary disease revealed a reactive HIV antibody and a positive western blot for all bands. The diagnosis of AIDS cholangiopathy was made based on characteristic bile duct abnormalities in the context of proper clinical and laboratory evidence.

959 Markedly Elevated CA 19-9 in a Case of Mirizzi’s Syndrome: An Atypical Presentation Saba Ahmad, MD, Hiral Shah, MD, Patrick Hickey, DO, Matthew Sullivan, DO. Lehigh Valley Health Network, Allentown, PA. Introduction: The CA 19-9 antigen is commonly used as a tumor marker for malignancies of the pancreas and biliary tract. It has been suggested that high levels of CA 19-9 (>300 U/mL) have a strong correlation with malignant biliary pathology. In this case report, we present a patient with exceptionally elevated levels of tumor marker (CA 19-9 >4000 U/mL) in the setting of Mirizzi’s syndrome. Case Report: A 51-year-old male with a several week history of epigastric pain presented to the emergency department with new onset jaundice, tea-colored urine, and light stools of 1-week duration. Total bilirubin was elevated at 19.6 mg/dL. Initial abdominal CT scan revealed markedly dilated intrahepatic and common bile ducts, the latter measuring 1.5 cm. No stones or masses were visualized. CA 19-9 levels were elevated at 4258 U/mL. Given his presentation, clinical suspicion was high for a biliary tract malignancy, specifically early pancreatic cancer or a lesion at the ampulla of Vater. The patient underwent endoscopic ultrasound examination demonstrating a large stone at the junction of the cystic duct and common bile duct with a markedly enlarged gallbladder concerning for Mirizzi’s syndrome with impending hydrops. ERCP was performed with occlusion cholangiogram and balloon sweep of the bile duct without evidence of stones. The wire was advanced into the cystic duct with contrast injected to confirm the large stone at the junction of the bile duct and cystic duct. Maneuvers to remove the stone were unsuccessful. A stent was placed in the bile duct to achieve adequate drainage upstream from the obstruction. The magnitude of the stone was such that subsequent cholangiogram did not demonstrate cystic duct filling beyond the level of obstruction. The patient subsequently underwent percutaneous cholecystostomy tube placement and was continued on antibiotics. He improved clinically with gradual decrease of his hyperbilirubinemia and underwent a laparoscopic cholecystectomy four weeks later with normalization of his CA 19-9 level and liver-associated tests. Discussion: There is a growing body of data that demonstrates elevated levels of CA 19-9 in benign biliary pathology. To our knowledge, there are only 3 other reports of CA 19-9 elevations of this magnitude secondary to Mirizzi’s syndrome. EUS as a diagnostic tool was not mentioned in any of these reports and diagnosis was discovered intraoperatively during cholecystectomy or, in one case, laparotomy for open liver biopsy. EUS can be a useful tool to evaluate for gallstones impinging on the common bile duct to further distinguish between malignant etiology and Mirizzi’s syndrome, which can be difficult to visualize with other imaging modalities. Disclosure - Dr. Shah - Speakers Bureau: US Endoscopy.

[960A]

Figure 1. Cholangiogram demonstrating diffuse strictures.

961 Intragastric Balloon Causing Pancreatitis Ahmad AL Dobyany, MBBS, Medicine. King Abdul Aziz Medical City, Makkah, Saudi Arabia. Introduction: Intragastric balloon (IGB) is a temporary alternative for weight loss. Nausea, vomiting, and abdominal discomfort are the most common side effects. Acute pancreatitis secondary to IGB has been reported 4 times in the literature. Case Report: Our patient failed to lose weight by diet and exercise. IGB was successfully deployed and filled with 500 mL saline. Two months later, the patient presented with acute abdominal pain with epigastric tenderness. Lab data were normal except serum amylase (1362 IU/L). CT revealed the IGB compressing the pancreatic tail. The IGB was removed and the patient’s symptoms and labs returned to normal values. Discussion: IGB is generally safe and well tolerated. Most adverse effects are nausea, vomiting, and epigastric discomfort. Rare complications include: gastric ulceration, bleeding, perforation, or acute pancreatitis. Conclusion: We conclude that acute pancreatitis can occur post IGB placement due to mechanical compression, so increasing the awareness about this complication.

960 AIDS Cholangiopathy: An Uncommon Presentation in the Antiretroviral Therapy Era Christopher Linz, MD, Meer Ali, MD, Seth Rotz, MD, Pierre Gholam, MD, John Dumot, DO. University Hospitals Case Medical Center, Cleveland, OH. Introduction: Biliary manifestations of HIV have become rare since the advent of potent antiretroviral therapy. AIDS cholangiopathy is an infectious form of sclerosing cholangitis, usually seen in patients with CD4 counts less than 100/mm3. The organism most commonly implicated is Cryptosporidium parvum, however Cytomegalovirus, Giardia lamblia, Mycobacterium aviumintracellulare, Cyclospora cayetanesis, Isospora belli, Histoplasma capsulatum, and Microsporidium have also been identified. Definitive diagnosis is made by ERCP, demonstrating papillary stenosis, intrahepatic and extrahepatic sclerosing cholangitis, or an isolated long extrahepatic bile duct stricture. Treatment is targeted at symptomatic relief and initiating antiretroviral therapy, not the underlying opportunistic infection. The overall survival of patients is independent of AIDS cholangiopathy and follows the natural progression of HIV/AIDS. Herein, we describe the case of a 32-year-old woman with a history of multiple sexually transmitted infections who presented with nausea, vomiting, abdominal pain, weight loss, and jaundice for 1 month. She took no medications. She denied any alcohol or drug abuse but had multiple sexual partners and did not use barrier protection. She was afebrile and hemodynamically stable upon presentation. Physical exam revealed abdominal tenderness in the right upper quadrant. Laboratory values were notable for an elevated total bilirubin of 7.3 mg/dL with a direct bilirubin of 5.3 mg/dL, AST of 145 U/L, ALT of 265 U/L, and an alkaline phosphatase of 313 U/L. ERCP was performed and demonstrated


962 Successful Treatment of Hypertriglyceridemia-Associated Pancreatitis With Insulin Aaysha Kapila, MD, Charles Rives, MD, Neil Barry, DO, Pranav Patel, MD, Mark Young, MD. East Tennessee State University, Johnson City, TN. Introduction: Hypertriglyceridemia-associated pancreatitis (HTGP) is a life-threatening complication; it is the third most common cause of pancreatitis preceded by alcohol and gallstone. Triglyceride levels of more than 1000 mg/dL are considered a risk for pancreatitis. Early clinical recognition of HTGP is essential to improve morbidity and mortality. The pathophysiology is secondary to the hydrolysis of triglycerides (TG) into toxic free fatty acids (FFA) by pancreatic lipases, thus causing lipotoxicity during an episode of acute pancreatitis (AP). Insulin acts by inhibiting the action of lipase and thus preventing formation of FFA. HTGP often presents in patients with uncontrolled diabetes, where insulin can decrease both triglyceride and glucose levels in these patients. A 64-year-old white male with hypertension, hypertriglyceridemia and diabetes mellitus presented to the emergency department with abdominal pain, nausea, vomiting, and decreased appetite for the past week. The abdominal pain was sharp, non-radiating, and located on the left side of the abdomen was rated as 8/10 on the pain scale. The patient denied alcohol use or past history of pancreatitis but had a strong family history of hypertriglyceridemia. His triglyceride levels were always in the range of 600-800 mg/dL. Physical examination was sig-


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Abstracts nificant for epigastric pain. Labs were significant for lipase 936 U/L (0 to 160 U/L), glucose 346 mg/dL (0-100 mg/dL), hemoglobin A1c 10.3% (4%-5.6%), calcium 9 mg/dL, WBC 13.3 cells/mL (4,500-10,000 cells/mL), and triglyceride 1575 mg/dL (12gm/dl, WBC 493/HPF, RBC 15/HPF, Lymphocytes 70%, Monocytes 25%. CEA of cystic fluid was 6.5 and fluid lipase was elevated consistent with cystic lymphangioma. Follow up ultrasound showed no evidence of recurrence at 6 months with resolution of abdominal pain. Lymphangioma are benign lesions that originate from lymphatic vessels and typically arise in the head, neck, and axillary region (95%); pancreatic cystic lymphangiomas are an extremely rare subgroup and account for less than 1% of all lymphangiomas and only 0.2% of pancreatic lesions. Pancreatic cystic lymphangioma consist of interconnecting cysts separated by septa, lined by epithelial cells, and contain serous, serosanguineous, or chylous fluid. Although rare, lymphangioma should be considered in the differential particularly in the setting of previous extensive abdominal or pelvic surgery and disruption of chylous drainage. EUS-assisted complete drainage is a viable option in treatment of these cystic lesions.

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Figure 1.

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973 Adenomyomatous Hyperplasia of the Ampulla of Vater Masquerading as Malignancy: A Case Series Patrick Hickey, DO, Saba Ahmad, MD, Matthew Sullivan, DO, Jeffrey Brodsky, MD, Hiral Shah, MD. Lehigh Valley Health Network, Allentown, PA. Introduction: Adenomyomas are benign lesions rarely seen in the ampulla of Vater, composed of heterotopic pancreatic tissue. Patients may present with biliary obstructive, abnormal liver tests, and/or imaging abnormalities, but may be found incidentally. Endoscopic sampling of the papilla may show epithelial cell atypia suggesting dysplasia. Patients often undergo invasive surgical resection for presumed malignancy. In this case series 2 patients underwent pancreaticoduodenectomy for distal common bile duct (CBD) brush cytology adequate for adenocarcinoma with ultimate surgical pathology diagnosis revealing benign adenomyomatous hyperplasia (AH). Case 1: A 74-year-old female with a history of cholecystectomy presents with recent colonic surgery complicated by an intra-abdominal abscess. Computed tomography (CT) imaging showed new significant dilatation of the CBD without pancreatic mass. The patient underwent endoscopic ultrasound (EUS), and endoscopic retrograde cholangiopancreatography (ERCP) to further investigate dilatation. Gross dilatation of the CBD to 18 mm down to the ampulla and pancreatic duct prominence of 3.5 mm was confirmed with EUS. Cholangiogram showed significant upstream CBD dilation and a 1-cm stricture of the distal CBD. She underwent sphincterotomy, cytology brushings of the distal CBD, and biliary stenting. Cytology was positive for malignant adenocarcinoma. A pancreaticoduodenectomy was performed. Surgical pathology showed AH of the ampulla of Vater and incidental focal low-grade pancreatic intraepithelial neoplasia. Her postoperative course has been uneventful and she is doing well. Case 2: A 73-year-old female with a history of cervical carcinoma, chronic kidney disease, and cholecystectomy presents with epigastric pain, back pain, dark urine, and weight loss. MRCP showed CBD dilatation to 20 mm. EUS revealed prominent pancreatic duct (3 mm) and CBD dilatation to 20 mm (10 mm in the distal CBD). Cholangiogram showed a shelf with abrupt tapering in the distal CBD. She underwent sphincterotomy, cytology brushings of the distal CBD, and biliary stenting. Cytology showed distal CBD high-grade biliary intraepithelial neoplasia; could not exclude adenocarcinoma. After pancreaticoduodenectomy, surgical pathology specimens of the ampulla of Vater showed features of AH without carcinoma. Her course has been uneventful after postoperative recovery. Discussion: Although uncommon, AH should be considered in the differential of CBD dilatation. Brush cytology may be highly suggestive of dysplasia and lead to surgical resection. Gastroenterologists should be aware of AH of the ampulla of Vater as a rare benign clinical entity which may mimic a pancreaticobiliary malignancy. Disclosure - Dr. Shah - Speaker’s Bureau: US Endoscopy.

974 A Rare Case of Hemobilia: Ruptured Cystic Artery Pseudoaneurysm With Ectopic Ampulla of Vater Porter Glover, MD,1 Jennifer Thompson, BS,1 Scott Swendsen, MD,2 Vu Nhu Nguyen, MD,2 Duc Vu, MD2. 1. Internal Medicine, Baylor Scott and White Hospital, Temple, TX; 2. Gastroenterology, Baylor Scott and White Hospital, Temple, TX. Introduction: An 80-year-old white male presented to the emergency department with profound fatigue for 2 days. History and physical exam were unrevealing. Laboratory testing was notable for hemoglobin of 11.9. Multiple episodes of melena and a drop in hemoglobin to 9.6 occured on hospital day 2. Esophagogastroduodenoscopy (EGD) and colonoscopy did not reveal a source of bleeding, but melena was noted throughout the colon and in the terminal ileum. Tagged red blood cell scan was negative. Capsule endoscopy revealed fresh blood in the proximal small bowel. Hemoglobin dropped below 7 requiring transfusion. Repeat EGD with side-viewing duodenoscope (ERCP), revealed bile and blood pouring from a sinus orifice at the opening of the pylorus. Major papilla was not identified in the second portion of duodenum. CT angiography showed a focus of arterial enhancement within the gallbladder lumen. Embolization was unsuccessful. Gallbladder was resected at the infundibulum with surgical pathology demonstrating hemorrhagic congested mucosa, four 2.5-cm yellow/green stones, and acute necrotic and chronic cholecystic changes with extensive hemorrhage. At 1-month follow-up, patient was asymptomatic with hemoglobin of 11.3. Hemobilia as a cause of symptomatic acute blood loss anemia is a rare phenomenon. Furthermore, pseudoaneurysm as a cause of hemobilia has only been reported in the literature with 22 documented cases. We report a case of hemobilia occurring in the setting of cystic artery pseudoaneurysm with the addition of an ectopic ampulla of Vater located in the duodenal bulb. There is suggestion in the literature that ectopic biliary drainage may predispose to gastrointestinal complications including cholangitis, cholecystitis, and gastric outlet obstruction. In multiple large case series, ectopic location of biliary drainage is observed in 0.43%-2% of ERCP evaluations. The incidence of pseudoaneurysm seen concurrently with ectopic biliary drainage is unknown. Our patient presented with symptomatic life-threatening anemia requiring extensive work-up with multiple procedures as well as blood transfusions. Early detection during endoscopy with side-viewing duodenoscope (ERCP) as well as CT angiography should be considered for early diagnosis during obscure GI bleeding. The purpose of this case is to highlight a possible association of cystic artery pseudoaneuysm with ectopic biliary drainage and to encourage the gastroenterologist to think about rare causes of acute upper GI bleed, like hemobilia, and its variations, such as this case with an ectopic ampulla.

Case Report: A 76-year-old Caucasian male, presented with a history of weight loss, painless jaundice and abdominal pain. His liver enzyme elevation was consistent with a cholestatic pattern. A CT abdomen revealed a 4.1 x 4.9 x 5.0 cm enhancing inhomogeneous malignant-appearing mass in the head of the pancreas with dilation of the common bile duct. Endoscopic retrograde cholangiopancreatography identified a biliary stricture and an ampullary stent was placed. Brushings from the stricture did not reveal any malignant cells. Cytological examination of an endosonographically-guided fine needle aspiration specimen confirmed the diagnosis revealing a moderately differentiated squamous cell carcinoma with no glandular differentiation and positive immunostaining for CK 5/6 and p63. No other primary site for squamous cell carcinoma was identified. Since the tumor was in close proximity to the superior mesenteric artery, the surgical risk was high. The patient was treated with concurrent chemotherapy (5-fluorouracil) and radiotherapy. The patient was closely followed with biliary stent changes and surveillance imaging. He has shown a progression free survival of 13 months, the longest so far reported in the literature. Pure pancreatic squamous cell cancer is very uncommon with an incidence of 0.5% to 2% of all exocrine pancreatic neoplasms. It is often presumed to be metastatic from another primary site unless proven otherwise. It is postulated to originate either in squamous metaplasia in a setting of chronic pancreatitis, in a pre-existing adenocarcinoma or differentiation of primitive multipotent cells with malignant transformation. CT imaging is helpful in staging or determining primary malignancies elsewhere if any. Enhancement of tumor on contrast CT and tumor blush on angiography helps to differentiate squamous cell from adenocarcinoma due to its rich vascularity. It is an aggressive tumor with a dire prognosis. Surgical resection is the best curative option but often limited by local and/or distant metastasis. Chemotherapeutic options include 5-fluorouracil, Gemcitabine and platinum based regimens, with variable success rates and a reported median survival of 3 months. We present a rare case of an aggressive primary pancreatic squamous cell cancer with the longest reported cancer free survival following chemotherapy.

976 A Severe and Long-term Abdominal Pain Caused by Gastroduodenal Artery Embolization Jian Ding, MD, DO. Digestive Department of the First Affiliated Hospital, Fujian Medical University, Fuzhou, China. Introduction: We report a case of a 44-year-old male who presented with 2-month history of abdominal dull pain and 1 episode of hematemesis (hematemesis 5 times and bloody stools twice within 5 days). Pain was generalized at right upper quadrant, relieved after hematemesis. The gastroendoscopy examination showed acute duodenal papilla hemorrhage. Angiography showed vascular malformations in the head of pancreas and descending part of duodenum. Embolization of the gastroduodenal artery was performed via the hepatic artery. Four days after the embolization, duodenoscopy revealed a small amount of blood oozing from the duodenal papilla and the clinical manifestations of abdominal pain of patient subsided. More severe abdominal pain and dull pain appeared after the bleeding stopped, and it was unbearable. The patient was admitted to our hospital after 25 and 50 days following embolization treatment. Electronic duodenoscopy showed ulcers and some imaging manifestations like ischemic necrosis around the duodenal papilla compared with the result of previous duodenoscopy examination. We think different from the first abdominal pain caused by vascular malformation; the second and third causes when the patient was admitted to the hospital with abdominal pain were the ischemic necrosis of duodenal ampulla after interventional therapy. As time went by, the pain gradually subsided and eventually disappeared after 4 months after embolization treatment. DSA interventional treatment can bring about local tissue necrosis and revascularization, which has a relationship with clinical manifestations such as abdominal pain lasting for several months.

975 Surviving Primary Pancreatic Squamous Cell Carcinoma: A Rare Entity Presidential Poster Harjot Kaur, MD, Arjun Vaid, MD, Jagpal Klair, MD, Rayburn Rego, MD. Internal Medicine, University of Arkansas for Medical Sciences, Little Rock. Introduction: The pancreas is devoid of any squamous cells and the origin of a pancreatic carcinoma with primary squamous morphology is rarely described with little known about the natural history following treatment.


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Figure 1.


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Abstracts 977

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A Case of Exenatide-Induced Recurrent Pancreatitis Despite Withdrawl of Drug Therapy

Sump Syndrome after Choledochoduodenostomy: An Atypical Case Refractory to Endoscopic Therapy

Varun Jain, MD,1 Deepak Sharma, DO,1 Vimala Ramasamy, MD,2 Ava Anklesaria, MD,1 Gayotri Goswami, MD2. 1. Icahn School of Medicine at Mount Sinai (Bronx) - James J Peters VA Medical Center, Bronx, NY; 2. North Central Bronx Hospital, Bronx, NY.

Amir Rezk, MD,1 Kimberly Fairley, MS, DO,2 David Diehl, MD2. 1. General Internal Medicine, Geisinger Medical Center, Danville, PA; 2. Gastroenterology, Geisinger Medical Center, Danville, PA.

Introduction: An increasing number of cases of Exenatide-Induced acute pancreatitis have been reported and the FDA has issued a warning regarding this potential side effect. However, we report a novel case of recurrent pancreatitis, despite the discontinuation of Exenatide, in the absence of other precipitating factors. We followed the case of a 50-year-old male with history of HTN, DM type 2 (previously on Metformin, NPH Insulin and Exenatide for 2 years) that presented with acute pancreatitis (based on clinical symptoms, lipase and amylase levels and CT findings). Common causes of pancreatitis, including alcohol, gallstones, hypertriglyceridemia, infectious etiologies, and other medications were excluded prior to establishing the diagnosis of Exenatide-induced pancreatitis. Exenatide was discontinued during the initial admission, and he was treated conservatively until symptoms resolved. This patient was followed over the course of 7 months and was found to have two subsequent admissions with pancreatitis, despite having discontinued Exenatide. He was re-admitted 2-3 weeks after his first admission with laboratory and radiologic evidence of necrotizing pancreatitis and a pseudocyst. The patient was treated conservatively with intravenous fluids, pain management and was kept NPO. Symptoms resolved within 2 days and the patient was discharged. Two months later he had a third episode of pancreatitis with stable pseudocyst, which was also treated conservatively. Again, other etiologies of pancreatitis were absent. Based on our literature search, about 40 cases of Exenatide-induced pancreatitis, 6 of which were necrotizing or hemorrhagic, have been reported to the U.S. Food and Drug Administration in post-marketing trials as of 2008. A subsequent study reported a >6-fold increase in the risk of pancreatitis with use of Exenatide. The mechanism of how Exenatide may predispose to pancreatitis is not clearly understood. Exenatide is a GLP-1 agonist; studies have demonstrated in animal models that GLP1 mimetic therapy may cause pancreatic acinar inflammation with elevated serum lipase levels. The association between exenetide and acute pancreatitis is well known, however recurrance of pancreatitis despite withdrawl of therapy has not been documented. Here we present the first case of Exenatide induced recurrent pancreatitis after withdrawal of drug therapy. Since recurrent and chronic pancreatitis are known risk factors for pancreatic cancer, this validates the concern that the drug may increase risk of pancreatic cancer. Further studies are warranted corroborate this hypothesis.

Introduction: Sump syndrome is an uncommon ailment that affects patients after choledochoduodenostomy (CDD). Treatment is primarily distal common bile duct (CBD) decompression at the level of the ampulla with endoscopic sphincterotomy (ES). We describe a case of sump syndrome which persisted despite adequate endoscopic therapy. Case Report: An 84-year-old woman had undergone ERCP and ES for biliary stones. Despite a full sphincterotomy, recurrent stones developed, which necessitated multiple (4) ERCPs for duct clearance. CDD was done and the patient was asymptomatic for 5 months, but then again had elevated LFTs with biliary pain. MRCP demonstrated intra- and extrahepatic ductal dilation with pneumobilia and numerous filling defects in a very dilated (2.1 cm) CBD. Another ERCP was done, and cholangiography showed multiple filling defects. Direct cholangioscopy was achieved through the CDD which demonstrated a widely patent anastomosis with solid food particles present in the duct. Complete removal was accomplished with a biliary extraction balloon. The patient presented 2 weeks later with recurrent symptoms. A pancreaticoduodenectomy was performed for definitive management, and the patient had an uneventful recovery. She has not had recurrent biliary stones over a 1-year follow-up. Discussion: Sump syndrome results after CDD when the segment of the CBD between the ampulla of Vater and biliary-enteric anastomosis serves as a receptacle for stagnant bile, debris, stones, bacteria, and food particles. This material can pass through the anastomosis yet cannot pass through the intact ampulla of Vater forming the “sump”. Its prevalence has been reported to be between 0.0 and 9.6% after CDD. Treatment ideally will prevent complications such as cholangitis and pancreatitis. Distal CBD decompression at the level of the ampulla with ES has been the treatment of choice. Patients who do not respond to this therapy can be treated with Roux-en-Y hepaticojejunostomy. The explanation for disease status post sphincterotomy can include a large burden of particles that are unable to transverse the sphincterotomy or recurrent ampullary stenosis. The syndrome has been reported in a case report after Roux-en-Y hepaticojejunostomy and that patient was managed by operative decompression and redo hepaticojejunostomy with creation of longer Roux limb. CDD is a safe and useful procedure for distal CBD decompression in benign and malignant pancreaticobiliary disease with sump syndrome representing a rare outcome. This case highlights the need for alternative procedures for CDD patients with benign distal biliary strictures to prevent or treat sump syndrome.


981 IgG4-Related Autoimmune Pancreatitis Presenting With Multiple Extrapancreatic Manifestations Ketan Shah, MD, MBA, Mazen Jamal, MD, MPH. Veterans Affairs Medical Center, Long Beach, CA.

979 A Case of Extrahepatic IgG4-Sclerosing Cholangitis Devon Charlton, MD, Steven Brandwein, MD, FACG. Internal Medicine, Danbury Hospital, Danbury, CT. Introduction: IgG4-sclerosing cholangitis (IgG4-SC) without pancreatic involvement is quite unusual and presents a diagnostic challenge as it may mimic primary sclerosing cholangitis or cholangiocarcinoma. We present a case of IgG4-SC isolated to the extrahepatic biliary tree. Case Report: A 50-year-old man with a history of nodular sclerosing Hodgkin’s disease, statuspost splenectomy and radiation therapy at age 21, and type 2 diabetes presented with jaundice and pruritis. Over a several week period his liver function tests were elevated in a waxing and waning pattern with no treatment. Initial labs included a total bilirubin 3, alkaline phosphatase 623, ALT 921, and AST 387. Ultrasound and serological work-up was unremarkable. Liver biopsy showed chronic nonspecific active hepatitis. MRCP demonstrated intrahepatic biliary ductal dilatation in both the right and left lobes with abrupt termination at the bifurcation. The main common duct was normal in caliber and not visualized on MRCP. Lastly, the pancreas and pancreatic duct appeared normal. ERCP exhibited segmental strictures of the common bile duct with several strictures in the main duct and a stricture at the bifurcation. The intrahepatic ducts were dilated but otherwise normal. Choledochoscopy demonstrated no villous or ulcerated features. Bilateral plastic biliary stents were placed. Brushings and biopsies were negative for malignant cells. Given segmental strictures and no evidence of a neoplastic process, there was suspicion of an inflammatory process. Initial IgG4 was high-normal at 116. Repeat ERCP for stent replacement demonstrated no change and repeat biopsies were negative; but IgG4 was elevated at 167. Thus, prednisone 40 mg daily was started for suspected IgG4-SC. After 4 weeks treatment, repeat ERCP demonstrated resolution of the strictures and stents were removed. Follow-up MRI and liver tests were normal. Discussion: Of critical importance, IgG4-SC is a clinical mimicker of extrahepatic cholangiocarcinoma and it must always be considered. Diagnostic criteria is in development and characteristic features of IgG4-cholangiopathy should include at least 2 of 3 major criteria: increased serum levels of IgG4, positive staining of IgG4-positive plasma cells on histology, and steroid responsiveness. If IgG4-SC is suspected, a trial of steroids should be started. In contrast to primary sclerosing cholangitis or cholangiocarcinoma, the most characteristic feature of IgG4-SC is steroid responsiveness. Our patient did not have enough tissue to allow for IgG4 staining, but did meet the other 2 criteria. This case demonstrates a patient with extrahepatic IgG4-SC who avoided surgery and had resolution of his disease with a course of steroids.

Introduction: A 43-year-old male presented with a 1-year history of an asymptomatic left inguinal mass. CT scan demonstrated a 5.3-cm well-circumscribed round heterogeneous mass in the left inguinal region, but also demonstrated a conglomerate nodal 13-cm mass surrounding the infrarenal aorta and proximal common iliac arteries, as well as pulmonary micronodules. Excisional biopsy of the inguinal mass demonstrated a benign reactive lymph node. One year later, the patient presented with an acute onset of epigastric abdominal pain and obstructive jaundice. His labs demonstrated an elevated total bilirubin of 5.6 mg/dL, alkaline phosphatase of 210 IU/mL, and ALT of 504 IU/mL, with normal previous values 3 months prior. Serum lipase was 70 units/L. MRI demonstrated a diffusely enlarged pancreas. There was also intra- and extrahepatic biliary ductal dilatation to 10 mm and mucosal enhancement of the bile duct and gallbladder. His symptoms did improve on antibiotics. His serum IgG4 eventually returned at 851 mg/dL with the remainder of IgG subclasses being normal. One month later, he was readmitted for recurrent painless jaundice. Labs demonstrated a serum total bilirubin of 14.7 mg/dL, alkaline phosphatase of 698, AST of 120, and ALT of 224. CT demonstrated worsened diffuse bile duct dilatation to 2.4 cm and complete effacement of the common bile duct at the pancreatic head with distal decompression. The pancreas was also persistently enlarged. The patient was started on prednisone 40 mg once daily. One week later, endoscopic ultrasound demonstrated heterogeneous pancreatic parenchyma with findings consistent with chronic pancreatitis with no focal pancreatic mass. The bile duct dilation improved to 12.5 mm. ERCP demonstrated a smooth stricture in the distal common bile duct with no filling defects. A sphincterotomy was performed and a plastic stent was placed. Fine needle aspiration of the pancreas was nondiagnostic. On follow-up 3 weeks later, the patient’s jaundice and laboratory abnormalities completely resolved. A serum IgG4 and repeat imaging have been ordered and are currently pending. His corticosteroid dose was tapered. This case illustrates interesting findings of type 1 IgG4-related autoimmune pancreatitis along with extra-pancreatic involvement consisting of IgG4related autoimmune cholangitis, periaortitis, pulmonary nodules, and inguinal lymphadenopathy, and hence his clinical picture meets 4 out of the 5 Mayo Clinic “HISORt criteria.” With corticosteroids, his symptoms of pancreatitis and cholestasis did resolve, as did his laboratory abnormalities. Follow-up imaging and serum IgG4 is currently pending and will be available to report by the time of presentation of this clinical vignette.

982 A Rare Case of Gastrointestinal Bleeding Mitesh Bhalala, MD, Shireen Pais, MD, Grigory Rozenbilt, MD, Brad Dworkin, MD, FACG. New York Medical College, Valhalla, NY. Introduction: Evaluation for gastrointestinal (GI) bleeding occurs on a daily basis. We present a rare case of a life threatening bleed.



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Figure 1. (A) Bleeding through the papilla of Vater. (B) Pseudoaneurysm in the distal gastroduodenal artery. (C) Embolization of pseudoaneurysm.

Case Report: 64-year-old man with history of vascular disease s/p multiple stents, hypertension, and alcoholic pancreatitis presented for catheterization due to vascular complaints. He was found to have a hemoglobin of 6.9 mg/dl. He reported intermittent hematemesis and melena for the last 6 months. On exam, he was in mild distress, heart rate 100 bpm, BP 123/56 mmHg, with epigastric tenderness. Other labs were normal except for a lipase of 675 U/L. EGD was normal except for pooled blood in the second portion of the duodenum. A side viewing endoscope showed blood emerging from the ampulla interspersed with bile. Angiography revealed a pseudoaneurysm of the gastroduodenal artery. The diagnosis was consistent with hemosuccus pancreaticus (HP). He underwent successful embolization. MRI revealed chronic pancreatitis. Discussion: HP is defined as GI bleed via the pancreatic duct. It’s a rare cause of bleeding with ~100 cases reported. Most common causes are acute and chronic pancreatitis. Tumors, vascular disease, iatrogenic, congenital anomalies, infections, and trauma are rare causes. The pathophysiology is related to pseudoaneurysm formation due to auto-digestion into the peri-pancreatic vessels. The pseudoaneurysm communicates with the pancreatic duct through the pseudocyst or a fistula. Once bleeding occurs, the blood coagulates and obstructs the duct. This leads to increase pressure temporarily tamponading the hemorrhage. As the clot dissolves, hemorrhage recurs, resulting in intermittent bleeding. Patients may present with abdominal pain, GI bleeding and/or hyperamylasemia. Prompt angiography and treatment with angiographic embolization of pseudoaneurysms or surgery is warranted to control bleeding. Failure to recognize and treat HP is associated with mortality up to 90%, declining to 8-37% with treatment. Conclusion: HP should be considered in all patients with a history of pancreatic disease and severe GI bleeding when routine endoscopic findings are non-diagnostic.

TIPS with a porto-hepatic vein pressure gradient of 20 mmHg was found. Treatment consisted of balloon dilatation and insertion of another telescoping TIPS stent. Patient did well and has had no further UGIB as of 1 year follow up. Hemobilia is an uncommon medical problem that presents in a varied fashion and clinical suspicion is paramount in establishing the diagnosis and treatment plan.


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[984A]

Figure 1. Hemobilia.

Not All Bleeding in Cirrhosis Are Variceal Tariq Hammad, MD, Usman Ahmad, MD, Yaseen Alastal, MD, Ali Nawras, MD, FACG. Gastroenterology, University of Toledo Medical Center, Toledo, OH. Introduction: Hemobilia is a rare cause of upper gastrointestinal bleeding (UGIB). A high level of clinical suspension in the proper clinical context is required. Transjugular intrahepatic portosystemic shunt (TIPS) is a mainstay treatment option for managing complications in liver cirrhosis and Doppler ultrasound is very accurate in detecting shunt thrombosis. In this report we describe an unusual case of hemobilia as a result of significant stenosis of a TIPS shunt not identified by Dppler ultrasound. A 48-year-old male patient presented with nausea, hematemesis, and melena for one day prior to admission. Medical history was significant for decompensated liver cirrhosis secondary to chronic alcohol abuse and having undergone a TIPS procedure one year prior to presentation to manage severe variceal bleeding. On presentation the patient was hemodynamically unstable with a blood pressure of 84/51 mmHg and heart rate of 115. Urgent esophagogastroduodenoscopy (EGD) was performed revealing large esophageal varices with stigmata of recent bleeding that were banded. No active variceal bleeding was noted. Examination of stomach and duodenum were limited due to the presence of fresh blood and instability of the patient. A TIPS Doppler ultrasound was performed which demonstrated appropriate shunt function. The patient was discharged and repeat EGD was performed 14 days after his initial one. Repeat EGD demonstrated smaller non-bleeding esophageal varices, portal hypertensive gastropathy, and fresh blood in the second portion of the duodenum. A side view scope was then introduced which revealed active bleeding from the papilla (Fig 1). The patient was sent for a mesenteric arteriogram which was unremarkable. Given the high level of clinical suspicion a formal TIPSogram was performed. Two areas of significant stenosis within the


985 A Case of Isolated Metastasis of Renal Cell Carcinoma to the Pancreas Michael Green, MD, Najla Itani, MD, Thomas Schulz, MD, William Salyers, MD, FACG. University of Kansas School of Medicine, Wichita, KS. Introduction: The most frequent metastatic sites for renal cell carcinoma (RCC) include the lungs, bones, and liver. However, metastasis of RCC to the pancreas is quite rare, with a reported incidence of 1.2-2.8%. Interestingly, the tumor cells have been shown to have a high affinity for pancreatic parenchyma. Pancreatic metastasis is usually found incidentally and the interval from time of initial resection of the RCC to metastasis can be quite long. Patients with a favorable prognosis include those with single, easily resectable lesions and a prolonged disease-free period. An 85year-old female with a history of clear-cell RCC status post right nephrectomy almost 13 years prior presented to her primary care physician for right upper quadrant pain. Work-up included an ultrasound followed by a CT scan of the abdomen and pelvis that showed an irregularly lobulated mass in the head of the pancreas. Subsequent endoscopic ultrasound confirmed the presence of a hypoechoic vascular tumor in the neck of the pancreas measuring 4.24 cm in its largest diameter, and involving the common hepatic artery. Fine needle aspiration revealed a tumor that had cellular changes suggestive of metastatic RCC. The tumor was positive for pankeratin, epithelial membrane


| OCTOBER 2014

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Abstracts antigen, anti-RCC, and vimentin. Given the mild common bile duct dilation noted and likelihood of progression, a biliary stent was placed. The patient was not a surgical candidate and therefore was started on sunitinib with repeat CT scan 1 month later showing stable disease. However, given her ongoing pain and nonresectable nature of her tumor she opted to refrain from further treatment. Given that RCC metastasizes to the pancreas following a prolonged disease-free interval, lifelong follow-up is essential. This should begin within the primary care setting where most of these patients will pursue their ongoing follow-up, as was the case in the patient presented above. In any patient with a history of RCC and a newly detected pancreatic mass, metastasis should be suspected. The first line treatment of metastasis is resection, which offers a favorable outcome. Hence, to ensure timely detection and an opportunity for resection, patients with RCC should be monitored long-term, and studies investigating the cost-effectiveness of extended imaging surveillance should be pursued.



988 Obstructive Cholestasis Secondary to Duodenal B-Cell Lymphoma With Large Cell Transformation Ahmed Abdulhamid, MSIV,2 Fouad Otaki, MD,1 Ira Jacobson, MD,1 Michel Kahaleh, MD, FACG,1 David Wan, MD1. 1. New York Presbyterian Hospital, New York, NY; 2. Weill Cornell Medical College in Qatar, Doha, Qatar. Introduction: The differential etiologies of cholestasis are commonly divided into extra- and intrahepatic causes. An acute presentation is highly suggestive of obstruction secondary to choledocholithiasis. We present a case of profound cholestasis with an unusually contradictory preliminary diagnostic work-up. A 64-year-old man with a history of resected pituitary adenoma and follicular lymphoma in remission after chemo- and immunologic therapy presented with new-onset lethargy and abnormal liver enzymes. The patient endorsed 1-day history of darkening of urine and painless jaundice; his physical exam was significant only for known splenomegaly and icterus. His alkaline phosphatase (ALP) was 2943 U/L on admission along with amminotransferases (AST and ALT) of 209 and 297 U/L, respectively. An abdominal ultrasound revealed a stable hemangioma, without any evidence of biliary obstruction or dilation. As his ALP continued to rise, we performed a liver biopsy noted for interlobular bile duct injury, patchy lobular inflammation, and occasional apoptotic liver cells. No significant canaclicular cholestasis or CK-7 staining was noted, which would have been typical of a cholestatic liver injury pattern. The specimen was consistent with drug injury. Despite holding all his nonessential medications his ALP peaked at 4725 U/L. On a MRI of the abdomen, there was mild asymmetrical intrahepatic biliary ductal dilatation with a normally tapering common bile duct, and incidentally the duodenum had circumferential thickening. In the absence of a definitive diagnosis the patient underwent endoscopic retrograde cholangiopancreatography, which was noted for mass in the second and third portion of the duodenum. Pathology revealed an aggressive recurrence of B-cell lymphoma with large cell transformation. The patient had a remarkable drop in ALP and bilirubin following the placement of a biliary stent. He is currently receiving an alkylating chemotherapeutic agent and his alkaline phosphatase has normalized. This case highlights the need to have a high index of suspicion for obstructive jaundice despite findings of druginduced liver injury on histology and the lack of extrahepatic biliary dilatation. Drug-induced liver injury remains a diagnosis of exclusion. Furthermore, while duodenal and periampullary lesions are only diagnosed in 4-6 per million patients, the abnormal CT findings, prior history of lymphoma, and lack of clinical improvement were concerning. Considering obstructive jaundice on the differential for severely elevated ALP with even subtle CT findings is important to provide prompt and effective treatment.

[989A]

989 Epidermoid Cyst of Intrapancreatic Accessory Spleen: A Diagnostic Dilemma Saloni Sharma, MBBS,2 Kaartik Soota, MD,1 Maisa Abdalla, MD,2 Guabao Wang, MM,2 Zhongren Zhou, BMed, PhD,2 Eva Galka, MD,2 Ashok Shah, MD,2 Shivangi Kothari, MD,2 Vivek Kaul, MD2. 1. Unity Health System, Rochester, NY; 2. University of Rochester Medical Center, Rochester, NY. Introduction: Epidermoid cyst of intrapancreatic accessory spleen (IPAS) is a rare diagnosis with only 32 cases reported in the literature. We present the case of a 39-year-old male who underwent distal pancreatectomy for presumed intraductal pancreatic mucinous neoplasm (IPMN) that was diagnosed to be an epidermoid cyst of IPAS. Case Report: A 39-year-old male with history of alcohol abuse was admitted to the hospital with complaints of abdominal pain, nausea, vomiting, and intermittent hematochezia associated with weight loss of 20 pounds in 2 months. Abdominal CT scan showed a 2 x 1.9 cm, well-circumscribed cystic mass in the pancreatic tail (Figure 1). Endoscopic ultrasound (EUS) also showed a cystic lesion in pancreatic tail (Figure 1). Fine needle aspiration cytology (FNA) revealed a few “atypical” cells with intra- and extracellular mucin. Cyst fluid CEA level of 10,460 ng/mL was noted, concerning for a mucinous neoplasm. The patient underwent distal pancreatectomy and splenectomy. However, pathology revealed epidermoid cyst of intrapancreatic accessory (heterotopic) spleen with low-grade pancreatic intraepithelial neoplasia. Discussion: Epidermoid cyst of IPAS was first reported by Davidson et al in 1980. It is believed that some unidentified genetic and/or environmental factors might play a role in its development as most of these cases have been reported from the Asian community. It is commonly found in adults in the age group 40-70 years and does not seem to carry any gender predilection. Clinically, patient is asymptomatic, and the lesions in found incidentally on abdominal imaging. It can easily mimic other pancreatic lesions including premalignant lesions like IPMN and mucinous cysts, as was the case in our patient. CT, MRI, and EUS-FNA are helpful but it can be difficult to establish an accurate diagnosis without gross pathology from a resected specimen obtained surgically. Epidermoid cyst of IPAS is a rare entity, but should be kept in mind in the differential diagnosis of cystic pancreatic lesions, particularly as it carries an excellent prognosis. Conclusion: Epidermoid cyst of IPAS is a benign lesion found incidentally on abdominal imaging and is difficult to diagnose without pathology obtained from surgical resection. It is a benign entity and patients should be reassured about the good prognosis. This is the fifth reported case of such a lesion from the western part of the world.

990 Cardiac Tamponade as a Complication of Pseudocyst in Chronic Pancreatitis Syed Amer, MBBS,1 Mohammed MuqeetAdnan, MBBS2. 1. Mayo Clinic, Phoenix, AZ; 2. University of Oklahoma Health Sciences Center, Oklahoma, OK. Case Report: A 45-year-old male with history of alcoholism and chronic pancreatitis presented to the emergency department with chief complaint of chest pain and shortness of breath. On physical exam, he was in severe distress, with distended neck veins, distant heart sounds, and bilateral crackles on lung exam. He was hemodynamically unstable with a blood pressure of 80/60 mm Hg and pulse of 110. Pulsus paradoxus with drop in systolic blood pressure on inspiration was also observed. A noncontrast chest CT showed massive pericardial effusion. The effusion was drained urgently and a pericardial drain was left in place. Following which, his blood pressure stabilized at 110/70. Pericardial fluid analysis showed WBC of 3750/mm3 with 97% neutrophils, RBC of 59400/mm3, LDH of 1387 u/L, total protein of 4.8 g/dL, glucose 116 mg/dL, amylase 101 u/L, and lipase 196 u/L. The pericardial drain was removed the next day after decreased output. Within hours, he became hypoxic and hypotensive. CT angiogram of the chest showed reaccumulation of fluid in the pericardium along with bilateral pleural effusions. It also revealed a pancreatic pseudocyst that was found to be extending close to the posterior mediastinum and abating the posterior pericardial wall with a fistulous tract from the pseudocyst into the pericardium. He was intubated due to hemodynamic instability and moved to the ICU. He then had a ERCP followed by an EUS-guided cystogastrostomy to drain the pseudocyst. His subsequent post-op course was uneventful. Discussion: Pseudocyst formation is a common complication of both acute and chronic pancreatitis. Approximately, 40% will resolve spontaneously within 6 weeks. Extra-abdominal extension of a pancreatic pseudocyst is uncommon. Mediastinal pseudocysts result from extension of enzyme rich proteolytic fluid through the diaphragm. Most common route is via the aortic or esophageal hiatus. Rarely, it occurs by direct erosion through the diaphragm or via foramen of Morgagni. Even rarer, does a mediastinal pseudocyst penetrate into the pericardial sac. CT scan, ERCP, and magnetic resonance pancreatogram

Figure 1.



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(MRP) are useful for diagnosis. The treatment modalities include (1) medical management, (2) ERCP with endoscopic pancreatic stent placement (endoscopic transpapillary/transmural technique), (3) surgery, and (4) endosonographic drainage. Conclusion: Pancreaticopericardial fistula should be considered in the differential diagnosis of pericardial effusion in a patient with known history of chronic pancreatitis and should be treated promptly.

991 Acute Pancreatitis Secondary to Gastrostomy Tube Placement: A Rare Complication Christine Granato, MD, Shivangi Kothari, MD, Viren Kaul, MBBS, Asad Ullah, MD, Truptesh Kothari, MD, Vivek Kaul, MD, FACG. University of Rochester Medical Center, Rochester, NY. Introduction: Acute pancreatitis secondary to gastrostomy tube (G-tube) balloon migration is a rare complication. We present a case of acute pancreatitis secondary to G-tube placement in a patient with Roux-en-Y foregut anatomy. Case Report: A 33-year-old African American female presented with a one-day history of acute onset epigastric pain with associated fever (100.4F). Past surgical history was notable for Roux-enY gastric bypass and cholecystectomy. The patient had no prior history of alcohol use. Two weeks prior to admission, the patient underwent laparoscopic assisted transgastric ERCP for Type II SOD (dilated CBD and severe biliary pain) and was found to have severe papillary stenosis. Biliary sphincterotomy was performed and a G-tube was surgically placed into the excluded stomach for luminal decompression and maintenance of access. On admission, physical exam was notable for hypoactive bowel sounds with tenderness to palpation in the epigastrum, without peritoneal signs. G-tube was in place with minimal erythema at the incision site. Labs were notable for ALT 90U/L, AST 71U/L, alkaline phosphatase 125U/L, total bilirubin 0.7mg/dL, amylase 284U/L, and lipase 683U/L. CT abdomen revealed post-gastric bypass anatomy with the G-tube balloon extending into the second portion of the duodenum. The balloon was seen at the level of the ampulla, exerting a mass effect on the pancreatic head with associated moderate intra- and extra-hepatic biliary ductal dilatation and minimal pancreatic duct dilation. MRCP confirmed mass effect on the distal CBD by the G-tube balloon, with the CBD measuring 1.1cm. There was no filling defect identified in the biliary tree. The G-tube was retracted and balloon partially deflated, with resolution of symptoms and lab abnormalities. Discussion: G-tube placement has known complications including dislodgement, local hemorrhage, perforation, leakage at PEG site, and buried bumper syndrome. Acute pancreatitis secondary to a G-tube is a rare complication. Pancreatitis in this setting is more often caused by balloon migration of replacement tubes and/or Foley tubes, and not by the primary G-tube as seen in our patient. Symptoms typically resolve with medical management and changing/retracting the G-tube. Conclusions: Acute pancreatitis secondary to balloon migration of G-tubes is a rare complication. Increased awareness of this potentially serious complication is prudent, and should be considered as a potential etiology of pancreatitis in all patients with G-tubes. To the best of our knowledge, less than 10 such cases have been reported in the literature.

cholangitis is supported by 1) segmental stricture with pre-stenotic dilation, 2) bile duct wall thickening, 3) an average of >10 IgG4 positive plasma cells on histology, and 4) effective response to steroid therapy. High IgE levels and peripheral eosinophilia are seen in IgG4-related disease and concurrent thrombocytopenia has been reported. Due to the presence of eosinophilia and the patient’s background, chronic infection with Clonorchis or Opisthorchis species needed to be excluded. Negative testing, lack of response to praziquantel, and steroid response confirmed the absence of a parasitic infection. We entertained the possibility of primary sclerosing cholangitis (PSC) or cholangiocarcinoma (CC). However, steroid response is not expected in either entity. Eosinophilic cholangitis (EC) is possible, but less likely as prior cases described involved predominantly young men and included the presence of a dense eosinophilic infiltrate on biopsies. The diagnosis of isolated extrapancreatic biliary lesions as IgG4 sclerosing disease remains challenging due to an overlap of features with PSC, EC, Churg-Strauss syndrome, CC, and chronic parasitic biliary infections.

993 Acute Pancreatitis: A Complication of Jejunostomy Tube Jehangir Ansari, MD, Samer Mohandes, MD, Sangeeta Agrawal, MD, FACG. Gastroneterology, Dayton VA Medical Center; Wright State University, Dayton, OH. Introduction: Acute obstructive pancreatitis (AOP) caused by gastrostomy tube migration and sphincter of Oddi obstruction has been described in a few case reports. We describe a case of acute pancreatitis caused by extrinsic compression of ampulla of Vater by a jejunostomy tube (JT). Case Report: A 60-year-old male nursing home resident was sent to the hospital for evaluation of a malfunctioning JT, which was placed earlier that year after he sustained traumatic brain injury. Abdominal exam was benign and JT flushed appropriately; however, some tension was noted when the tubing was withdrawn into the attachment device. Labs on admission revealed amylase 1519, lipase 971, AST 184, ALT 442, alkaline phosphatase 749, total bilirubin 1.0, and direct bilirubin 0.4. A CT scan without contrast was performed and revealed intrahepatic ductal dilatation, common bile duct diameter (CBD) of 10 cm, and mild fat-stranding surrounding the pancreas. Endoscopic retrograde cholangiopancreatography was performed and the JT was found compressed across the ampulla with associated ulceration. An attempt to canalize the CBD was unsuccessful, dye extruded from the ampulla immediately after injection. The JT was removed after balloon deflation. An endoscopic sphincterotomy was then performed and occlusion cholangiogram did not reveal any fi lling defects. His liver function test abnormalities gradually resolved and he was discharge to nursing home. Discussion: A review of the literature disclosed no documented association between JT and acute pancreatitis. Based on this patient’s endoscopic findings and resolution of pancreatic enzymes and liver function abnormalities after removal of JT, it is deduced that extrinsic compression of the biliary tract and inflammation of the sphincter of Oddi with subsequent obstruction of bile outflow caused pancreatitis directly due to the presence of a tightly wedged JT. Our case highlights the fact that clinician should have a strong index of suspicion of AOP secondary to JT when a patient with a JT presents with acute pancreatitis.

992 A Case of Abdominal Pain, Jaundice, Eosinophilia, and Thrombocytopenia Teresa Valentin, MD,1 Marina Serper, MD,2 Gregory Ginsberg, MD, FACG,2 Maarouf Hoteit, MD2. 1. Department of Medicine, Hospital of the University of Pennsylvania, Philadelphia, PA; 2. Division of Gastroenterology, Hospital of the University of Pennsylvania, Philadelphia, PA. Introduction: A 69-year-old Chinese woman with a history of pancreatitis, recurrent cholangitis, and allergic rhinitis presented with jaundice and epigastric pain. Labs were notable for cholestatic injury, thrombocytopenia, eosinophilia, and elevated IgE. Physical exam revealed enlarged, nontender submandibular glands. ERCP showed a stricture in the bifurcation affecting secondary and tertiary intrahepatic ducts. Stool and bile ova/parasites were negative and empiric praziquantel was ineffective. Bile duct biopsy showed chronic inflammatory infiltrate, no fibrosis, and 14 IgG4 plasma cells per high-powered field. Cytology was negative for malignancy. During a similar episode 7 months ago, serum IgG was elevated at 1890 mg/dL, with peak IgG4 of 134 mg/dL. After starting prednisone 40 mg daily, her labs normalized within 2-3 weeks. Repeat ERCP showed improvement of strictures and an 8-week follow-up MRI showed persistence of the right intrahepatic duct stricture with overall improvement in inflammation. She continues on a prednisone taper while taking 100 mg of daily azathioprine. According to adapted HISORt criteria and clinical diagnostic criteria of IgG4-SC 2012 by Ohara et al, a diagnosis of IgG4-sclerosing

[992]

Table 1. Platelets (103/μL)

Eosinophils (103/μL)

Total bili (mg/dL)

AP (U/L)

AST (U/L)

4/1/2014

321

0.00

0.9

100

19

20

3/10/2014

237

3.10

1.5

428

146

141

ALT (U/L)

3/5/2014

7

3.20

6.6

633

189

195

1/27/2014

29

14.40

0.7

409

84

109

8/26/2013

306

0.93

1.0

156

29

21

8/9-8/12/2013

260

11.49

1.7

423

118

102


[993A]

Figure 1.


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Abstracts 994 Pancreatitis Caused By Diverticulitis Avani Sinha, MD, Kunal Karia, MD, David Wan, MD, Ira Jacobson, MD. New York Presbyterian Hospital, New York, NY. Introduction: Colonic involvement from pancreatic disease has been reported in the literature. Though rare, colonic obstruction, perforation, and hemorrhage have occurred due to the close proximity of the pancreas. The reverse, however, has yet to be reported. We present a case of acute pancreatitis due to diverticulitis. The patient is a 53-year-old male with history of recurrent diverticulitis and rare alcohol consumption who was started on ciprofloxacin and metronidazole for left lower quadrant pain consistent with diverticulitis with initial improvement. However, 3 days later the patient developed an acute onset of postprandial left upper quadrant and left flank pain. On presentation, exam was notable for left-sided tenderness and labs significant for amylase 718 U/L and lipase 268 U/L. Computed tomography (CT) of the abdomen and pelvis revealed a short segment of descending diverticulitis with fluid and edema extending into the adjacent anterior pararenal space and pancreatic tail suspicious for pancreatitis without evidence of cholelithiasis or choledocholithiasis. The patient was made NPO, fluid resuscitated with lactated ringer’s solution, and continued on piperacillin/tazobactam for diverticulitis with improvement in symptoms. Diet was advanced on hospital day 2, which was also notable for fevers and diarrhea with positive Clostridium difficile toxin. A repeat CT obtained on hospital day 4 showed resolving diverticulitis and pancreatitis. The Clostridium difficile responded to oral vancomycin. Common etiologies of pancreatitis include gallstones, alcohol consumption, and sometimes hypertriglyceridemia, hypercalcemia, and autoimmune pancreatitis. Though there are reports of pancreatitis secondary to small bowel diverticulitis, this is the first report of pancreatitis secondary to adjacent colonic diverticulitis.

drink alcohol and a subsequent MRCP did not observe any evidence of common bile duct dilation or filling defect and showed resolving pancreatitis without obvious complications. The patient was kept NPO and her Lialda was stopped. However, the patient could not tolerate a diet and started to have watery, bloody, non-mucoid, explosive diarrhea 5 times per day associated with crampy, abdominal pain similar to her ulcerative colitis flares. She was started on mesalamine rectal enemas and Asacol®. Her diet was advanced and she was initially doing well, until she had abdominal pain after taking mesalamine. Due to concern over recurrent mild pancreatitis, the mesalamines were stopped and budesonide was started. The patient tolerated the medication well and was discharged with resolution of gastrointestinal symptoms. While azathioprine and mercaptopurine have been widely associated with acute pancreatitis (between 1-6% of exposed individuals develop acute pancreatitis), mesalamine-induced pancreatitis is rare. A population-based case-control study by Munk et al did not discern a significant association between the use of 5-ASA agents and increased risk of acute pancreatitis. In fact, Munk et al observed that patients with ulcerative colitis had a 1.5-fold greater risk of developing pancreatitis than patients without ulcerative colitis. Lialda-induced pancreatitis was only observed in 2 cases in clinical trials, both of which were attributed to hypersensitivity reactions. In this case, the patient likely first developed a Lialda-induced pancreatitis and then an ulcerative colitis flare once the Lialda was held. She was tried on an alternative 5-ASA agent but again developed abdominal pain possibly secondary to a mild pancreatitis. These episodes of drug-induced pancreatitis may have been due to the pH-dependent coating Lialda and Asacol share or to a general class effect of 5-ASA agents. This case describes a rare side effect of a common ulcerative colitis medication. In the future, physicians should consider pancreatitis on their differential for chronic abdominal pain in patients taking Lialda or other 5-ASA agents.

996 Taking an Alternate Route Home: Stenting of Choledochoduodenal Fistula Jayakrishna Chintanaboina, MD, MPH, Matthew Moyer, MD, MS. Penn State Hershey Medical Center, Hershey, PA. Introduction: Choledochoduodenal fistulas (CDFs) may occur secondary to inflammatory or neoplastic causes or as a consequence of XRT therapy. Rarely, this may represent as the only available pathway for biliary drainage. We report a case of 53-year-old male who underwent stenting of a CDF connecting the duodenal bulb and the proximal biliary tree, which was the only route available to allow biliary drainage. A 53-year-old male with past medical history of adenocarcinoma of rectum with subsequent metastasis to the right lobe of the liver and lymph nodes in the portahepatis region status post right hemihepatectomy, with portal lymph node and retroperitoneal lymph node dissection and external beam radiation therapy to that region. He initially underwent biliary stenting with a 10 Fr x 12 cm polymer stent by endoscopic retrograde cholangiopancreatography (ERCP) due to aggressive distal common bile duct (CBD) stricture. At the time of planned stent exchange, after removal of the previous stent, the guidewire could not be reintroduced into the proximal biliary system despite numerous techniques and maneuvers, due to the complicated stricture at the CBD-common hepatic duct interface. Several maneuvers were unsuccessful in traversing the wire through the CBD stricture included use of the SpyScope® system for directed wire access. At this point, a small fistula was noted by contrast fluoroscopy extending between proximal biliary tree/portahepatis and the duodenal bulb likely secondary to previous chemoradiation. This fistula was used to access the intrahepatic biliary system with a 035 jag wire whereupon a 7 Fr x 7 cm stent was placed in the fistula using a 9 mm upper scope and a standard introducer for palliation. Patient did well for several months and underwent stent upsizing on a scheduled basis until his disease advanced to overwhelm the entire liver parenchyma with metastatic disease. The patient was referred for possible hyperthermic intraperitoneal chemotherapy for palliation and hospice care. CDFs are rarely reported and form most commonly due to inflammatory, neoplastic, traumatic, or infectious causes. CDF may occur as a result of increasing pressure traversing along the pathway of the fistula as a result of obstruction in the distal CBD. Surgical choledochoduodenostomy was routinely performed as a side-side procedure with cholecystectomy prior to the advent of ERCP if retained stones or debris were noted intraoperatively in the distal CBD. CDFs can be treated surgically; however, a surgical option may not be appropriate in patients requiring palliative care. As demonstrated here, endoscopically stenting these CDFs may serve as the only route for allowing biliary drainage and palliation.

997 Acute Pancreatitis as the Initial Manifestation of Small Cell Carcinoma of the Lung

[994A] Figure 1. Coronal view of diverticulitis encroaching and causing inflammation of adjacent pancreas.

995 A Case of Lialda®-Induced Pancreatitis Alina Kutsenko, MD,1 Keri Herzog, MD,2 Michelle Cohen, MD,1 David Wan, MD,1 Brian Bosworth, MD,1 Michel Kahaleh, MD, FACG1. 1. New York Presbyterian Hospital, New York, NY; 2. Memorial SloanKettering, New York, NY. Introduction: A 63-year-old woman with a 5-year history of ulcerative colitis controlled with Lialda® for 2 years, psoriasis, and atrial fibrillation presented with acute pancreatitis. For the past several months, the patient experienced intermittent severe epigastric pain that radiated to her right upper quadrant and shoulder associated with nausea and vomiting. Her symptoms persisted despite a cholecystectomy for cholelithiasis in January 2014. In March, she had severe pancreatitis with a lipase level of 3000 U/L and a CT abdomen/pelvis showing inflammation surrounding the pancreas. She did not


Muhammad Ali Khan, MD, Sehrish Kamal, MD, Faraz Luni, MD, Yaseen Alastal, MD, Tariq Hammad, MD, Ali Nawras, MD, FACG. University of Toledo, Toledo, OH. Introduction: Small cell carcinoma of the lung is an aggressive disease that tends to metastasize early in its course and has a poor prognosis. Pancreatic metastasis generally constitutes a late manifestation of this disease and most patients do not have organ specific symptoms. We hereby present an interesting case of small cell carcinoma of lung with acute pancreatitis as the initial manifestation of the disease. Case Report: A 71-year-old female with significant history of tobacco abuse presented with complaints of epigastric abdominal pain radiating to the back for 2 days. She also reported weight loss of 40 lbs during the past 4 months. No history of alcohol abuse or gallstones. Physical examination was unremarkable except for epigastric tenderness and scleral icterus. Amylase 1469 U/L, lipase 1632 U/L, total bilirubin 3.9 mg/dL, alkaline phosphatase 332 IU/L, ALT 79 IU/L, AST 88 IU/L, and calcium 8.6 mg/dL. Diagnosed with acute pancreatitis, she had MRCP that showed multiple hyper intense hepatic nodules on background of iron deposition and mild dilation of biliary system. ERCP revealed displaced major papilla, distal common bile duct indentation, which was suspicious for distal bile duct stricture. Shelving was also noted with poor drainage of the contrast for which a plastic biliary stent was placed. Brushing from the common bile duct showed atypical ductal proliferation. Tumor markers revealed CA 19-9 624 U/mL, CEA 62.8 ng/mL, and AFP 1 U/mL. CT of the chest revealed a 2.5-cm irregular mass in the superior hilar aspect of the right lower lobe of lung with irregular margins. A CT-guided biopsy of the liver lesions showed


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malignant cells with immunostaining positive for TTF-1, chromogranin, and synaptophysin; Ki67 revealed nuclear reactivity for about 95% of tumor cells. Flow cytometric studies demonstrated that the tumor cells expressed CD56 (neuroendocrine marker) but were negative for lymphohemotopoietic markers. All these findings were compatible with a diagnosis of metastatic small cell carcinoma of lung. Conclusion: Small cell carcinoma of lung having acute pancreatitis as the initial presentation is a rare event. Possible mechanisms for metastatic cancer inducing pancreatitis include obstruction of the pancreatic duct by metastases or peripancreatic compression secondary to regional lymph node or vascular compromise by neoplastic destruction. However, in some patients there is no evidence of pancreatic metastasis raising the question if this is a paraneoplastic manifestation.

to show high-grade obstruction at the splenic flexure with resolution of the pancreatitis. ERCP was performed, which demonstrated pancreatic colonic fistula. Pancreatic duct stents were placed with subsequent improvement of abdominal pain and abdominal distention. Repeated ERCP 3 months later showed no pancreatic colonic fistula present. Pancreatic colonic fistulas are mostly found postoperatively with only 2% being found prior to surgery with ERCP. In patients with resolved pancreatitis and evidence of obstruction on CT imaging, possible exploration with ERCP prior to surgery may discover pancreatic colonic fistula and reduce the need for high-risk abdominal surgery, allowing treatment with pancreatic duct stenting.

1000 998

Unusual Adrenal Gland Dissemination From Primary Pancreatic Adenocarcinoma

Painless Jaundice: A Rare Presentation of Primary Biliary Cirrhosis Aaysha Kapila, MD, Pranav Patel, MD, Patrick Costello, MD, Mark Young, MD. East Tennessee State University, Johnson City, TN. Introduction: Primary biliary cirrhosis (PBC) usually presents with fatigue, pruritus, and rheumatologic manifestations like Sjögren’s and CREST syndrome. Most commonly associated findings are portal hypertension, osteoporosis/osteopenia, vitamin D deficiency, and hyperlipidemia. The diagnosis of PBC can be established by 2 of the 3 criteria: elevated alkaline phosphatase, presence of AMA, and histologic evidence of non-suppurative destructive cholangitis and destruction of interlobular bile ducts. Painless jaundice is a rare presentation of PBC. We present the case of a 69-year-old man who was admitted to the hospital with jaundice and weight loss of 50 pounds in the last 4 months, nausea, and decrease in appetite. Family history was significant for a brother with pancreatic cancer. Vitals at the time of presentation were unremarkable except for a heart rate of 96/min. Systemic examination was significant for scleral icterus and jaundiced skin. Lab work was significant for total bilirubin 7.7 mg/dL, direct bilirubin 4.2 mg/dL, alkaline phosphatase (ALP) 259 IU/L, AST 51 IU/L, ALT 47 IU/L, GGT 105 IU/L, albumin 2.9 g/dL, Hb/hct 11.9/34.9, ANA positive, CPR 39.7 mg/dL, AMA 128 U (020), smooth muscle IgG antibody and endomyseal antibody Ig A were negative. Elevated IgG levels 1717 (650-1600), IgM and G levels were normal. Computed tomography demonstrated no acute process, but age indeterminate L1 and L4 compression fractures were determined. Subsequent MRCP demonstrated no biliary abnormality. This was followed by a CT-guided liver biopsy, pathological analysis of the liver sample confirmed PBC with portal/periportal fibrosis and biliary metaplasia (stage 2 of 4), with evidence of mild steatosis (Figure 1 and 2). No evidence of autoimmune hepatitis/ PBC overlap syndrome was observed. The patient was started on ursodiol, which lead to stabilization of bilirubin levels and transaminases. Four weeks post-discharge, there was marked improvement in ALP, AST, ALT, and total bilirubin. DEXA bone density study was performed on the outpatient which illustrated osteoporosis, likely secondary to “low turnover osteoporosis”. Compression fractures were treated conservatively and vitamin D and calcium supplementation.

999

Motaz Ashkar, MD,1 Sandeep Krishnan, MBBS, PhD, FACG2. 1. Department of Medicine, Steward St. Elizabeth’s Medical Center, Brighton, MA; 2. Division of Gastroenterology, Steward St. Elizabeth’s Medical Center, Brighton, MA. Introduction: The lethality associated with pancreatic cancer has been shown to be directly related to its potential to disseminate early to other solid organs. However, the adrenals represent an underappreciated site of metastasis in patients with pancreatic cancer. We report a case of primary pancreatic adenocarcinoma with rare metastasis to the left adrenal gland. A 72-year-old woman presented from a nursing home with a 1-month history of non-bloody diarrhea, poor oral intake, anorexia, weight loss, and progressive painless jaundice along with dark urine. The patient was afebrile, and her physical examination revealed deeply icteric sclerae and skin along with mild epigastric tenderness without evidence of rebound or hepatosplenomegaly. Laboratory data revealed hemoglobin of 11.1 g/dL, WBC of 12.3 k/cmm, total bilirubin of 24 mg/dL, alkaline phosphatase of 227 U/L, aspartate aminotransferase of 70 U/L, and an alanine aminotransferase of 130 U/L. Serum electrolytes were within normal limits. Her CA 19-9 antigen was 494 U/mL. Contrast-enhanced CT scan of the abdomen and pelvis revealed a 33 x 29 mm hypoenhancing mass at the pancreatic head suspicious for malignancy, with intrahepatic and extrahepatic biliary dilatation and main portal vein encasement with occlusion. A 25 x 12 mm nodule was also noted in the left adrenal gland. Endoscopic ultrasound (EUS) was then performed and revealed a malignant appearing 26 x 26 mm oval hypoechoic and homogeneous pancreatic head mass with poorly defined borders. A malignant-appearing 5 x 3 mm peri-pancreatic lymph node was seen. Endosonographic visualization of the left adrenal revealed a 25 x 19 mm oval and hypoechoic lesion. The left hepatic lobe was normal with no mass lesions. Endoscopic fine needle biopsy (EUS-FNB) of the pancreatic mass confirmed adenocarcinoma. Endoscopic fine needle aspiration (EUS-FNA) of the left adrenal lesion demonstrated adenocarcinoma, consistent with metastatic pancreatic cancer. FNA was not attempted on the lymph node due to its small size. The vast majority of distant metastatic sites of pancreatic cancer are found in the liver and regional lymph nodes, but the incidence of hematogenous spread to the left adrenal gland in some reports is only 0.4%. Usually the adrenal dissemination is silent, but as reported it could have clinical features of adrenal insufficiency. Obtaining tissue samples utilizing EUS-FNA when possible has become a preferred approach in diagnosing pancreatobiliary malignancies. Its application extends to tissue procurement from left adrenal gland and is generally considered a less invasive and safe approach.

Acute Pancreatitis Causing a Highway to the Colon With Subsequent Road Closure Justin Cochrane, DO, Gregory E. Schlepp, MD, Wichit Srikureja, MD. Providence Sacred Heart Medical Center, Spokane, WA. Introduction: Acute pancreatitis is a common disease with a variety of different etiologies. Its complications range from necrotizing pancreatitis to ileus formation secondary to inflammation that causes slowing colonic transit time. Rare colonic complications can be pseudo-obstruction, secondary to pancreatic colonic fistula formation to the splenic flexure, with incidence around 6%. Following is a case of a 73-year-old female who presented with abdominal distention and was discovered to have pancreatic colonic fistula through ERCP intervention and treated with pancreatic stents. A 73-year-old female with history of recurrent pancreatitis initially presented to an outside hospital with abdominal pain, distention, and jaundice. A physical exam showed normal vitals with diffuse abdominal pain without rebounding or guarding, and diffuse abdominal distention with no obvious fluid wave or shifting dullness. Liver function test total bilirubin 0.7, INR 1.2, albumin 3.0, liver enzymes ALP 143, AST 20, ALT 6, lipase 469, hemoglobin 11.5, WBC 19, and PLT 265. CT imaging demonstrated obstruction with transition point around the splenic flexure. A colonoscopy showed no visible signs of mechanical obstruction around the splenic flexure. She was transferred to a tertiary hospital secondary to worsening of abdominal pain and no resolution of her abdominal distention. Repeat imaging continued

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1001 Chylous Ascites Secondary to Necrotizing Pancreatitis: A Fortuitous Diagnosis by ERCP Allison Yang, MD, Todd Baron, MD, FACG, Philip Hart, MD. Mayo Clinic, Rochester, MN. Case Report: A 68-year-old man was admitted for management of complications secondary to necrotizing pancreatitis. One month prior to admission, he underwent laparoscopic cholecystectomy for gallstone pancreatitis. He was readmitted with symptoms of gastric outlet obstruction, weight gain, significant abdominal distention, and pitting edema of the abdominal wall and bilateral lower extremities to the level of the thighs. CT scan demonstrated a large area of walled of pancreatic necrosis with moderate abdominal and pelvic ascites. EUS-guided cystgastrostomy with 3 direct endoscopic necrosectomies were performed over the next 2 months. Symptomatic ascites persisted, which required serial therapeutic paracenteses. ERCP performed 3 months after onset of pancreatitis demonstrated a large pancreatic duct leak. Transpapillary stent placement was performed with clinical improvement and decrease in ascites. At follow-up ERCP 1 month later for stent removal, milky-appearing fluid was emerging from the papilla. The suspicion for chylous ascites was confirmed by fluid analysis demonstrating a triglyceride level of 427 mg/dL.

Figure 1. (A) Florid duct lesion- biliary epithelial destruction by granuloma. (B) Portal tract with absence of interlobular bile duct and mild lymphoplasmacytic infiltrates.



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Abstracts Discussion: Chylous ascites is an uncommon cause of ascites, which occurs when lymph enter the abdominal cavity. It can develop secondary to any disruption of the lymphatic system due to traumatic injury, obstruction, or inflammation. Potential etiologies include abdominal malignancies, cirrhosis, lymphatic abnormalities, and various inflammatory conditions including constrictive pericarditis, radiation therapy, and Whipple’s disease. Acute and chronic pancreatitis are also recognized as uncommon causes of chylous ascites. Management of chylous ascites involves treatment of reversible underlying causes, dietary management (involving institution of a high protein, low fat diet with medium-chain triglycerides [MCTs]), and diuretic therapy. MCTs, in contrast to long-chain triglycerides, are absorbed directly into intestinal cells and transported as free fatty acids and glycerol directly to the liver via the portal vein, reducing the production and flow of chyle. In patients with severe malnutrition who are refractory to medical therapy, surgical shunts have been considered. This patient was treated with dietary modifications, including MCT supplementation (15 mL 3 times per day), and furosemide. Additional paracenteses were not required. After serial pancreatic duct stenting resolution of the pancreatic duct leak was achieved over a 4-month period. At last follow-up, his ascites had clinically resolved. This case of chylous ascites demonstrates an uncommon complication of acute pancreatitis, which was fortuitously diagnosed at the time of an ERCP.

iting. Past medical history was significant for hyperlipidemia and hypothyroidism. At presentation, vital signs were stable. Abdominal examination revealed epigastric tenderness with no guarding or rigidity. Bowel sounds were present. Laboratory work: white blood cell counts of 11.4 K/mm3, total bilirubin of 1.7 mg/dL, direct bilirubin of 0.4 mg/dL, and alkaline phosphatase, aspartate and alanine aminotransferase levels of 106 U/L, 584 U/L, and 915 U/L, respectively. Viral hepatitis serology was negative. Gallbladder ultrasound revealed multiple echogenic gallstones and dilated common bile duct (CBD) of 9 mm. HIDA scan showed evidence of radiotracer activity in gallbladder and possibly in the right hemicolon. CT scan showed no definite communication between the gallbladder and ascending colon. Patient underwent ERCP which revealed multiple filling defects in cystic duct (Figure 1A) causing compression of bile duct. In addition, contrast extravasation into the ascending colon was noted during occlusive cholangiogram (Figure 1B). Sphincterotomy was performed followed by biliary stenting. Patient was taken to surgery; fistula was identified from the inferior edge of the gallbladder to the hepatic flexure. Roux-en-Y hepaticojejunostomy and cholecystectomy was performed. Pathology study of the gallbladder revealed chronic cholecystitis with multiple cholelithiasis. Cholecystocolonic fistula could be a complication of Mirizzi syndrome. ERCP is essential to confirm the diagnosis and to guide further surgical management.

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Mirizzi Syndrome Type I Complicated by Cholecystocolonic Fistula: A Rare Complication for a Rare Disease

Pancreatic Lipoma Masquerading As A Cystic Neoplasm

Yaseen Alastal, MD, Tariq Hammad, MD, Syed Hasan, DO, Osama Alaradi, MD, Ali Nawras, MD, FACG. University of Toledo, Department of Internal Medicine, Division of Gastroenterology, Toledo, OH. Introduction: Mirizzi syndrome is a rare disease of the biliary tract. Cholecystocolonic fistula (CCF) is an uncommon complication of biliary diseases, occurring in 0.06%-0.14%. The combination of both diseases is extremely rare. Only 1 case of CCF was reported with Mirizzi syndrome type I. Herein we present another case of of Mirizzi syndrome type I associated with CCF. A 51-year-old female patient presented to emergency department with epigastric pain for 1 day, associated with nausea and vom-

Katie Agnello, MD,2 Lalit Gurtoo, MD,1 Manoj Kumar, MD, MPH,2 Andrew Bain, MD,1 Amanpal Singh, MD, MS1. 1. Roswell Park Cancer Institute, Buffalo, NY; 2. University at Buffalo, Buffalo, NY. Introduction: Incidental pancreatic lesions are commonly found through a variety of diagnostic imaging modalities. These findings may correlate with a patient’s symptomatology, and often leads to further diagnostic tests to evaluate for malignancy. One of the rare findings fitting this scenario includes pancreatic lipomas. Case Report: Patient was an 80-year-old male with a history of node negative colon cancer status post resection who underwent a routine surveillance CT abdomen at an outside facility, which

[1002A]

Figure 1. (A) ERCP reveals multiple filling defects in cystic duct (B) contrast extravasation into the ascending colon during occlusive cholangiogram.

[1003A] lesion.

Figure 1. CT image (left) of a 1.5-cm hypodense lesion in pancreatic head/uncinate process. EUS image (right) shows the corresponding isoechoic to mildly hyperechoic



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showed a low-density lesion measuring 1.6 cm in the pancreatic head/uncinate process (Figure 1). The hypodense appearance of the lesion raised the suspicion of a cystic lesion. There was suggestion of fat component because of negative Hounsfield units (-95 HFU), however neoplastic process could not be ruled out. Endoscopic ultrasound (EUS) was recommended for further evaluation. Examination with a curvilinear array echoendoscope showed a 18 x 15 mm isoechoic to mildly hyperechoic lesion in the uncinate process suggestive of lipoma (Figure 1). No anechoic lesions to suggest a cystic neoplasm were noted. The remainder of the pancreas appeared unremarkable. Considering the appearance of the lesion on the EUS and its correlation with the CT findings, fine needle aspiration was not considered necessary. Discussion: Our case demonstrates a rare scenario of a pancreatic lipoma confused as a cystic neoplasm on CT scan. EUS examination was helpful to confirm the final diagnosis. Pancreatic lipomas are rare mesenchymal tumors, accounting for only 1-2% of all pancreatic neoplasms, consist of adipose cells, surrounded by a thin fibrous capsule. Pancreatic lipoma is often a well-circumscribed, homogeneous mass with densities ranging from -30 to -120 Hounsfield units on CT scan. Most of these lesions are asymptomatic and require no further intervention. Rarely, the lipomas can become large and cause pain requiring surgical resection.

1004 Pleomorphic Giant Cell Carcinoma of Pancreatic Tail Diagnosed By Endoscopic Ultrasound Yaseen Alastal, MD, Tariq Hammad, MD, Syed Hasan, DO, Osama Alaradi, MD, Usman Ahmad, MD, Roaya Khalaf, MD, Ali Nawras, MD, FACG. University of Toledo, Department of Internal Medicine, Division of Gastroenterology, Toledo, OH. Introduction: Pleomorphic giant cell carcinoma of the pancreas is a very rare malignant tumor with aggressive behavior and poor prognosis. Here we present a case of pleomorphic giant cell carcinoma of pancreas diagnosed by endoscopic ultrasound-guided fine needle aspiration (EUS-FNA). Case Report: A 67-year-old white male patient presented to outpatient clinic with mild left upper quadrant abdominal pain for 1 year, which was progressively worsening recently. He reports 8 pounds weight loss over 1 month. Patient denies nausea, vomiting, or change in bowel habits. Past medical history was significant for hypertension and obstructive sleep apnea. He doesn’t smoke or drink alcohol. No significant family history of malignancies. Vital signs were stable. Body mass index was 51 kg/m2. Abdominal exam revealed mild epigastric tenderness with no palpable masses. The patient had CT scan of the abdomen which revealed bulging in the distal pancreatic body (Figure 1). CA19-9 and CEA were 136.9 units/mL and 0.6 ng/mL, respectively. MRI/MRCP of the abdomen revealed a pancreatic tail mass suspicious for malignancy. CT-guided fine needle aspiration and biopsy revealed atypical cells with no confirmed malignancy. The patient underwent endoscopic ultrasound which showed large, hypoechoic, heterogeneous mass with well-demarcated border at the tail of the pancreas measuring 48.6 x 30.6 mm (Figure 2A). The mass was encasing the splenic vein with no invasion to the

splenic artery. EUS-FNA was performed for the pancreatic tail mass in the presence of cytopathologist who confirmed the adequacy of the samples (Figure 2B). Pathology study of the samples revealed numerous pleomorphic malignant tumor cells consistent with pleomorphic giant cell (anaplastic) carcinoma of the pancreas. Conclusion: Pleomorphic giant cell carcinoma of the pancreas is a rare type of pancreatic malignancies. EUS-FNA can help in the diagnosis of this rare neoplasm.

1005 When Might Endosonographic Decompression of Courvoisier’s Gallbladder Be Required With Palliative Metallic Biliary Stenting? A Case Series Tariq Hammad, MD, Yaseen Alastal, MD, Muhammad Bawany, MD, Muhammad Ali Khan, MD, Usman Ahmad, MD, Osama Alaradi, MD, Ali Nawras, MD, FACG. University of Toledo, Department of Internal Medicine, Division of Gastroenterology, Toledo, OH. Introduction: Metallic stents (MS) has been used as palliative drainage in malignant common bile duct (CBD) strictures. Cystic duct (CD) obstruction with resultant cholecystitis and empyema is a rare potential post metallic biliary stenting complication in specific high-risk situations. After encountering 2 incidences of post palliative metallic biliary stenting cholecystitis; we adopted the practice of endosonographic (EUS)-guided aspiration of gallbladder (GB) at the time biliary stenting in carefully selected patients. Here we report 3 patients where the distended GB was decompressed at the time of palliative stenting of CBD using EUS-guided fine needle aspiration (EUS-FNA). Case Reports: Two patients with presumed stage 4 adenocarcinoma of the head of pancreas and 1 patient with stage 4 metastatic sacomatoid carcinoma of the lung to the pancreatic head presented with jaundice. In all patients, liver function test showed obstructive pattern. Abdominal CT showed a mass in the head of pancreas, biliary ductal dilatation (BDD), and massively distended GB. The patients were referred to our endoscopy unit for EUS-FNA confirmation of the diagnosis and for endoscopic retrograde cholangiopancreatography (ERCP) for potential palliative CBD stenting. EUS-FNA of the pancreatic masses was done. Onsite cytopathological exam confirmed malignancy. EUS again showed severely distended GB. The patients underwent ERCP, which showed either high-grade med or distal CBD strictures with significant extrahepatic BDD. Strictures were dilated and stented with partially covered self-expandable metallic biliary stents. CD take off was either at the level of covered part of the MS or not identified. Hence, EUS-guided decompression of the GB by FNA was performed at the end of the procedure without any complications. Conclusion: Although GB decompression is not necessary for the vast majority of palliative metallic biliary stenting; it should be considered in subset of patients with high potential risk for post stenting cholecystitis (Figure 1). Further large studies are required to validate these observations.

1006 Metastatic Adenosquamous Cell Carcinoma of the Pancreas Presenting With Upper Gastrointestinal Bleeding Roopjeet Bath, MBBS, Navkiran Brar, MBBS, Haleh Vaziri, MD. Gastroenterology & Hepatology, University of Connecticut, Farmington, CT. Introduction: An 81-year-old man with a history of coronary artery disease and porcine aortic valve on clopidogrel and aspirin presented to the emergency room with a 3-day history of black tarry stool. The patient’s hemoglobin was 6.1 at presentation, decreased from his baseline of 14. He underwent an upper endoscopy that revealed 2 ulcers in the upper stomach. One was 2 cm with a small adherent clot, the other was 1 cm with a clean base. Biopsies were taken from the edge of the ulcers. Pathology showed moderately differentiated squamous cell cancer with focal glandular differentiation as well as H. pylori. A subsequent CT of the abdomen/pelvis showed a large necrotic soft tissue mass involving the pancreatic body/tail and inframedial stomach measuring 6.5 x 6.5 cm with areas of low attenuation consistent with necrosis. There were 6 ill-defined hypodensities in the liver consistent with metastases as well as intraperitoneal lymphadenopathy. The patient’s serum CA 19-9 was 4564 (0-37) U/mL. CEA was 16.7 (0-5) ng/mL, and CA 125 was 96 (0-35) U/mL. The patient was evaluated by the surgical service and oncology service, including review at a specialized cancer institute. After reviewing imaging, pathology, and tumor markers, it was agreed that the patient had a primary adenosquamous cell carcinoma (ASCCP) of the pancreas with metastases. ASCCP is a rare tumor of the pancreas, representing 1-4% of pancreatic exocrine malignancies.[1] It is also referred to “adenocanthoma” and “mucoepidermoid carcinoma”.[2] ASCCP has a clinical presentation similar to that

[1004A]

Figure 1. CT scan reveals mass in the pancreatic tail.

[1004B]

Figure 2. (A) Endoscopic ultrasound reveals large, hypoechoic, mass at the tail of the pancreas. (B) EUS-guided fine needle aspiration of the mass.



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[1005A]

Figure 1. Algorithem showing when decompression of Courvoisier’s gallbladder is required with palliative metallic biliary stenting.

of adenocarcinoma of the pancreas but with an overall worse prognosis.[1] Due to its rapid growth, necrosis within the tumor is common. Compared with adenocarcinoma of the pancreas, ASCCP is associated with a larger mass at time of diagnosis, increased likelihood of lymph node involvement and is more poorly differentiated. Median survival is reported to be 5.7±4.1 months.[3] The optimal treatment of patients with metastatic ASCCP is not established, and current treatment guidelines are based on pancreatic adenocarcinoma management. Our patient was initially started on a palliative chemotherapy regimen as part of a modified clinical trial using gemcitabine and abraxane, later to switched to capecitabine but eventually transitioned to comfort measures only and passed away 6 months after diagnosis. References: [1] Simone CG et al. Gastrointestinal Cancer Res 2013. [2] Coakley BA et al. J Gastrointest Oncol 2011. [3] Boyd CA et al. J Surg Res 2012.

1007 How Can Adenocarcinoma of the Pancreas Mimic Klatskin Tumor? Tariq Hammad, MD, Yaseen Alastal, MD, Aijaz Sofi, MD, Osama Alaradi, MD, Ali Nawras, MD, FACG. University of Toledo, Department of Internal Medicine, Division of Gastroenterology, Toledo, OH. Introduction: Klatsin tumor is a cholangiocarcinoma involving biliary hilum, which results in right and left hepatic duct (HD) dilatation. Here we present a case of adenocarcinoma of the pancreas presented like Klatskin tumor. A 78-year-old female presented with pruritus, jaundice, and dark urine for a month. Physical exam was pertinent for jaundice. Liver function test showed total bilirubin of 10.55 mg/dL, direct bilirubin of 7.5 mg/dL. Alkaline phosphatase, aspartate and alanine aminotransferase of 311 U/L, 75 U/L and 155 U/L, respectively. Albumin, prothrombin time, and complete blood counts were normal. Abdominal computed tomography showed intrahepatic biliary ductal dilatation (HBDD). Further evaluation by magnetic resonance cholangiopacratography

[1007A] Figure 1. (A) EUS image shows hypoechoic mass of 21.3 x 17.2 mm at the superior surface of the neck of pancreas. (B) ERCP image shows dilated right and left main HD with low biliary hilum . Biliary hilum is invaded by the mass mimicking Klatskin tumor. (C) ERCP image shows 2 plastic stents positioned up to the right and left main HD.



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showed intra- and extra-HBDD to the level below junction of cystic duct (CD) and common HD. No stones were identified. Initially, she had endoscopic retrograde cholangiopancreatogram (ERCP) at other facility that showed stricture in the common bile duct (CBD). Stricture was dilated and stented with a 10 French x 5 cm plastic stent. Brush cytology was negative. Patient’s symptoms persisted, so she was referred to our institution for further evaluation. Endoscopic ultrasound (EUS) and ERCP were performed. EUS showed hypoechoic well-defined mass of 21.3 x 17.2 mm at the superior surface of the neck of pancreas invading the splenic vein and artery (Figure 1A). Fine needle aspiration was done and on site cytology evaluation showed moderately differentiated adenocarcinoma of pancreas. Old stent was removed. ERCP was repeated and showed dilated right and left main HD with low biliary hilum at the level of superior surface of pancreatic neck. The biliary hilum was invaded by the pancreatic mass mimicking Klatskin tumor (Figure 1B). CD was communicating with the right HD. Strictures were dilated and stented with 2 plastic stents positioned up to the right and left main HD (Figure 1C). Patient was referred for Whipple surgery with hepaticojejunostomy based on the cholangiographic findings. Pancreatic malignancy associated with CBD anomaly of low biliary hilum mimics Klatskin tumor. Combined ERCP and EUS were essential for proper diagnosis and guiding the surgical plan.

present a case of pancreatic involvement by RD of a 38-year-old African American female who came to office as a new patient with complaints of abdominal pain and nodules in her neck. She had an abnormal abdominal ultrasound that showed possible pancreatic mass along the anterior margin of pancreatic head and generalized abdominal lymphadenopathy. She also had a CT of neck with contrast and CT abdomen that showed diffuse cervical lymphadenopathy and hypodensity along the anterior margin of pancreas. She was treated symptomatically and was referred for lymph node biopsy. One of her cervical lymph nodes was biopsied and it was consistent with SHML. The lymph nodes show a markedly thickened fibrotic capsule and nodal architecture distorted by expansion of the sinuses by large histiocytes which show positivity for S-100 immunohistochemically. Some of the histiocytes contain red blood cells and a few contain white blood cells. There is a marked increase in plasma cells in the remaining lymphoid tissue. Flow cytometry was negative for a monoclonal process. Rosai-Dorfman disease (RD) is a rare disorder with important pathologic characteristics that includes presence of positive immunostaining of S-100 protein and CD 68. Very few cases of SHML (10 g/d, CA125 was 828 U/mL, but other tumor markers were normal. PET-CT confirmed hepatomegaly, ascites, enlarged left and atrophic right kidney. Uptake in the jejunum suggested inflammation. Echocardiography showed left atrial enlargement, left ventricular wall thickening, and diastolic dysfunction. EGD showed multiple ulcers in gastric angle and gastric corpus, and erosive gastritis while colonoscopy showed multiple hemorrhagic focuses and mucosal edema in the rectosigmoid. Colon biopsies (30 cm, 12 cm, and 8 cm from


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Abstracts anus) revealed chronic inflammation accompanied with erosion in colonicmucosa, and mild dysplasia in focal glandular epithelium. Congo red staining showed the vascular wall was positive. Both Congo red staining and amyloidosis was positive in tonguebiopsy. Renal biopsy indicated primary renalamyloidosis (λlight chain). Discussion: Although renal involvement with nephrotic syndrome is most common in patients older than 50, gastrointestinal and hepatic manifestations can also occur with primary amyloidosis, as was the case with our patient. Ascites precluded safe liver biopsy, so other organs, tongue and colon, were sampled to make the diagnosis. Monoclonal plasma cells produce amyloid proteins and the protein deposition in extra-cellular matrix or blood vessel wall impacts the normal physiological functions of affected organs. According to clinical manifestations, amyloidosis can be characterized as primary, secondary, or hereditary, while subtyping can also be based on the kind of amyloid proteins produced. There is not specific treatment for amyloidosis, but our patient received lipid reducers, anticoagulation andantiplatelet therapy to improve microcirculation and renal function protection, gastrointestinal mucosa protection, nutritional support, and albumin infusion. VAD chemotherapy or Velcade combined with high-fluxhemodialysis was offered, but because of associated risks, the patient declined

1086 Primary Splenic Lymphoma: A Rare Incidental Diagnosis Jae Yoon Park, MD, Vandana Nehra, MD. Mayo Clinic, Rochester, MN. Introduction: An 87-year-old man presented for evaluation of incidentally identified splenic lesions. Two indeterminate solid hypodense lesions in the anterior aspects of the spleen were noted on CT of the abdomen and pelvis 2 months prior during evaluation of abdominal pain. His medical history was notable for type 2 diabetes mellitus, hypertension, hyperlipidemia, and congenital hepatic cysts. At time of evaluation, he was asymptomatic and denied any fevers, chills, night sweats, weight loss, headaches, vision changes, dyspnea, chest pain, hemoptysis, abdominal pain, nausea, vomiting, hematochezia, melena, or bone pain. Physical exam was unremarkable, without evidence of hepatosplenomegaly or palpable lymphadenopathy. Initial laboratory evaluation was only notable for mild thrombocytopenia of 110 x 10^9/L (normal: 150-450 x 10^9/L). The peripheral smear showed no diagnostic abnormalities. Extended electrolyte panel, liver function tests, lactate dehydrogenase, serum and urine protein electrophoresis, and prostate specific antigen were all within normal limits. MRI of the abdomen was obtained, which showed multiple solid lesions in the spleen measuring 4.8 cm, 3.3 cm, and 2.1 cm in maximal dimensions. Further imaging with fludeoxyglucose (FDG) F18 PET scan revealed FDG-avid lesions in the spleen with maximal standardized uptake value (SUV) of 6.1, suspicious for lymphoma. Also, there was an incidental FDG update with maximal SUV of 6.2 in the right prostate, concerning for prostate cancer. There was no FDG avid lymphadenopathy. An ultrasound-guided biopsy of the splenic lesion demonstrated grade 1-2 follicular lymphoma, with an elevated proliferation index (40-50% per Ki-67 staining). The cells were also positive for CD10, CD20, BCL-2, and BCL-6, suspicious for being lambda light chainrestricted. To rule out prostatic involvement, he underwent transrectal ultrasound-guided biopsy of the prostate. This demonstrated Gleason 3+4 prostatic carcinoma with less than 5% of gland involvement. Given diagnosis of splenic lymphoma without systemic involvement, after discussion with the patient, close medical follow-up was decided without further interventions. This illustrates a rare case of primary splenic lymphoma. Incidental splenic lesions are frequently encountered on imaging for unrelated reasons. The differential for splenic lesions is broad, and includes infectious, inflammatory, lymphoid and vascular neoplasms, and metastatic disease. Of these, primary splenic lymphoma is a rare, yet important diagnosis with prognostic and therapeutic implications. Clinical suspicion and early diagnosis followed by appropriate medical and interventional therapies are keys to successful management.

ally the treatment of choice in surgical candidates. Octreotide and bevacizumab (a vascular endothelial growth factor inhibitor) have been recently reported as promising medical therapies in patients with pulmonary LM. However, the experience of this approach in patients with intra-abdominal LM is still limited due to the rarity of the disease.

1088 Unusual Cause of Gastrointestinal Bleeding and Encephalopathy Chung-Jyi Tsai, MD, PhD, FACG, Ibrahim Hanouneh, MD. Cleveland Clinic, Cleveland, OH. Introduction: A 76-year-old woman presented with a 12-month history of obscure GI bleeding. EGD and colonoscopy were unrevealing. Capsule endoscopy revealed a moderate amount of red blood in the distal small bowel without an identifiable source. She was referred for retrograde double balloon enteroscopy. However, 2 months prior to the office visit and prior to double balloon procedure, she has developed recurrent episodes of altered mental status. She was brought to the emergency service on these occasions, where the patient was confused and oriented to name only. Physical exam was unremarkable except conjunctival pallor. Neurologic exam was non-focal. Labs were significant for iron deficiency anemia - hemoglobin 8.2 gram/dl and elevated ammonia level of 123. Liver function tests were normal. Brain CT was negative. CT enterography showed suspicious intestinal varices. The patient’s past medical history is significant for ruptured appendicitis with appendectomy 18 months prior to evaluation. She has neither known history of liver disease nor risk factors for chronic liver disease. The patient was started on lactulose, which helped restore her mental function. MR angiography revealed spontaneous communication between the superior mesenteric and right gonadal veins, along with multiple mesenteric varices. Mesenteric angiography with selective venogram of right gonadal vein confirmed the presence of portosystemic shunt. Direct blood sampling from the shunt revealed highly elevated ammonia level (230), further confirming that the portosystemic shunt was contributing to the patient’s hyperammonia. Coil embolization of the right gonadal vein and portosystemic shunt was performed to restore normal venous return. Patient tolerated the management well and was discharged with no further GI bleed or altered mental status. Ectopic isolated mesenteric varices in the absence of portal hypertension are rare. To our knowledge, this represents the first such case reported in the literature. As previous abdominal surgery was the only predisposing risk factor in this patient, it is probable that the varices arose as a result of intra-abdominal adhesions following appendectomy.

1087 Recurrent Gastrointestinal Bleeding: A Rare Presentation of Intestinal Lymphangiomatosis Kunut Kijsirichareanchai, MD, Alexander Hewlett, DO. University of Nebraska Medical Center, Omaha, NE. Introduction: Lymphangiomatosis (LM), an aberrant sequestration of lymphatic vessels during development, is an extremely rare condition in adults. It is usually diagnosed in the neck, axilla, mediastinum, and, infrequently, mesentery. We are presenting a recurrence of intestinal LM as a cause of gastrointestinal bleeding (GIB). A 69-year-old white female with remote history of surgical resection of mesenteric LM admitted to the hospital with melena and symptomatic anemia. Initial laboratory showed hematocrit of 12%, normal white blood cell and platelet, and normal coagulograms. Upper endoscopy and colonoscopy revealed diffuse erythema and mucosal oozing of blood in the small intestine and colon. Similar findings were confirmed by capsule endoscopy and double balloon enteroscopy. Endoscopic intervention was not attempted due to the diffuse nature of the lesions. Visceral angiography showed no extravasation, but multiple areas of pseudoaneurysms in superior mesenteric artery territory. Computed tomography of abdomen found multifocal mesenteric nodule, consistent with LM. Intestinal LM as a potential source of bleeding was suspected. Several medical therapies including bowel rest, octreotide, propanolol, and bevacizumab, were initiated but failed to control the bleeding. Surgical intervention was considered to be high risk due to the amount of bowel involved. She continued to have melena and became transfusion-dependent, requiring 2 units of blood transfusion every 1-2 days (a total of 60 units in 30 days.) After a multidisciplinary discussion, she decided to pursue comfort care without further transfusion. She was discharged home and eventually expired in a few weeks. Final autopsy found multiple areas of ectatic, thin-walled, endothelial-lined space in the submucosa, and mesentery of the small and large bowels. Special staining confirmed this as dilated lymphatic channels at epithelial lining. These findings were compatible with the final diagnosis of intestinal LM as the cause of death. Intestinal LM is a rare, benign tumor of the lymphatic system that is uncommonly recognized as a cause of recurrent GIB. Three possible underlying pathogeneses include 1.) hemorrhage into the cystic space from trauma, 2.) hemangioma as a component of angiomatous process, and 3.) blood from venolymphatic communication, as in our case. Surgical intervention is usu-


[1088A]

Figure 1.


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1089 Abdominal Tuberculosis Initially Diagnosed as Crohn’s Disease Xi Chen, MD, Daniel Eshtiaghpour, MD, Viktor eysselein, MD. Harbor UCLA Medical Center, Torrance, CA. Introduction: Only 1-3% of tuberculosis cases are extrapulmonary. Twelve percent of those cases are abdominal, of which 65-75% have gastrointestinal involvement. Intestinal tuberculosis (TB) presents most commonly with abdominal pain, weight loss, fever, and change in bowel habits, and has similar radiological, histological, and endoscopic features compared to Crohn’s disease, presenting a diagnostic dilemma. A 28-year-old female with a history of Crohn’s disease presented with 3 days of left upper quadrant abdominal pain accompanied by nausea, vomiting, and PO intolerance without hematemesis or hematochezia. CT scan showed significant fibrosis in the mid-jejunum and inflammatory changes to the colon causing small bowel obstruction. Supportive treatment with IV fluids and decompression was initiated with no resolution of her pain and no bowel movements. Diagnostic laparoscopy found severe Crohn’s disease including creeping fat and transmural inflammation of the terminal ileum with 2 proximal strictures at skip lesions. Ileocecectomy and stricturoplasty were performed. Pathology showed inactive Crohn’s disease of the terminal ileum with a healed ulcer and a necrotizing granuloma, which tested positive for acid fast bacteria. Of note, the patient had a colonoscopy 2 years prior with pathology negative for TB, at which time she completed a 9-month course of isoniazid therapy for latent TB. The patient was referred to infectious disease, where she was started on RIPE therapy and followed by public health. The DNA from her pathology sample was degraded, and testing was limited. PCR was negative for TB and positive for non-tuberculous mycobacterium; however, given the high pretest probability, isoniazid and rifampin were continued. The differentiation of intestinal TB from Crohn’s disease is often difficult. The most reliable method is a positive culture for acid-fast bacilli; however, only 1/3 of the mucosal biopsies test positive. PCR is another reliable method, but can be falsely positive in some patients with Crohn’s disease. Colonoscopy is the diagnostic study of choice, but our patient required emergent laparoscopy for a non-resolving small bowel obstruction. Crohn’s disease typically presents with longitudinal, fissuring ulcers, cobblestoning, and non-caseating granulomas, while intestinal TB presents with transverse ulcers, nodularity, caseating granulomas, and hypertrophic, mass-like lesions. Our patient had both acute intestinal TB and inactive Crohn’s disease. Thus, she had pathologic features of both diseases, contributing to her initial misdiagnosis of intestinal TB as an acute flare of Crohn’s disease.

pletely recanalize in the embryo’s foregut. This residual web matures secondary to peristalsis until it becomes symptomatic. Symptoms typically arise in the fourth decade of life and present with obstructive symptomatology, including, pain, nausea, vomiting, pancreatitis, and bleeding. Diagnosis is confirmed by upper GI contrast study and endoscopy. Location is vital to identify before intervention due to the risk of compromising hepatopancreatic drainage. Endoscopic intervention has been reported with varying complications, but overall, has shown success in treatment and resection of IDD.

[1091A] Figure 1. Visualization of both lumens upon entering the duodenum. The red arrow notes the windsock diverticulum.

1090 A Parasitic Journey Vinay Yalamanchi, DO, Wallace Wang, MD, Moshe Rubin, MD, FACG, Ellen Gutkin, DO, FACG. Internal Medicine, New York Hospital of Queens, New York, NY. Introduction: A 42-year-old male presented with a 4-week history epigastric abdominal pain and intermittent non-bloody, non-bilious vomiting. History was notable for travel to Peru 2 months prior. Physical exam was remarkable for midepigastric tenderness. Laboratory results revealed a mild leukocytosis (12.82 K/uL ) with an eosinophil count of 1.02 K/uL. Computed tomography (CT) of the abdomen without contrast was suspicious for obstruction at the proximal to mid-jejunum, thought to be secondary to post-operative adhesions or an inflammatory process. At endoscopy, within the second portion of the duodenum, a long, white, actively moving parasite was seen and retrieved with a Roth net. Capsule endoscopy was performed the next day, and did not reveal any additional parasites. Pathology confirmed the diagnosis of Ascaris lumbricoides. The patient was treated with 400 mg of albendazole, and it was suggested that his family also undergo treatment. More than 1 billion people are infected with Ascaris lumbricoides, and tropical countries have the highest prevalence. The ability to recognize the symptoms associated with parasitic infection is crucial, and timely diagnosis may prevent further complications. In general, the burden of worms correlates with the progression of symptoms. Children tend to develop worm clusters, and their status can shift rapidly towards complications such as sepsis. Adults may present with acute non-specific symptoms that progress to more complicated sequelae, even with only a single adult worm. Suspicion of parasitic enteritis warrants immediate CT of the abdomen with and without contrast to assess for obstruction or hepato-pancreato biliary involvement. Depending on the degree of obstruction or worm burden, endoscopy and laparascopy may be warranted. A thorough history of a patient’s travels and water or food handling can be a tremendous aide in the diagnosis of this type of infection. This case underscores the importance of obtaining a travel history in the setting of nonspecific gastrointestinal symptoms.

[1091B]

Figure 2. A Billroth II papillotome used to perform the diverticulotomy.

1092 Massive Upper GI Bleeding Due to Pseudoaneurysm of Right Gastroepiploic Artery in Chronic Pancreatitis: A Rare Presentation Sherry Levio, MD, Prathab Devaraj, MD, Srinivasan Ganesan, MD. WVU, Morgantown, WV.

1091 A Rare Cause of Abdominal Pain, Nausea, and Vomiting: A Windsock Diverticulum Jason Rubinov, MD, Dovid Moradi, MD, Andrew Korman, MD, Joseph Kim, MD, FACG, David CarrLocke, MD, FACG. Mount Sinai Beth Israel, New York, NY. Case Report: A 23-year-old female with a history of asthma and GERD presented to her PMD with intermittent nausea, vomiting, and epigastric pain for 5-6 months. Outpatient CT scan revealed a closed intraluminal duodenal diverticulum (IDD), otherwise known as a windsock diverticulum. She was referred for therapeutic endoscopy. Physical exam was significant for moderate epigastric tenderness. Laboratory values and vital signs were unremarkable. An upper endoscopy was performed. Upon entering the duodenum, 2 lumens were noted. The patent lumen was traversed without difficulty. The second lumen was a blind pouch consistent with the patient’s previous diagnosis per CT imaging of a windsock diverticulum of the duodenum. A diverticulotomy was performed using a Billroth II papillotome to cut the free wall of the diverticulum, ensuring that the major papilla was not compromised. The patient was discharged on hospital day 3 with significant improvement of her symptoms. Discussion: An intraluminal duodenal diverticulum is a rare entity, with less than 100 reported cases since 1885. The likely origin is a vestigial remnant of the medial or lateral vacuole, which does not com-


Introduction: Pseudoaneurysms of the right gastroepiploic artery are extremely rare, and are associated with significant morbidity and mortality related to massive bleeding and hemorrhagic shock. To date, pseudoaneurysms of the right gastroepiploic artery have only been reported in the setting of iatrogenic injury during PEG placement and in the setting of Churg-Strauss syndrome. The following case report involves a pseudoaneurysm of the right gastroepiploic artery in a patient with chronic pancreatitis due to alcohol abuse presenting as massive upper gastrointestinal bleeding secondary to direct erosion of the vessel through the duodenal wall. Case Report: A 67-year-old male with past medical history of chronic pancreatitis from alcohol abuse presented with 1-day history of bright red blood per rectum. He denied abdominal pain, nausea, vomiting, or diarrhea. His hemoglobin on presentation was 13 g/dL. The following day, he developed abdominal pain with hematemesis, and hemoglobin dropped to 7.9 g/dL. He became hypotensive and was transfused 6 units of PRBCs. His post-transfusion hemoglobin was 10.9 g/dL. NG lavage showed maroon blood and he was taken for urgent EGD, which demonstrated a 1-cm ulcer in the posterior duodenal bulb with overlying pulsatile clot. Epinephrine 1:10,000 was injected into the submucosa and the clot was removed, revealing a large visible vessel in the ulcer bed, which began to bleed more briskly. In spite of epinephrine injection and placement of 3 hemoclips, bleeding continued. He underwent emergent mesenteric angiography, which revealed a pseudoaneurysm of the proximal right gastroepiploic artery. IR coil embolization was successful in providing hemostasis, and the patient recovered without further bleeding complications.


| OCTOBER 2014

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Abstracts Discussion: Visceral artery pseudoaneurysms are a rare cause of potentially life-threatening hemorrhage. The most common artery affected is the splenic artery, followed by the gastroduodenal, pancreaticoduodenal, and the hepatic arteries. The clinical presentation involves abdominal pain and peritoneal signs related to intra-abdominal bleeding. Pseudoaneurysms of the right gastroepiploic artery are extremely rare. Until now, they have not been reported in the setting of chronic pancreatitis with massive upper GI bleeding, resulting from direct erosion of the vessel through the duodenal wall. Endoscopists should be aware of this entity, and right gastroepiploic artery pseudoaneurysm should be on the differential for upper gastrointestinal bleeding in patients with a history of chronic pancreatitis, especially if bleeding is not amendable to endoscopic intervention.

1093 Bouveret’s Syndrome: Definitive Diagnosis With Esophagogastroduodenoscopy Patrick Hickey, DO, Matthew Sullivan, DO, Saba Ahmad, MD, Hiral Shah, MD. Lehigh Valley Health Network, Allentown, PA. Introduction: Bouveret’s syndrome is a rare variant of gallstone ileus characterized by upper GI obstruction from an impacted gallstone in the setting of bilioenteric fistula. Typically, Bourveret’s presents with nausea, vomiting, and upper abdominal pain in elderly females. Diagnosis is usually made with imaging or endoscopy. Patients may present with Rigler’s triad of gallstone ileus, which consists of a small bowel obstruction, pneumobilia, and an ectopic radiopaque gallstone on x-ray. The most common treatment is surgical removal, but endoscopic extraction and lithotripsy have been described. We report a rare case of Bouveret’s syndrome and describe its endoscopic diagnosis and surgical management. Case Report: An 80 year-old-female presents with intractable nausea and vomiting of 2 days’ duration associated with mild right upper quadrant pain. CT evaluation at an outside hospital was found to have evidence of a possible cholecystoduodenal fistula with pneumobilia, a possible non-opaque gallstone within the third portion of the duodenum, and upper gastrointestinal obstruction. The patient was transferred to our institution for further management. Given the patient’s symptoms and findings on imaging, an EGD was performed for definitive diagnosis and attempted treatment. Two liters of bilious fluid and gastric contents were removed from the esophagus and stomach, suggestive of a gastric outlet obstruction. Endoscopy revealed granulated ulceration and pus in the second portion of the duodenum, consistent with cholecystoduodenal fistula. Advancement of the endoscope into the distal third portion of the duodenum revealed complete lumen obstruction with a mass of black and white material composed of gallstones and debris. The entire mass could not be mobilized, despite efforts with the needle knife to break the stone. Subsequent exploratory laparotomy allowed surgical removal of a 5.5 x 3.5 x 3.5-cm gallstone from the duodenotomy site. During the surgical procedure, the fistula was left intact because it was scarred and not well visualized. A gastrojejunal tube was placed for tube feedings and she was quickly advanced to a solid diet. She was discharged home in stable and improved condition a week after surgical intervention, and continues to do well in follow-up. Dicussion: French internist Leon Bouveret first described the syndrome in 1896. Bouveret’s syndrome is a rare differential diagnosis for upper gastrointestinal obstruction in elderly patients. Surgical awareness and possible intervention is warranted in such complicated cases. In this case, we demonstrate the value of endoscopy to diagnose and guide the treatment of Bouveret’s syndrome with non-diagnostic imaging. Disclosure - Dr. Shah - Speakers Bureau: US Endoscopy.

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1095 A Rare Case of Gastrointestinal Bleeding Due to Primary Intestinal Melanoma Ashish Zalawadia, MD, Yousuf Siddiqui, MD. Henry Ford Hospital, Detroit, MI. Introduction: We present a rare case of primary small intestine melanoma. Case Report: A 69-year-old male with a history of colon polyps presents with dark stool and fatigue. His hemoglobin dropped from 16 to 11. EGD showed possible Barrett’s esophagus. Biopsy was negative for metaplasia. He had a nodule of the second portion of the duodenum. Biopsy showed normal mucosa. Colonoscopy showed hemorrhoids, diverticulosis, and normal terminal ileum. A 3-mm tubular adenoma was removed from the colon. Small bowel (SB) capsule showed a moderate-sized semi-circumferential mass in the jejunum with areas of ulceration and bleeding. A CT abdomen showed small bowel mass in the distal jejunum. Adjacent enlarged lymph nodes (LN) are suspicious for metastatic disease. The patient underwent exploratory laparotomy and partial SB resection. Pathology reveals malignant melanoma. LN was negative for metastasis. Skin evaluation by dermatology did not find any lesions that were concerning for dysplastic nevi. Ophthalmology evaluation was normal. MRI of the brain revealed no metastatic process. PET-CT revealed intense hypermetabolism in the small bowel at the area of the surgical site without any evidence of metastatic disease. He followed up with oncology and his repeat PET scan and capsule endoscopy remained negative for recurrence of cancer. Discussion: Intestinal melanomas can be primary tumors or metastases of cutaneous, ocular, or anal melanomas. Primary intestinal melanoma is extremely rare. Most cases of SB melanoma are metastases from cutaneous melanoma. Metastases to the gastrointestinal tract are found at autopsy in 60% of patients who die with malignant melanoma. The clinical picture of SB melanoma is similar to the clinical presentation of other tumors involving the SB. Thus, patients with a history of cutaneous melanoma who have intermittent abdominal pain or anemia should be investigated to rule out intestinal metastases. Diagnosis can be made by ultrasound, barium studies, endoscopy, CT, or PET. A combination of imaging techniques is recommended to improve the sensitivity and specificity of radiological imaging. No standard therapy exists for the treatment of intestinal melanoma, although surgical removal is the treatment of choice in all patients with resectable melanoma. Accurate preoperative diagnosis and assessment of the extent of intestinal metastases is essential when selecting patients for surgery. Systemic chemotherapy regimens show no benefit to overall survival. The prognosis is poor, with an overall median survival of 6-9 months and a 5-year survival rate of less than 10%. Conclusion: Primary intestinal melanoma is very rare condition with poor prognosis. Early detection and surgical resection are vital to disease survival.

1096 An Unusual Cause of Partial Small Bowel Obstruction in a Young Male With HTLV-1 Varun Jain, MD,2 Deepak Sharma, DO,2 Tatjana Gavrancic, MD,2 Ava Anklesaria, MD,2 Vimala Ramasamy, MD,1 Sherrie White, MD,1 Andrey Iliev, MD1. 1. North Central Bronx Hospital, Bronx, NY; 2. Icahn School of Medicine at Mount Sinai (Bronx) - James J Peters VA Medical Center, Bronx, NY. Introduction: There are several causes of small bowel obstruction; in developed countries, these include adhesions, malignancy, and Crohn’s disease. Here, we present an unusual etiology of partial small bowel obstruction and weight loss in a young male. A 45-year-old male who had emigrated from Ghana presented with one year of post-prandial nausea, vomiting, associated 50-pound weight loss, and a diffusely tender abdomen. Laboratory tests revealed 6% eosinophils without leukocytosis

Generalized Lymphangiectasia in a Patient Presenting With Overt Obscure Gastrointestinal Bleeding Maen Kamal, MD,1 Jason Mader, DO,1 Rezwan Ahmed, MD,1 Muralikrishna Mukkamala, MS,1 Teresa Limjoco, MD,2 Yaser Rayyan, MD, FACG1. 1. Internal Medicine, Marshall University, Huntington, WV; 2. Marshall Pathology, Marshall University, Huntington, WV. Introduction: Intestinal lymphangiectasias (IL) are disorders characterized by dilated intestinal lacteals. Often reported in children, and less commonly in adults, its presentation is subtle, causing a slow loss of lymph into the gastrointestinal tract. In this case, we describe a rare presentation of overt obscure gastrointestinal bleeding (OOGIB) caused by generalized lymphangiectasia (GL). A 61-year-old white male presented to the hospital with a 1-week history of fatigue, worsening dyspnea with moderate exertion, and melena. His past medical history was significant for CAD, iron deficiency anemia (IDA), and HIV with a last reported undetectable viral load treated with efavirenz, emtricitabine, and tenofovir. His vital signs were stable and complete blood count was consistent with IDA. His Hgb and HCT on presentation were 6.4gm/dL and 21.5%. The patient was transfused and had improvement to his anemia. Further work-up revealed serum iron of 33 uL/dL, TIBC of 395 ug/dL, iron saturation of 8.4%, transferrin of 370mg/dL, and serum ferritin of 5.6 ng/mL. His stool was positive for occult blood and serum folate, and B12 levels were within normal range. The patient underwent upper and lower endoscopy that showed a duodenal diverticulum, mild diverticulosis in the ascending and transverse colon, and streaks of blood without an identified source. The patient’s vital signs and hemoglobin were closely monitored post-procedure, and he subsequently required a second blood transfusion. Capsule endoscopy (CE) was then performed and showed an actively bleeding polypoid mass in the jejunum, limiting visualization to the cecum. A single-balloon enteroscopy (SBE) was done next and identified an actively bleeding tumor at the distal jejunum. The patient underwent exploratory laparotomy and had resection of his jejunal mass as well as a Meckel’s diverticulectomy. With the exception of an ileus, the patient did well post-operatively and tissue pathology of the mass confirmed GL. IL may be associated with hypoproteinemia, hypogammaglobulinemia, hypoalbuminemia, and lymphopenia. The common clinical features of IL, which our patient did not exhibit, include bilateral lower limb edema, pleural effusion, and chylous ascites. Patients may have steatorrhea with increased loss of fecal fat and protein, while others may present simply with IDA. Most lymphangiectasias detected in adults appear to have little to no clinical features of malabsorption. Our case demonstrates an unusual presentation of OOGIB secondary to IL, which, to our knowledge, has not been reported. It is important to promptly identify this condition, and we would like to emphasize the role of CE and SBE in securing the diagnosis.


[1096A]

Figure 1. Duodenal biopsy.


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and positive HTLV-1 antibodies. Abdominal x-ray revealed a 3.5-cm dilated jejunum in the upper abdomen and multiple air-fluid levels, suggestive of partial proximal small bowel obstruction. The patient was treated with conservative management with IV fluids and nasogastric tube drainage. Given his history of persistent nausea, vomiting, and weight loss, an EGD was performed, which revealed inflammation of the antral and duodenal mucosa with some ulcerations. Gastric and duodenal biopsy results were positive for Strongyloides stercoralis (Figure 1). A diagnosis of S. stercoralis infection with partial small bowel obstruction was established. He was treated with albendazole 400 mg twice daily for 3 days and Ivermectin 200 mcg/kg daily for a total of 6 weeks. The patient was relieved of his symptoms and was noted to gain weight with conservative management. Strongyloides stercoralis is a nematode that burrows in the mucosa of the small intestine. Duodenal obstruction is a rare complication of strongyloidiasis, with only few cases reported in the medical literature. It can occur in severe infection with the parasite due to mucosal edema and inflammation. Widespread strongyloidiasis can also cause paralytic ileus. HTLV-1 affects cell-mediated immunity and increases the risk of severe infection. Parenteral therapy is not available for strongyloidiasis, which makes conservative management of duodenal obstruction and paralytic ileus in this setting challenging. Although surgical management of duodenal obstruction has been reported in the literature, if an early diagnosis is made, then conservative treatment may be used with favorable outcomes, as seen in this patient.

1097 A Unique Cause of Gastrointestinal Bleed With Innovative Treatment Tarek Sawas, MD, Farzin Rashti, MD, Mitesh Patel, MD, FACG. Georgetown University Medstar Washington Hospital Center, Washington, DC. Introduction: An 85-year-old female with a history of scleroderma and peptic ulcer disease presented to the emergency room with shortness of breath, weakness, abdominal pain and black, tarry stools for 3 days. She had been using aspirin, but denied using NSAIDs. She denied nausea, vomiting, or hematochezia. Her hemoglobin was 4.6 g/dL and she was admitted for symptomatic anemia. She was started on intravenous protonix and received volume resuscitation and blood transfusions. Upper endoscopy was performed and showed gastric atrophy, but the source of bleeding was not identified. A colonoscopy showed pan-diverticulosis with clots and red blood in the entire colon. Video capsule endoscopy revealed multiple oozing arteriovenous malformations (AVMs) in the distal duodenum and proximal jejunum. Due to the location of the AVMs, single-balloon enteroscopy was performed with successful thermal therapy, with argon plasma coagulation of multiple non-bleeding AVMs. Despite treatment, the patient continued to have persistent bleeding and refused further endoscopic therapy. She opted for therapy with segmental resection of the small bowel with intraoperative enteroscopy for intraluminal identification of potential bleeding sites. Multiple AVMs were identified intraoperatively throughout the proximal to mid jejunum with 1 site noted to be actively bleeding. The exact locations were marked for resection with the use of surgical sutures. Pathology of the small bowel showed amyloid deposits in multiple submucosal blood vessels, which was confirmed by Congo red staining. Symptoms secondary to gastrointestinal (GI) primary amyloidosis are extremely rare (1%) and GI bleeding is rarely encountered as an initial symptom or the only manifestation of the disease. Amyloidosis can involve any part of the GI tract, but isolated small bowel amyloidosis is uncommon. Appearance on endoscopy and colonoscopy varies between friable mucosa, ulcers, mass, sub mucosal hematoma, and telangiectasias. Treatment often requires endoscopic intervention, surgical resection, or angiogram with embolization. There is only 1 reported case of segmental small intestinal resection with intra-operative enteroscopy for amyloidosis in the literature. We present the first case of GI bleeding as an initial manifestation of isolated small bowel amyloidosis secondary to AVMs, and only the second case to be treated with segmental small intestinal resection with intra-operative enteroscopy. Although it is exceedingly rare to develop GI bleed from amyloidosis, clinicians must be aware of this rare, but possible cause of GI bleeding.

1098 Resolution of Intestinal Failure with Prolonged Parenteral Nutrition, Bowel Rest, and Intravenous Antibiotics in an HIV Patient With Chronic Cystoisospora belli Diana Snyder, MD, Lena Palmer, MD. Loyola University Medical Center, Maywood, IL. Introduction: Cystoisospora belli, formerly Isospora belli, is a protozoal parasite causing chronic diarrhea and weight loss after ingestion of food or water contaminated with oocytes. It is endemic in India, Africa, and South America. In the United States, it mainly affects immunocompromised patients, such as those with HIV. Sulfamethoxazole/trimethoprim (Bactrim®) is first-line treatment. The few published studies report a high rate of relapse and death, despite immune reconstitution. Our patient is a unique case of chronic cystoisosporiasis leading to intestinal failure, which resolved after parenteral nutrition (PN), bowel rest, and IV antibiotics. Case Report: A 48-year-old Indian male with HIV (CD4 count of 166, viral load undetectable on highly active anti-retroviral therapy [HAART]), and chronic hepatitis B was admitted with severe diarrhea, malnutrition, and profound weight loss [35 kg, BMI 13]). Stool studies detected Cystoisopora belli, and duodenal biopsy showed villous attenuation, severe duodenitis with eosinophilia, and Cystoisospora. He was admitted to the hospital almost monthly for a year, and treated with sulfamethoxazole/trimethoprim, ciprofloxacin, and nitazoxanide, but the intestinal failure persisted despite a CD4 count >200 and no detectable HIV virus. Home PN, bowel rest, and IV ciprofloxacin were ultimately initiated, resulting in dramatic symptom improvement. Persistent Cystoisospora was found on duodenal and jejunal biopsies 7 months into PN therapy, despite symptom improvement. Therapy continued, and he was able to wean from PN 3 months later. He has not been admitted since initiating PN. Discussion: Our case is unusual in that it shows a positive outcome in severe cystoisosporiasis via PN, IV antibiotics, and bowel rest, despite persistent intestinal colonization. Two case series reported HIVinfected patients failed to eradicate Cystoisospora belli even after immune reconstitution, as was seen in our patient. The patients remained symptomatic leading to hospitalization and even death in 5 of 6 patients. These studies suggest there may be incomplete restoration of gastrointestinal CD4+ T cells leading to only partial intestinal immunity in those with chronic cystoisosporiasis.


Conclusion: PN is an effective method to treat intestinal failure from Cystoisospora belli infection when HAART and antibiotics have failed. Patients may have chronic colonization of Cystoisospora belli despite symptom resolution.

1099 A Case of Eosinophilic Gastroenteritis Initially Misdiagnosed as Idiopathic Intestinal Angioedema Vinay Patel, MD, Kunal Karia, MD, David Wan, MD. Weill Cornell Medical College, New York, NY. Introduction: We present the case of a 31-year-old white woman with a 7-year history of recurrent jejunal thickening manifesting as worsening abdominal pain, nausea, and vomiting. These episodes started in 2008, at 25 years old. A CT demonstrated small bowel wall edema and endoscopy with biopsies was normal. Her symptoms resolved with a course of corticosteroids. She subsequently had flares every 3-6 months. She presented to us in 2009. Stool culture, ova and parasites, and other labs including infectious, hereditary angioedema, and autoimmune work-ups were normal. CT was remarkable for >20cm-long segment of jejunum with >1.5-cm circumferential wall thickening and ascites. Balloon enteroscopy showed edematous jejunal folds, but mucosal biopsies from the stomach, duodenum, and jejunum were normal. She was diagnosed with idiopathic intestinal angioedema. EGD and colonoscopy with biopsies in 2013 were again normal. In 2014, she was admitted to our institution, and MRI was consistent with previous CT findings, with the same jejunal segment involved. IgE levels were normal and CBC on admission showed 11,100/μL leukocytes with 1,200/μL eosinophils. She had increasing eosinophilia over the next 6 days, peaking at 3,500/μL. IL5 levels were 15pg/mL (normal: 50 mitotic rates per HPF. After complete surgical resection, she was started on 400 mg /day of imatinib. She has shown no evidence of relapse in the last 10 months.

1173 Pseudomelanosis Duodeni: Innocent Speckling Ruby Jhaj, MD, Jose Parungao, MD, Michael Piper, MD, FACG, Freddy Sosa, MD, Laurence Stawick, MD. Providence Hospital and Medical Centers, Southfield, MI. Introduction: Pseudomelanosis duodeni is a rare endoscopic finding displaying discrete brownish-black speckled duodenal mucosa consisting of pigment-laden macrophages containing ferrous sulfide. Usually occurring in females over 60, it is rarely noted in settings other than chronic kidney disease, hypertension, and diabetes mellitus. Some associated medications include ferrous sulfate, hydralazine, and furosemide. Case Study: A 71-year-old female with a past medical history of hypertension, chronic kidney disease, anemia, and diabetes presented to the hospital with a 4-day history of constant, dull left upper quadrant pain bearing no relation to exertion, position, or meals. She denied any changes in diet or medications, recent antibiotic use, or travel. Laboratory data and imaging were inconclusive. She was started on IV fluids, Protonix, Zofran and Reglan. With failure of conservative management, an EGD was performed, revealing gastritis and pseudomelanosis duodeni (Figure 1), which was confirmed by pathology demonstrating iron deposits in the mucosa (Figure 2). Protonix dosing was increased to twice a day and her pain had resolved. The patient never used laxatives. She had been taking furosemide and hydralazine for several years and used oral iron supplementation consistently for 2 months over a year ago. Conclusion: Although a rare endoscopic finding, pseudomelanosis duodeni has been demonstrated to have characteristic disease and medication associations, as seen in our patient. It is important to be cognizant of these facts in order to prevent unnecessary work-up pursuing alternative diagnoses. However, the significance, prognosis, and surveillance guidelines have not been established.

[1173A]

Figure 1.

[1173B]

Figure 2.

Uncommon Intra-abdominal Tumors May Have Common Presentations: Gastrointestinal Stromal Tumor Sana Siddique, MD, Indumathy Varadarajan, MD. Medicine, Mount Auburn Hospital, Cambridge, MA. Introduction: Gastrointestinal stromal tumours (GIST) are uncommon but aggressive stromal neoplasms of the gastrointestinal (GI) tract, which represent 5/50per HPF. Discussion: Pathogenesis of GIST can be accounted by mutations in the c-KIT gene or the plateletderived growth factor gene that enables the up regulation of the tyrosine kinase, increasing its oncogenic potential. Most GIST express CD 117, as they are a component of the tyrosine kinase receptors that are over-expressed in these tumors. Patients present with vague, nonspecific complaints, but fatal complications like intraperitoneal tumor rupture, tumor dissemination leading to intraperitoneal sarcomatosis, warrant urgent surgery. Size (>10 cm) and mitotic rates more than 50 per HPF are the most significant variables that predict malignant behavior. Imatinib, a potent tyrosine kinase inhibitor, has shown to



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1174 A Rare Case of Malignant Melanoma to the Jejunem, Diagnosed on Small Bowel Enteroscopy Sadra Azizi, MD, Emory Manten, MD, Jesse Green, MD. Albany Medical Center, Albany, NY. Introduction: A 63-year-old male was transferred to our center from an outside hospital after presenting with complaints of left hand numbness and dizziness, which had been ongoing for a few days. A head CT revealed 2 masses, which led to his transfer in order to evaluate for a likely malignancy and subsequently, a metastatic work-up. The patient denied any nausea, vomiting, diarrhea, constipation, abdominal pain, fevers, melena, and hematochezia. He also denied any prior endoscopic procedures. The patient had a contrast CT of the chest, abdomen, and pelvis, which revealed a 4 x 5-cm right atrial mass (later thought to be a thrombus based on MRI), and a 9 x 7-cm mid small bowel mass with surrounding lymphadenopathy and fat stranding, concerning for a primary small intestinal malignancy. Small bowel enteroscopy was performed and a large circumferential, fungating, ulcerated, and infiltrated mass with no bleeding was found in the proximal jejunum at 50-60 cm from the pylorus. This was biopsied and pathology returned positive for metastatic melanoma. After further evaluation, the patient was also found to have a lesion on the skin of his back, which was also biopsied and returned positive for melanoma in situ. The patient was then started on whole brain radiation and trametinib for palliative therapy. The patient underwent a complicated hospital course, which ultimately resulted in comfort care measures and ultimately, expiration. Small bowel tumors only account for 3-6% of all GI tumors, and only 1.5-4% of GI metastases from cutaneous melanoma are ever diagnosed in a patient’s lifetime. Our case highlights a rare presentation that lent itself to diagnosis via push enteroscopy. While there is some suggestion of the possibility for primary GI melanoma, some authors have suggested that there is no such entity and that they all result from a non-GI primary site, such as a regressed cutaneous source. The gold standard for therapy at this time remains surgical resection of metastatic bowel, but as a means of palliation and not cure. Newer systemic chemotherapies and immunotherapies are being FDA-approved in recent years, which may show promise in the coming future.

1175 Whipple’s Disease Presenting as Endocarditis Ryan Meinen, DO, David Payton, PA-C, Joseph Fares, MD, Walid Almuti, MD. GI, John C. Lincoln, Phoenix, AZ. Introduction: Whipple’s disease is a systemic disorder caused by Tropheryma whipplei and commonly presents with GI complaints such as chronic diarrhea. Its appearance varies, and we therefore report the case of a patient with this rare condition who presented with atypical endocarditis. Case Report: An 84-year-old Asian male presented with 3 months of myalgias, weight loss, generalized weakness, and poor appetite. He had also recently developed lower extremity edema. He denied abdominal pain, dysphagia, vomiting, or diarrhea. He also had no fever, chills, rigors, or rashes. His past medical history included Parkinson’s disease, hypothyroidism, and arthritis, but no GI or cardiac issues. Of note, the patient had a dental procedure without antibiotic prophylaxis 4 months prior to hospital admission. His physical exam revealed a soft, non-tender abdomen without appreciable masses. The cardiac exam noted a diastolic murmur. An outpatient transthoracic echocardiogram suggested mitral valve vegetation. On admission, a transesophageal echocardiogram subsequently confirmed a 1.2 cm x 0.7 cm vegetation on the anterior leaflet of the mitral valve. Blood cultures were negative. Serologic testing done for Q fever, Bartonella, Legionella, tuberculosis, coccidomycosis, rheumatoid factor, and ANCA was negative. These results, coupled with afebrile endocarditis, weight loss, and hypoalbuminemia raised concern for Whipple’s disease. EGD biopsies revealed benign small bowel mucosa with submucosal collections of foamy macrophages/histocytes with PAS positive material. The AFB stain was negative. Together, these histologic findings confirmed the Whipple’s diagnosis. The patient was then placed on IV ceftriaxone for 2 weeks and TMP-SMX for 1 year. Discussion: Although cardiac manifestations are common in Whipple’s disease, it is unusual for its initial presentation to be cardiac in nature without overt GI symptoms. In this unique case, the patient presented with generalized weakness and weight loss, but no abdominal pain or diarrhea. It is also important to note the patient had also been afebrile without chills or rigors despite having endocarditis. Although there are more common causes of endocarditis, most patients present with fever. This case is a worthwhile reminder to keep Whipple’s disease in the differential when evaluating patients with afebrile endocarditis, even in the absence of GI complaints.

1176 A Case of Adult Intussusception Sheila Reddy, MD,1 Boris Blechacz, MD2. 1. University of Texas at Houston, Houston, TX; 2. Department of Gastroenterology, Hepatology, and Nutrition, MD Anderson Cancer Center, Houston, TX. Introduction: A 38-year-old Indian man with B-cell adult lymphocytic leukemia on chemotherapy was admitted with diarrhea, nausea, vomiting, and worsening abdominal pain. On presentation, a CT of his abdomen and pelvis found a mild colonic and small bowel distention. The patient was managed with IV fluid hydration and pain medication, and his symptoms improved. Three days later, the patient developed severe colicky abdominal pain. On abdominal exam, he had peri-umbilical tenderness with guarding. The patient was neutropenic and thrombocytopenic throughout his hospital stay, with a WBC of 500/μL and platelets of 16000/μL. Given his acute change in symptoms, another CT scan was performed, which showed small bowel intussusception. Surgery evaluated the patient, and given his neutropenia and thrombocytopenia, opted for conservative management. Five days later, the patient had a repeat CT scan that showed resolution of the intussusception and the patient was eventually discharged home and continued on his chemotherapy regimen. Intestinal invagination or intussusception is the leading cause of intestinal obstruction in children. Intussusception in adults accounts for only 5% of intussuception cases. Intussusception can present as acute, intermittent, cramping, and abdominal pain with nausea and vomiting; however, vague abdominal symptoms


is a common presentation. While in children, 95% of cases are idiopathic, about 90% of causes of intussusception in adults are due to a distinct pathologic abnormality. In the small bowel, this consists of benign neoplasms, inflammatory lesions, and adhesions. Malignant lesions are found in only 30% of cases of intussusception in the small intestine, in contrast to 60% in colonic intussusception. Abdominal x-rays often show signs of intestinal obstruction, and can give information regarding the site of obstruction. CT has been reported to be the most useful diagnostic tool for the diagnosis of intussusception, with an accuracy of 58-100% with a finding of a homogenous mass that is target or sausage-shaped. The optimal management of adult intussusception is controversial, particularly in the small bowel. While resection of colonic intussusception is generally advocated due to the high percentage of associated malignancies, small bowel intussusception is less commonly due to malignancy, and thus intraoperative manual reduction with careful palpation of the intestinal wall might allow for limited bowel resection. Intussusception in adults is rare, and can present with non-specific abdominal complaints. Gastroenterologists should be aware of this rare condition for abdominal pain and the current treatment methods.

1177 Zip Tie: A Simple Fix for Gastrostomy Tube Dislodgement Pancreatitis Siegfried Yu, MD, Sherman Chamberlain, MD, FACG. Internal Medicine, Georgia Regents University, Augusta, GA. Introduction: Gastrostomy tubes are safe, inexpensive, and easy to place, and are commonly used to provide long-term enteral nutrition to individuals who have inadequate or absent oral intake. Although they can be placed endoscopically, surgically, or radiologically, the complications related to the various techniques are similar. Our case report describes a rarely reported cause of acute pancreatitis as a complication of gastrostomy tube utilization. We also propose a simple, inexpensive solution to this problem. Case Report: A 48-year-old male with a history of stroke with dysphagia requiring percutaneous endoscopic gastrostomy (PEG) feeding had his original PEG tube dislodged, and had a replacement PEG tube placed in the original PEG site. He subsequently presented to our hospital with chest and abdominal pain radiating to the back, and was found to have acute pancreatitis with lipase elevated to 674 U/L. His evaluation excluded common causes of acute pancreatitis. On the second hospital day (HD), a CT revealed the inflated replacement PEG tube balloon at the junction between the third and fourth portion of the duodenum. On examination, it was clear that there had been migration of the replacement PEG tube inner balloon despite the outer bumper being intact. The tube was pulled back into place with the outer bumper at 2 cm, and secured with a zip tie fastener placed tautly around the PEG tube just above the outer bumper to inhibit any slippage of the outer bumper (but still loose enough not to impinge on liquid flow). EGD on the 5th HD confirmed that the PEG tube balloon remained in place at the distal gastric body wall. The patient’s pancreatitis resolved promptly, and he was discharged home on the ninth HD. Discussion: PEG tubes have overall complication rates from 470%. Serious complications include gastric perforation, gastric bleeding, and hematoma development. Acute pancreatitis is rarely reported, but can occur as a result of tube dislodgement with migration of the PEG tube inner bumper/balloon, resulting in direct mechanical irritation of the major and/or minor papilla. The outer bumper of replacement PEG tubes should be, but are not commonly, sutured in place. The zip tie fastener, also known as a hose tie, zap-strap, or cable tie, is commonly used to organize cables and wires. Utilizing zip ties to secure the outer bumper of PEG tube replacements will avoid potential complications from inner balloon slippage if the PEG tube replacements are not sutured to the outer abdominal wall. This case demonstrates the zip tie method for securing PEG tubes, which offers a cost-effective quality improvement to enhance patient safety, and avoids unnecessary complications of PEG tube dislodgement.

1178 Fish Bone Ingestion as an Etiology for Intramural Duodenal Hematoma James Katsis, MD, Philip Sarges, MD, Mark Mattar, MD. Medstar Georgetown University Hospital, Washington, DC. Introduction: Intramural duodenal hematoma (IDH) is a rare cause of gastric outlet obstruction. It is most often reported in pediatric populations and in those with hematologic disorders or on anticoagulant therapy. The majority of IDH form as a result of external or internal trauma. Case Report: A 36-year-old woman with sickle cell anemia presented with sudden onset of severe, sharp epigastric abdominal pain associated with nausea and non-bilious, non-bloody emesis. She was found to have an elevated lipase level and was diagnosed with pancreatitis. Initially, she was treated conservatively for pancreatitis. The patient continued to have persistent abdominal pain, nausea, and vomiting. An abdominal CT showed gastric outlet obstruction secondary to an intramural duodenal hematoma. The patient later stated that she intentionally chewed and swallowed fish bones, which is typical for her diet. Physical exam revealed a soft but diffusely tender abdomen, mainly in the epigastric region with mild distention. Labs were notable for an elevated total and direct bilirubin of 3.2 and 2.2, respectively, a lipase of 180, and INR of 1.3. She was managed conservatively with supportive care and total parenteral nutrition (TPN). After eight days, she began to tolerate liquids and was transitioned back to oral nutrition. She was discharged in good condition. Discussion: The course of events that leads to an IDH typically occurs from a traumatic injury, whether it be external, such as a motor vehicle accident, or internal, such as endoscopic procedures, biopsies, or ingestion of sharp or rigid materials, as in this case. The presence of a hematologic disorder or use of anticoagulant therapy also contribute to the risk of hematoma formation. There are case reports of spontaneous IDH formation as well, but these are rare. The complications from IDH formation are from mass effect, mainly resulting in gastric outlet obstruction. In our case, and in many other cases, the patient developed pancreatitis, presumably due to obstruction of the duodenal papilla or compression of the pancreas caused by the hematoma. Recognition of this syndrome is important in order to avoid any unnecessary operations, as the outcome is usually excellent with conservative management.


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Abstracts 1179 A Rare Case of Pseudomelanosis Duodeni in a Heart Transplant Patient Sahil Patel, MD,1 Amir Kalani, MD PhD,1 Seth Kaufer, DO,2 BhaviK Bhandari, MD2. 1. Drexel University School of Medicine, Division of Internal Medicine, Philadelphia, PA; 2. Drexel University School of Medicine, Division of Gastroenterology, Philadelphia, PA. Introduction: Pseudomelanosis of the duodenum is a rare and asymptomatic finding of the gastrointestinal tract. First described in the literature in 1976, less than 50 cases have been reported since. It is typically discovered incidentally on endoscopy as flat, brown to black spots giving a speckled appearance to the duodenum. Risk factors include primarily oral iron intake, but conditions such as diabetes mellitus, chronic renal failure, arterial hypertension, gastrointestinal bleed, as well as intake of drugs like hydralazine, furosemide, and propranolol have also been implicated as possible etiologies. The pigmentation was originally believed to be due to melanin or melanin-related compounds, but has since been shown to be a product ferrous sulfide deposition. Histologically, hemosiderin-laden macrophages are demonstrated at the tips of the villi in the duodenum and diagnosis is confirmed with iron staining. Here, we report a 76-year-old male with a history of heart transplant, hypertension, diabetes mellitus, and chronic kidney disease who presented with early satiety and a 40-pound weight loss over 6 months. Laboratory findings were significant for iron deficiency anemia. He underwent an EGD, which revealed pseudomelanosis throughout the duodenum, and a colonoscopy, which showed polyps and diverticulosis, but no melanosis or pseudomelanosis. Duodenal biopsies were positive for iron staining, although the patient denied any previous use of iron supplements.

produced by these agents or be non-functional and be diagnosed after causing obstruction or mass effect. NETs can be well-differentiated (including carcinoid tumors that are slow) or poorly differentiated with tendency of being aggressive and rapid. GI NETs are relatively rare, but the most common primary tumor of small intestine. Case Report: An asymptomatic 66-year-old female with PMH of HTN and HLD was sent by her PMD for screening colonoscopy and was found to have a 2 x 3-cm mass in terminal ileum, which was diagnosed with grade lll B T2 N1 (regional lymph nodes), well-differentiated neuroendocrine carcinoma of terminal ileum, with no distant metastasis, positive for chromogranin, synaptophysin, and serotonin. The patient also had elevated 5 -HIAA. She underwent surgery, no adjuvant chemotherapy was recommended, and she remained asymptomatic with no recurrence in 2 years’ follow-up. Discussion: Most of the reported NETs have regional or distant metastasis at the time of diagnosis with poor survival if distant metastasis has occurred. The prevalence of distant metastasis increases with the size of primary tumor. Ileum is the most common site of GI NETs; however, diagnosis of intestinal tumors is difficult, and these tumors get to be diagnosed either with obstruction/mass effect or by symptoms of functional tumors, which mostly have already metastasized. Conclusion: As we described in this rare case, if all the attempted colonoscopies (screening and diagnostic) reach ileum, most of the tumors of distal intestine can be diagnosed in early stages when distant metastasis has not yet occurred, hence better prognosis and survival for patients could be achieved.

1182 1180

Primary Ewing’s Sarcoma of Jejunum Presenting as a Small Bowel Obstruction: A Case Report

Cytomegalovirus Ileitis Divya Sadaram, MBBS, Srivatsa Kowsika, MBBS, PA-C, Sree Kowsika, MD, Murthy Madhira, MS, MD. Gastroenterology, Monroe Gastroenterology Clinic, Monroe, MI. Introduction: Cytomegalovirus (CMV) involvement of gastrointestinal tract was described in both immune-competent and immune-compromised patients. Small bowel involvement was 4.3% of all CMV infections of GI tract. We are reporting a case of CMV Ileitis in a patient treated with rituximab. A 78-year-old white female was treated for non-Hodgkins lymphoma (NHL) with rituximab-based chemotherapy in 2006. The lymphoma recurred in 2011, and she has been receiving rituximab every 6 months, with the last dose in February 2014. The patient was seen for postprandial diarrhea, dyspepsia (early satiety), weight loss, and for colon cancer screening. The patient denied rectal bleeding, abdominal pain, and night sweats. She underwent EGD and colonoscopy. EGD revealed huge duodenal diverticulum and H. pylori-negative gastritis, and colonoscopy revealed colonic diverticulosis and severe ileitis (ulcerative ileitis with stenosed ileocecal valve). Biopsies revealed active erosive ileitis with positive immunohistochemical staining for CMV. CMV serology was positive (IgG), but CMV PCR was negative. IBD markers were negative. CTE revealed a short, active inflammatory stricture in terminal ileum. The patient was suggested to be treated with vanganciclovir for a period of at least 3-6 weeks. However, she discontinued the treatment after 2 weeks due to financial reasons. The patient’s diarrhea completely resolved and the patient felt better. We suggest a high index of suspicion in all immunocompromised and immunocompetent patients who present with chronic diarrhea, weight loss, and right lower quadrant abdominal pain. Symptoms of CMV Ileitis can range from mild anorexia, diarrhea, to severe complications like GI hemorrhage, perforation, fistula formation, and even death.

1181 A Case Of Asymptomatic Metastatic Neuroendocrine Tumor of Terminal Ileum, Accidentally Found in Screening Colonoscopy Negar Niknam, MD, Negin Niknam, MD, Farzin Farpour, MD, Saphwat Eskaros, MD, FACG. Internal Medicine, Icahn School of Medicine at Mt. Sinai, Queens Hospital Center, Jamaica, NY. Introduction: Neuroendocrine tumors (NETs) arise from neuroendocrine cells distributed in most organs, can be functional, produce hormones, peptides, amines, and be diagnosed by the symptoms

Kartik Valluri, MD,1 Marvin Lopez, MD,1 Michael Monzel, MD, FACG,1 Ashley Lankford, MD2. 1. Internal Medicine, University of Miami Miller School of Medicine Palm Beach Regional Campus, Boynton Beach, FL; 2. University of Miami Miller School of Medicine Palm Beach Regional Campus, Atlantis, FL. Introduction: Primary Ewing’s sarcoma/ PNET of the jejunum is a very rare presentation of Ewing sarcoma family of tumors (EFT) of extra-osseous origin. Case reports of duodenal, rectal, and abdominal Ewing’s sarcoma can be found in the literature, but to our knowledge, this is the first case of primary jejunal Ewing’s sarcoma. Case Report: A 48-year-old male with no past medical history presented to an urgent care facility with a 3-day history of constipation, not relieved by laxatives with associated abdominal pain. On physical examination, vital signs were stable, but the patient appeared uncomfortable with mild distention of the abdomen and hypoactive bowel sounds. The patient was prescribed laxatives and referred to a gastroenterologist. Over the course of the week, the patient’s symptoms worsened. An outpatient CT-scan of the abdomen with IV and PO contrast revealed a jejunal intussusception. The patient underwent an exploratory laparotomy revealing a 10-cm jejunal intussusception 12 inches from the ligament of Trietz with a large polyp as a lead point. Gross inspection of the resected specimen showed a fungating, ulcerative, obstructing tumor of the jejunum. Pathology revealed a tumor invading through the muscularis propria into the subserosa. A histological diagnosis was grade 4 PNET/Ewing sarcoma. FISH showed a EWSR1 (22q12) gene rearrangement and CD45 (-) /CD56 (+) cells ruling out hematolymphoid origin. Immunoperoxidase stains revealed CD99 positive marker for Ewing’s sarcoma. Subsequent bone scan and PET-studies failed to demonstrate any osseous primary sources or other sites of metastasis. The patient was referred to oncology for chemotherapy with vincristine, doxorubicin, and cyclophosphamide alternating with ifosfamide and etoposide (VDC/IE). Discussion: The majority of Ewing’s sarcoma are predominantly cancers of children and rarely seen after the age of 30. Molecularly, they have variable translocations of EWSR1 gene. Immunohistochemical staining is essential in differentiating amongst the various subtypes. Treatment of localized disease is surgical resection, preferably before chemotherapy with (VDC/IE) based on the IESS-III study. We believe this case is the first described primary jejunal Ewing’s sarcoma, presenting in the gastro-intestinal tract masked by common symptoms in a patient with no family history of malignancy. These tumors carry a poor prognosis regardless of surgical or chemotherapeutic management. It is always beneficial to identify the cause and ascertain the pathological diagnoses for prompt treatment to prevent metastases and improve prognosis of individuals affected by Ewing’s sarcoma.

1183 An Unsual Case of Enteritis: ACEI of Spades Srikar Mapakshi, MD, Catalina Negulescu, MD, Brandon Amant, MD, Neelima Reddy, MD. Internal Medicine, Baton Rouge General-Tulane Internal Medicine Residency program, Baton rouge, LA.

[1181A]

Figure 1. Mass in terminal ileum, seen in endoscopy.


Case Report: A 37-year-old black female with ADD and newly diagnosed HTN presented with a 2-week history of generalized post-prandial abdominal pain associated with nausea, emesis and diarrhea. At an OSH abdominal ultrasound demonstrated gallstones without cholecystitis. She was discharged with a diagnosis of gastroenteritis. Persistent post-prandialgastrointestinal symptoms lead to an outpatient surgical evaluation and a laparoscopic cholecystectomy. Despite surgery, her symptoms persisted and gastroenterology consultation prompted inpatient admission. PMH was notable for a normal colonoscopy done 1 year prior for self-limited abdominal pain. She denied drug allergies and use of tobacco, alcohol, or illicit drugs. On admission, she was afebrile and hemodynamically stable. She had only mild transaminitis with AST 52 and ALT of 54. Stool studies including Clostridium difficile were negative. Contrast-enhanced CT abdomen and pelvis revealed multiple loops of small bowel wall thickening extending to distal ileum with adjacent mesenteric edema and ascites empiric intravenous antibiotics started without improvement of symptoms. She recalled a self-limited episode of lip swelling 2 days prior to admission and stated that she had started taking Lisinopril recently. Given the strong temporal correlation between symptom onset and initiation of ACE inhibitor (ACE I), a diagnosis of drug-induced visceral angioedema was made and ACE I was discontinued. Within 24 hours of ACE I discontinuation, the patient reported significant symptom improvement.


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Discussion: A PubMed literature search revealed few reported cases of ACE I-induced visceral angioedema. Visceral angioedema poses a diagnostic challenge because it involves internal organs that are not classically affected by ACE I induced angioedema. ACE I-induced visceral angioedema is more commonly seen in women (82%) compared to men. Abdominal pain (100%), vomiting (86%), ascites (71%), diarrhea (50%), and leukocytosis (44%) are commonly associated. Contrast enhanced CT of the abdomen and pelvis is the imaging modality of choice to evaluate for bowel wall thickening and free fluid consistent with visceral angioedema. Several theories for the etiology of angioedema have been proposed, but brady kinin associated vasodilatation is the most widely accepted. Symptoms usually resolve within 48 hours of ACE I discontinuation. We hope this case will increase awareness of ACE I-induced visceral angioedema as an important and under-recognized complication of ACE inhibitor therapy. Drug-induced visceral angioedema should be part of the differential for abdominal pain and a through medical history, along with appropriate work-up, can avoid unnecessary invasive procedures and health care costs.

1184 Olmesartan-Associated Sprue-like Enteropathy Justin Hartke, MD, Arushi DeFonseka, MD, Anne Tuskey, MD, Brian Behm, MD. University of Virginia Health Systems, Charlottesville, VA. Introduction: Olmesartan has been implicated as an etiology of sprue-like enteropathy characterized by duodenal villous atrophy refractory to a gluten-free diet, negative celiac serologies, and resolution of symptoms following discontinuation of olmesartan. We present a series of 3 patients with olmesartan-associated enteropathy identified at our institution. Three patients were identified with olmesartan-associated enteropathy; all 3 were white females with a mean age of 64.7 years. All were taking olmesartan for several years prior to development of symptoms. Symptoms at presentation were characterized by chronic progressive diarrhea, weight loss, and abdominal pain. Celiac serologies including tissue transglutaminase IgA and quantitative IgA levels were normal. Upper endoscopy showed histologic findings suggestive of celiac disease, including severe duodenal villous atrophy and increased intra-epithelial lymphocytes in all patients. Colonoscopy with biopsies revealed microscopic colitis in 2 patients and was normal in the third. One patient was HLA-DQ2 heterozygote-positive and one patient was HLA-DQ8 heterozygote positive. Two patients were started on gluten-free diets without symptomatic improvement. All 3 patients were prescribed budesonide without symptomatic improvement. One patient was prescribed mesalamine while another was prescribed prednisone, which did not resolve symptoms. Complete symptom resolution was noted a mean of 5 weeks following discontinuation of olmesartan. No patient developed recurrent symptoms with alternative antihypertensive medications. This case series highlights the association of olmesartan and the development of sprue-like enteropathy, which may present years after initiation of olmesartan therapy. It corroborates previous findings with complete resolution of symptoms after discontinuation of olmesartan. Thus, in patients with seronegative villous atrophy and symptoms suggestive of celiac disease, clinicians should consider olmesartan as a potential cause of symptoms.

1185 Sclerosing Mesenteritis Presenting as Duodenal Obstruction Sasha Mangray, MBBS, Alan Brijbassie, MBBS , MD, FACG. Carilion Clinic, Roanoke, VA. Introduction: A 60-year-old male with a history of hypertension and hypothyroidism presented for evaluation of abdominal pain, emesis, and singultus for 5 days. He denied fever or prior surgical history. On physical examination, abdomen was diffusely tender with normal bowel sounds. Laboratory results showed a mild leukocytosis of 13.5 K/uL and creatinine of 3.52 mg/dL. Un-enhanced computed tomography (CT) of the abdomen revealed a dilated distal esophagus, very distended stomach, and dilated C loop that gradually tapered to the third part of the duodenum. Endoscopy identified a stricture 30 cm from the duodenal bulb, which was biopsied; however, histopathology was equivocal. Surgical referral was made and the patient underwent exploratory laparotomy, which demonstrated a mesenteric mass involving the third and fourth portions of the duodenum and encasing the superior mesenteric artery. A gastrojejunostomy was done and biopsy results of the mass showed fibrous tissue, fat necrosis, and chronic inflammation, consistent sclerosing mesenteritis. Sclerosing mesenteritis (SM) is an umbrella term that describes a spectrum of rare, non-neoplastic diseases that affects the small bowel mesentery. The pathophysiology of SM remains unknown, but various mechanisms have been postulated, including hypoxic, allergic, infectious, and autoimmune. Men account for 70% of patients and disease usually occurs in the sixth and seventh decades. The most frequent presenting complaints were abdominal pain, bloating, diarrhea, bowel obstruction, and weight loss. The small bowel mesentery is affected at its root in most cases, with a propensity for jejunal mesentery. Exceptionally, the inflammatory process may extend into the retroperitoneum and affect the pancreas, duodenum, and inferior vena cava. Forty percent of patients had prior abdominal surgery, and concurrent intra-abdominal pathology was noted in 18%. These included ovarian tumors, nonHodgkins lymphoma, colon, renal cell, and gastric carcinoma. SM can co-exist with fibrosclerotic disorders in other organs, including retroperitoneal fibrosis and Sjogren’s syndrome. Treatment is reserved for those patients who are symptomatic. Surgery is indicated if patients have symptoms of obstruction, but this has shown to only be 10% effective in ameliorating symptoms. Some series have shown improvement with tamoxifen and prednisone. Our case represents an unusual presentation, in that the duodenum was affected and produced almost complete bowel obstruction. Although the overall prognosis for SM is good, in 20% of cases, it is associated with significant morbidity and a chronic debilitating course.

1186 Rare Presentation of Mucinous Cystadenoma of the Appendix John Anong, MD, John Litchfield, MD, Mark Young, MD, Thomas Borthwick, MD. Internal Medicine, East Tennessee State University, Johnson City, TN. Introduction: Appendiceal mucinous cystadenoma is a rare slow-growing tumor of the appendix, also called a neoplastic mucocele. Incidence rates are lacking, but this entity represents only 0.2-0.3% of all appendectomies. It is usually symptomatic and can mimic acute appendicitis. It must be differentiated from mucinous cystadenocarcinoma, which carries a poor prognosis. Complications include cyst rupture leading to “pseudomyxoma peritonei.” As such, timely and careful surgical resection is essential. We present a rare case of rapidly progressing appendiceal mucinous cystadenoma in an asymptomatic elderly male associated with multiple pancreatic cysts. Case Report: An 86-year-old male with history of celiac sprue, prostate cancer status radiation complicated by radiation proctitis, and stable pancreatic cysts was referred to our facility after he was found to have an enlarged and thickened appendix on CT concerning for an appendicocele or possible malignancy. Multiple stable cystic lesions of the pancreas were noted, but the appendiceal mass was not seen on recent previous imaging, suggesting it was rapidly progressing. He did not have any symptoms or recent history of nausea, vomiting, altered appetite, abdominal discomfort, diarrhea, or melena. He was treated with flexible sigmoidoscopy and argon plasma coagulation for radiation proctitis 2 months prior. Physical examination revealed a non-toxic appearing elderly male without any abdominal discomfort or palpable masses. Routine laboratory examination on admission showed no abnormalities except for elevated glucose and hemoglobin of 11.4. The patient underwent uncomplicated laparoscopic appendectomy, and there was no evidence of spillage/rupture or peritoneal implants. Pathological examination of the mass showed mucinous distention of the appendiceal specimen with low-grade dysplastic changes consistent with mucinous cystadeoma. The postoperative course was complicated by transient hypoxia; however, the patient had an uneventful recovery and has had no evidence of disease recurrence. Conclusion: This represents an unusual presentation of appendiceal mucinous cystadenoma, as our patient had multiple cystic pancreatic lesions, showed no symptoms, and his diseased evolved quickly. Indeed, simultaneous occurrence of these 2 tumors has only been reported once. Any patient with thickened/enlarged appendix should prompt consideration for appendectomy. If not addressed promptly, these neoplasms can progress to cystadenocarcinoma or have other serious complications.

1187 Small Bowel Obstruction: A Novel Complication of Superior Mesenteric Vein Thrombosis Pratap Singh, MD, Ankur Varma, MD, MPH, Modushudan Bhattacharjee, MD. Internal Medicine, University of Texas Health Science Center at Houston, Houston, TX. Introduction: Superior mesenteric vein thrombosis (SMVT) is rare condition, and it accounts for 1 in 5,000 inpatient admissions for abdominal pain. It is usually an incidental finding or a diagnosis found during work-up of abdominal pain. Intestinal infarction is one of its well-recognized complications. Here, we report an unusual case of small bowel obstruction (SBO) secondary to SMVT. A 71-year-old woman with a history of colon cancer (had chemotherapy and transverse hemicolectomy 5 years ago) presented with complains of persistent vomiting for the past 2 days and abdominal pain for 1 day. Her vital signs were temperature 98° F, pulse 90 beats/minute, blood pressure 120/70 mm Hg. Physical examination was remarkable for distended abdomen with no rigidity or guarding. Laboratory work showed metabolic acidosis with lactic acid 5.77 mg/dL, hemoconcentration (hematocrit 46%). CT

[1187A]


Figure 1. SMVT (arrow).


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Abstracts abdomen with contrast showed SBO due to an ill-defined mass at the ileo-transverse colonic anastomosis, which was contiguous with the mural thickening. It also showed bowel wall edema, SMVT (Figure 1) and superior mesenteric artery (SMA) narrowing. Surgical intervention was planned, but was not done, as the patient preferred conservative management. She responded well to hydration and nasogastric suction with resolution of lactic acidosis. She tolerated regular diet before discharge. During her third admission within a month with similar presentation, CT scan abdomen was repeated, which showed interval resolution of ileo-transverse colonic mass as seen on previous imaging, unchanged bowel edema, SMVT, and narrowing of SMA. Small bowel follow-through confirmed absence of luminal obstruction along with non-uniform caliber of the small bowel consistent with SMVT. She was diagnosed as a case of SMVT presenting as SBO. She was managed with therapeutic anticoagulation and a clear liquid diet, which was later transitioned to regular diet. To the best of our knowledge, this is the first case of SMVT presenting as SBO. A high index of suspicion is required to diagnose SMVT as a cause of SBO since early initiation of therapeutic anticoagulation forms the essential component of management.

and pelvis was remarkable for a 13-cm tubular mass-like structure anterior to the aorta at the level of the fourth portion of the duodenum, extending inferiorly to the level of the jejunum. A push enteroscopy was performed and demonstrated a 6 x 6-cm mass around the ligament of Treitz. Biopsies of the mass revealed leiomyosarcoma, epithelioid variant, cytomorphologically similar to the previously resected uterine mass, desmin +, caldesmon +, actin weakly +, CD34-, S100-, CD117-. The patient was subsequently taken to the OR for laparotomy and resection of the tumor to prevent recurrent duodenal intussesception. Discussion: In adults, intussesception is usually caused by a pathologic lead point in 90% percent of the cases. Our patient’s intussesception presented secondary to a duodenal metastatic mass. Small bowel metastases are uncommon and account for 10% of all small bowel tumors. Metastatic leiomyosarcomas very rarely occur in the GI tract. When leiomyosarcomas do metastasize to the GI tract, they occur predominantly in the stomach and are exceedingly rare in the small bowel.

1189 1188

Whipple’s Disease: A Rheumatoid Masquerader

Duodenal Intussusception Secondary to Metastasis From Uterine Leimyosarcoma Tina Seecharan, MD, Javed Sadiq, MD, Dimitrios Georgostathis, MD, Veronika Dubrovskaya, MD, FACG. SUNY Downstate Medical Center, Brooklyn, NY. Introduction: This is a rare case of adult duodenal intussesception secondary to metastatic uterine leiomyosarcoma. Case Report: A 65-year-old female with distant history of leiomyosarcoma of the uterus s/p TAH/SBO presented with intermittent periumbilical pain and 10-15-pound weight loss. The CT of the abdomen

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Fnu Sanna, MD, Simranjit Singh, MD, Davendra Ramkumar, MD, FACG. University of Illinois at Urbana-Champaign, Urbana, IL. Introduction: Whipple’s disease (WD) is a rare systemic infectious disease with an incidence of approximately 30 cases per year worldwide. The disease is difficult to diagnose, and a high index of suspicion is often required. We present a case of WD that highlights the fact that unexplained rheumatologic symptoms, even in the absence of gastrointestinal symptoms, can predate other manifestations by years. Case Report: A 38-year-old white male presented for evaluation of burning epigastric pain and fatigue. He also had mild intermittent diarrhea for several weeks without any melena. He had a 4year history of generalized joint pains, for which he was receiving nonsteroidal anti-inflammatory drugs (NSAIDS). Labs were notable for a microcytic anemia (hemoglobin of 10.9 G/dL) with iron studies suggestive of deficiency. Colonoscopy was unremarkable. Upper endoscopy showed dilated lacteals in the duodenum. Histology from duodenal biopsies revealed widened villi packed with foamy macrophages containing granular periodic acid-schiff-positive inclusions corresponding to bacterial structures consistent with the diagnosis of WD. CNS and cardiac involvement were ruled out and he was treated with ceftriaxone for 2 weeks, followed by trimethoprim-sulfamethoxazole (TMP-SMX); because of an adverse reaction, TMP-SMX was switched to doxycycline, and he is completing a year of therapy. His gastrointestinal symptoms resolved within 1-2 weeks, and he had dramatic improvement of his rheumatologic symptoms, including polyarthritis 4-6 weeks after initiation of therapy. Discussion: Whipple disease is a systemic infection caused by Tropheryma whippelii. The most common manifestations are diarrhea, weight loss, abdominal pain, and arthralgia. However, marked variability in presentation can delay the diagnosis by years. Low-grade fever, migratory arthralgia, neurological involvement (cognitive changes, supranuclear gaze palsy, altered level of consciousness), cardiovascular (endocarditis) are a few of the many different presenting features. Polyarticular inflammatory arthropathy preceding the diagnosis of Whipple’s disease is seen in more than 65% of patients and is commonly misdiagnosed as an inflammatory rheumatoid disease, as seen in this case. The dilated lacteals were likely as a result of occlusion of the lymphatics by macrophages within the duodenal mucosa and submucosa. This case also highlights that prompt diagnosis and antibiotic therapy can result in dramatic clinical response in this rare but potentially lethal disease. For clinicians, unexplained arthritis, diarrhea, weight loss, and low-grade fever in middle-aged male, should raise suspicion for possible WD.

Figure 1. Tubular mass detected on CT.

1190 Use of the New NaviAid Enteroscopy System for Treatment of Bleeding Terminal Ileal Hamartoma Harshit Khara, MD, Mustafa Huseini, MD, Kimberly Fairley, MS, MD, Kimberly Chaput, MD, Chuan Long Miao, MD, David Diehl, MD, Amit Johal, MD. Department of Gastroenterology & Nutrition, Geisinger Medical Center, Danville, PA. Introduction: Recent balloon-assisted enteroscopy modalities have been successful in diagnostic and therapeutic interventions in the small bowel, in both anterograde and retrograde manner. However, they each have their unique platforms and cannot be used between different scope systems. The NaviAid enteroscopy is a new system which utilizes a through-the-scope balloon catheter as an anchor for advancement into the small bowel, and can be used through the biopsy channel of various scope systems. Case Report: We report a unique case of a 36-year-old female who presented with melena and symptomatic anemia, requiring blood transfusions. She underwent a non-diagnostic upper endoscopy; however, on colonoscopy exam, she had altered blood in the ileo-cecal valve. Terminal ileal intubation showed a bleeding distant polypoid lesion that could not be reached with the colonoscope. Biopsies showed a hamartamatous lesion. Video capsule endoscopy did not show any other lesions in the entire small bowel. A NaviAid-assisted retrograde enteroscopy was successful in reaching the lesion in the terminal ileum, which was successfully resected endoscopically. The path report showed an isolated hamartomatous polyp with negative margins and no signs of malignancy. She recovered uneventfully without any recurrence of bleeding or anemia. Discussion: The NaviAid balloon-assisted enteroscopy is a safe and effective single-operator system for performing deep enteroscopy using a conventional colonoscope. It eliminates the need of an overtube or special scope platforms. Recent studies have shown an overall diagnostic yield of 45%, with average depth of insertion of 89 cm when used in a retrograde manner. Our case demonstrates its successful clinical utility in complete endoscopic resection of bleeding distant small bowel lesion.

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Figure 2. Endoscopic view of metastatic leiomyosarcoma.



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CLINICAL VIGNETTES/CASE REPORTS - LIVER

1193 Shunt Myelopathy in a Non-cirrhotic Patient Nongnooch Poowanawittayakom, MD,1 Bhaumik Brahmbhatt, MD,2 Surakit Pungpapong, MD2. 1. Internal Medicine, Advocate Illinois Masonic Medical Center, Chicago, IL; 2. Mayo Clinic, Jacksonville, FL.

1191 Pegylated Interferon-Induced Cardiomyopathy: A Rare Presentation in A Patient Treated for Hepatitis C April Elam, MD, MS, Erica Isom, MD, Punita Kaveti, MD, Kelly Schrapp, MD, Marvin Crawford, MD. Morehouse School of Medicine, Atlanta, GA. Introduction: Since the release of the new U.S. Preventative Services Task Force guidelines recommending HCV screening in high-risk persons and patients born from 1945-1965, an increasing number of people are being diagnosed with Hepatitis C. Subsequent treatment usually includes triple therapy inclusive of pegylated interferon. We report a case of a patient on triple therapy for HCV presenting with new onset CHF. Interferon related cardiotoxicity is rare, and has only been reported 4 times in past literature. Case Report: A 53-year-old male with cirrhosis secondary to chronic HCV presented with worsening SOB for 2 weeks. He endorsed early satiety, decreased exercise tolerance, PND, orthopnea, and bilateral lower extremity swelling. He had previously been a null responder to dual therapy with ribavirin and telaprevir, and initiated on pegylated interferon for 11 of 48 weeks. He had no significant cardiac history, but had a 23-year remote history of polysubstance abuse and family history of CHF and CAD. Clinical signs of CHF were present, CXR showed cardiomegaly with pulmonary edema and new bilateral pleural effusion; BNP was 1501. Echo showed nonspecific cardiomyopathy with moderately dilated ventricles and atria, severe left ventricle (LV) global hypokineses and EF 10-15%. Due to the acuity of functional decline and negative work-up for an alternative etiology, new onset cardiomyopathy secondary to interferon therapy was diagnosed. Discussion: Hepatitis C is one of the most common curable viral infections worldwide. Cure rate has increased from 6-90% over the last 25 years, with pegylated interferon being responsible for the success in 70-80% of cases. Cardiac toxicity is rare and presents as arrhythmia, myocarditis, HTN, ischemic heart disease, pericarditis, pericardial effusion, and rarely, cardiomyopathy. LV function improvement is reported within 1-2 months following cessation of interferon; however, prognosis is poor. Emanuele, Durante-Mangonia, et al report that pegylated interferon may be safely offered to patients with coexisting, clinically significant heart disease. However, clinicians must be aware of potential cardiac toxicity and implement monitoring to detect symptoms early, aborting pegylated interferon therapy prior to irreversible damage. Conclusion: Pegylated interferon is a beneficial medication in the treatment of hepatitis C. Due to the increasing number of patients receiving therapy, we propose obtaining a baseline echo to assess LV function, particularly in high cardiac risk patients, prior to initiation of this therapy. Considering the poor prognosis of pegylated interferon-induced cardiomyopathy, physician awareness and close cardiac monitoring is imperative.

1192 A Case of Drug-Induced Cholangitis and Cholestasis From Amoxicillin/Clavulanic Acid and Levofloxacin Rafael Rojano-Marin, MD,1 Amir Rezk, MD,1 Chuan Miao, MD, MPH, MS,2 Nina Ahuja, MD2. 1. General Internal Medicine, Geisinger Medical Center, Danville, PA; 2. Gastroenterology, Geisinger Medical Center, Danville, PA. Introduction: Drug-induced liver injury (DILI) continues to be an important disease in clinical practice. Amoxicillin/clavulanic acid and levofloxacin are commonly used with a good safety profile. We describe a case of drug-induced cholangitis and cholestasis from amoxicillin/clavulanic acid and levofloxacin. Case Report: An 89-year-old male presented with a 1-day history of jaundice, dark urine, and pale stools. He was treated with 2 10-day courses of amoxicillin/clavulanic acid for a urinary tract infection, followed by a 10-day course of levofloxacin for pneumonia 1 week before presentation. He does not drink alcohol and had no personal or family history of liver disease. Physical exam was significant for jaundice. Laboratory evaluation demonstrated a total bilirubin of 11.1 mg/dL, direct bilirubin of 9.1 mg/dL, alkaline phosphatase of 1001 U/L, gamma-glutamyl-transpeptidase of 793 U/L, alanine aminotransferase (ALT) of 343 U/L, aspartate aminotransferase (AST) of 427 U/L, INR of 1.03, and albumin of 3.3 g/dL. Magnetic resonance cholangiopancreatography (MRCP) was negative for extrahepatic and intrahepatic biliary dilation. A liver biopsy revealed inflammation infiltrating the bile ducts and hepatocanalicular cholestasis consistent with drug-induced cholangitis and cholestasis. His liver function tests started to improve gradually within days after stopping levofloxacin. Discussion: DILI continues to be an important disease in clinical practice. Its diagnosis is mainly based on the exclusion of alternative causes of liver damage. Amoxicillin/clavulanic acid is a combination of amoxicillin and the β-lactamase inhibitor clavulanic acid. The latter component seems to be the prime offender for the liver injury. Amoxicillin/clavulanic acid has been reported to cause drug-induced intrahepatic cholestasis due to a metabolic idiosyncrasy or a hypersensitivity mechanism. It has also been reported to cause ductopenia. Levofloxacin is a fluoroquinolone commonly used to treat respiratory infections. Fluoroquinolones have been associated with drug-induced liver injury, ranging from a brief rise in transaminase level or cholestatic jaundice to severe hepatotoxicity. Levofloxacin has been associated with acute hepatitis, fulminant hepatic failure, and death. The mechanism of levofloxacin-induced hepatotoxicity is not known. Treatment for DILI is mainly the cessation of the offending drug, which may lead to recovery in liver enzyme abnormalities. We believe that our patient suffered from amoxicillin/clavulanic acid and levofloxacin-induced cholestasis and cholangitis. Clinicians should be familiar with the potential hepatoxicities from amoxicillin/clavulanic acid and levofloxacin.


Introduction: Portosystemic myelopathy (PSM) is a rare complication in 2% of transjugular intrahepatic portosystemic shunt (TIPS) procedures. The shunt can also occur spontaneously in cirrhotic patients or can be surgically made. We report a patient with bilateral legs weakness 14 years after having surgical splenorenal shunt. A 44-year-old man with history of congenital non-cirrhotic portal hypertension leading to hepatoportal sclerosis presented with progressive spastic weakness in bilateral legs for 5 months. In 1989, he presented with recurrent esophageal variceal bleeding, which was successfully managed with surgical splenorenal shunt with its revision in 1992. He denied any history of hepatic encephalopathy, ascites, or gastrointestinal (GI) bleeding after the shunt was placed. Five months ago, he had insidious onset of spastic weakness in bilateral legs, right side more than left side. No numbness or weakness in face or upper extremities. Physical exam revealed mild muscle weakness with spasticity and ankle clonus in both legs, leading to spastic gait and hyperreflexia in lower extremities. Babinski sign was positive at the right foot only. Romberg test and sensory exam were negative. Abnormal laboratory includes AST 76 U/dl, ALT 89 U/dl, Alk phosphatase 211 U/dl, GGT 316 U/dl. The patient underwent an extensive work-up including CT brain with contrast, CT myelogram of cervical, thoracic, and lumbar spine, lumbar puncture (LP), electromyelogram (EMG) study, and arteriogram, which were all unremarkable. With baclofen, he had no improvement in his spastic gait. Given the concern of portosystemic shunt myelopathy, an exception to his MELD score was given and he got liver transplant (2 years after his onset of myelopathy) with clinical improvement in myelopathy. PSM is a rare complication after shunt creation. The pathogenesis of PSM is still unclear. The decrease of ammonia clearance and reduced blood flow to spinal cord are the current hypothesis. The duration of PSM after the shunt creation varies between 6 months to 10 years. Most of the cases had hepatic encephalopathy before developing myelopathy. In our case, he had no history of hepatic encephalopathy and developed the myelopathy 14 years after the shunt placement, which was interesting and unreported. The occlusion of splenorenal shunt either surgically or with embolization can be considered for treatment. However, it is associated with higher mortality and morbidity. Liver transplant in cirrhotic patients with PSM reported good result and outcome. Portosystemic myelopathy is an uncommon complication after shunt creation. We report PSM case after a surgical splenorenal shunt creation, which improved after liver transplant.

1194 A Rare Case of Eosinophilic Myalgia Syndrome Edward Villa, MD, Eric Kallwitz, MD, Sherri Yong, MD. Loyola University of Chicago, Maywood, IL. Introduction: A 57-year-old female with a history of hypertension, hyperlipidemia, and osteoarthritis presented to a community hospital with altered mental status, severe bilateral upper and lower extremity myalgias, and arthralgias in her metacarpophalangeal joints bilaterally. Her only medications were hydrochlorothiazide and melatonin. She had no constitutional symptoms, rashes, nausea, vomiting, or diarrhea. At presentation, she was found to have WBC count of 14.5 with 43% eosinophils, ALT 1141, AST 630, total bilirubin 2.9 (predominantly direct bilirubin), and alkaline phosphatase 337. Abdominal ultrasound revealed mild gallbladder wall thickening with gallstones present, but no intra-/extra-hepatic ductal dilatation and normal common bile duct diameter; CT abdomen/pelvis was unremarkable. There was a weakly positive antismooth muscle antibody at titer of 1:40 as well as mildly elevated IgG of 1950 with negative ANA. Liver biopsy showed extensive eosinophilic infiltration, rare plasma cells, severe acute hepatitis with syncytial multi-nucleated giant cells, and focal centrilobular injury and piecemeal necrosis, which was not entirely consistent with autoimmune hepatitis. Bone marrow biopsy showed extensive eosinophilia not consistent with any hematologic malignancy, and flow cytometry was unrevealing. Further hematologic, neurologic, infectious, and rheumatologic studies were negative. She was diagnosed with eosinophilic myalgia syndrome. She was subsequently treated with oral steroids and discontinuation of melatonin, and her liver tests continued to improve, as did her confusion, myalgias, and arthralgias.

1195 Fitz-Hugh Curtis: A Rare Cause of Ascites Susanne Shokoohi, MD, Adam Zivony, MD, Gene Bakis, MD, Alice Fung, MD, Kian Keyashian, MD, Joseph Ahn, MD, MS, FACG. Oregon Health and Science University, Portland, OR. Clinical Presentation: A 16-year-old, previously healthy female presented to an outside hospital with right upper quadrant (RUQ) pain and hypotension requiring dopamine and norepinephrine. Exam was significant for RUQ tenderness without stigmata of chronic liver disease. Significant labs were: WBC 11 with 56% bands, lactate 8.6, creatinine of 1.7, AST 151, ALT 225, alk phos 113, t.bili 3.5. Subsequent tests were negative for hepatitis A, B, C, ANA, and ASMA. She was treated empirically with vancomycin, zosyn, and doxycycline, and was transferred to our ICU. Abdominal ultrasound was notable for moderate ascites and diffusely thickened edematous gallbladder wall with thickening measuring up to 1.5 cm without cholelithasisis, concerning for acute acalculous cholecystits. MRCP demonstrated gallbladder wall thickening without biliary dilation and moderate free peritoneal fluid. Gynecological examination revealed purulent cervical discharge and cervical motion tenderness. Gonorrhea and chlamydia PCR was negative. Sepsis was attributed to culture negative pelvic inflammatory disease (PID) with peri-hepatitis and gallbladder abnormalities due to Fitz-Hugh Curtis syndrome. Her liver enzymes normalized and abdominal pain improved over 5 days. She was discharged on a 14-day course of oral metronidazole and doxycycline, and on follow-up 3 weeks later, she had no complaints and had normal liver enzymes. Discussion: Fitz-Hugh-Curtis(FHC) is a syndrome of perihepatic inflammation that can occur in up to 14% of PID cases. It typically affects young, sexually active women who present with acute RUQ


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Abstracts pain. Causative organisms are typically Chlamydia trachomatis or Neisseria gonorrhea, although in up to 25% of cases, etiology is unknown. Ultrasound is the usual initial test to evaluate the gallbladder and liver for other common cause of RUQ pain. Typically, hepatic capsular enhancement in the arterial phase on CT is helpful in making the diagnosis and avoiding laparoscopic evaluation. Broad spectrum antimicrobial treatment with anaerobic coverage is recommended if FHC is suspected. Most patients recover completely after appropriate treatment. FHC should be considered when a young woman presents with RUQ pain and pelvic examination is obligatory in this setting. Ascites is an extremely rare finding in patients with FHC, and other causes of ascites should be excluded prior to attributing it to FHC.

1196 An Uncommon Cause of Upper Gastrointestinal Bleeding in a Post-liver Transplant Patient: Hepatic Arteriojejunal Fistula Emilie Regner, MD, Stuart Amateau, MD, PhD, Lisa Forman, MD. Internal Medicine, University of Colorado, Denver CO, CO. Introduction: We present an unusual case of massive GI bleeding in a 55-year-old man with a history of ulcerative colitis requiring total proctocolectomy with end ileostomy and primary sclerosing cholangitis requiring liver transplant with roux-en-Y hepaticojejunostomy. The patient presented with complaints of vomiting, abdominal pain, and black stools, and physical exam was notable for a non-distended, nontender abdomen and an ostomy bag containing melena. Vitals were notable for mild tachycardia and labs for anemia (Hct 32), leukocytosis (WBC 12), and mild coagulopathy (INR 1.4). IV esomeprazole and fluid boluses were administered; however, shortly after admission, the patient became severely hypotensive, tachycardic, and syncoped. His ostomy bag rapidly filled with bright red blood. He was transferred to the ICU, where he developed hematemesis and a tense abdomen. Massive transfusion protocol and vasopressors were started. Bedside EGD was notable for bright red blood in the upper GI tract, but no source of active bleeding. Invasive hepatic arteriography was notable for a ruptured pseudoaneurysm of the post-transplant proper hepatic artery which was coiled. Small bowel enteroscopy was performed, which revealed a full thickness defect with several visible IR coils deep to the defect in the roux limb of the hepaticojejunostomy. The defect was closed with endoclips for tissue approximation. Resuscitation efforts required 40 units FFP, 35 units PRBCs, and 6 units of platelets. Broad spectrum antibiotics and antifungals were administered as an infected hepatic artery pseudoaneurysm was the suspected cause for fistula formation. The patient developed ischemic hepatitis; however, liver ultrasound revealed patent vessels including patent hepatic artery, non-dilated biliary tree, and normal liver parenchyma. The patient was discharged to home in stable condition on hospital day 20. Hepatic artery pseudoaneurysm is a rare, life-threatening complication of liver transplant with an incidence of 1-2%, usually occurring in the setting of biliary leak or anastomotic infection. GI hemorrhage from hepatic arteriojejunal fistula is an even rarer complication of hepatic artery pseudoaneurysm. Mortality rate from pseudoaneurysm rupture is estimated at 70%. Standard approaches to treatment include endovascular hepatic artery stenting, coil embolization, and open surgery with arterial reconstruction. The practicing gastroenterologist should consider this diagnosis in addition to esophageal variceal bleed, gastric variceal bleed, gastric ulcer bleed, duodenal ulcer bleed, and anastomotic ulcer bleed in the differential diagnosis of upper GI bleeding in the late post-transplant period.

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coronary artery disease initially presented to an outside facility 23 days prior, with complaints of melena and angina. Upper endoscopy revealed a Mallory Weis tear. An abdominal MRI was performed, demonstrating cirrhotic changes, prompting a liver biopsy. Amyloid deposition was seen within the hepatocytes, space of Disse, sinusoids, and vessels. Mass spectrometry revealed AL kappa-type amyloidosis. He was transferred to our facility for further care, and he had no new complaints on presentation. Physical exam was notable for scleral icterus, lower extremity edema, and ascites. Hepatic function panel was significant for a total bilirubin of 13.4mg/dL, a direct bilirubin 8.3mg/dL, albumin 2.3g/dL, AST 70U/L, ALT 33U/L, and alkaline phosphatase 338U/L. His presenting model for end-stage liver disease score was 21. Colonoscopy was significant for severely erythematous inflamed mucosa in the ascending colon, which was not amenable to treatment by endoscopy. He was transferred to the hematology service and was diagnosed with a plasma cell myeloma following bone marrow biopsy. He was started on cyclophosphamide, bortezomib, and dexamethasone, but on day 9 of treatment, he died following a massive GI bleed and acute liver failure. Amyloidosis presenting with a lower gastrointestinal bleed is more common with localized disease rather than systemic disease. Although liver manifestations are common, affecting nearly 70% of patients, findings are usually limited to increased alkaline phosphatase. The median survival of patients with jaundice and hyperbilirubinemia in amyloidosis is approximately 1 month. Evaluation of patients presenting with massive lower GI hemorrhage must be approached with a high suspicion for uncommon presentations of rare conditions in order to expeditiously treat potentially fatal underlying illnesses.

1198 Hepatic Cysts With an Unusual Twist: Smooth Muscle Tumor by Epstein-Barr Virus Sricharitha Krishnamoorthy, MD, Arup Maitra, MD, Jennifer Bolyard, MD, Zuoliang Xiao, MD. Canton Medical Education Foundation,An Affiliate of Northeast Ohio Medical University, Canton, OH. Introduction: Transplantation of solid organs is becoming increasingly common due to the widening of the pool of acceptable candidates and advancements in post-transplant care. Despite advances in immunosuppressive regimens, increased risk of post-transplant Epstein-Barr virus (EBV)-associated diseases remains significant. We present an unusual case of hepatic cysts with EBV-associated smooth muscle tumor in a renal transplant recipient. A 63-year-old male presented with a high fever. He was 8 years post-renal-transplant, maintained successfully on immunosuppressive therapy. During the course of his work-up, imaging showed incidental findings of multiple liver cysts in CT scan of the chest. MRI liver confirmed diffuse rim-enhancing cystic lesions (Image 1). Tumor markers and initial liver biopsy were insignificant. Repeat liver biopsy showed spindle cells with eosinophilic cytoplasm and EBV encoded RNA, suggestive of EBV-associated smooth muscle tumor. Mycophenolate was discontinued and the hepatic cysts resolved. EBV has been associated classically (10%) with nasopharyngeal carcinoma, lymphomas, and post-transplant lymphoproliferative disease (PTLD), but proliferation of mesenchymal/ stromal cells giving rise to post-transplant smooth muscle tumor(PTSMT) is very rare (0.7%). PTSMT is a slowly progressive tumor with late onset (median 48 months) after transplant. PTSMT differs from leiomyosarcoma by absence of atypia or tissue necrosis, and characteristically has less mitotic activity. Gene expression analysis showed the mammalian target of rapamycin (mTOR/Akt) pathway with the overexpression of transcription factor Myc. No association with a particular immunosuppressant has been reported. The clinical presentation of PTSMT is nonspecific and depends on the location of the mass. The prognosis varies based on the number of organs involved and the presence of intracranial tumors. Hence, early diagnosis is necessary for best prognosis, especially when it can prevent intracranial involvement. Surgical removal or dose reduction or discontinuation of immunosuppressant is associated with best clinical outcomes.

Massive Lower Gastrointestinal Bleed With AL Amyloidosis Salvatore Savona, MD, Allison Rossetti, MD, Christina Arnold, MD, A. James Hanje, MD. Ohio State Wexner Medical Center, Columbus, OH. Introduction: AL amyloidosis is a rare disease of abnormal beta-pleated sheet protein deposition, often related to an underlying hematologic disorder. When affecting the gastrointestinal (GI) tract, symptoms include macroglossia, melena, dysmotility, and early satiety. In systemic AL amyloidosis, the small intestine is most commonly affected, followed by the stomach and colon. A 58-year-old male with history of

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Figure 1. MRI Liver showing multiple hepatic cysts.


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1199 A Rare Case Report of Spontaneous Resolution of Hepatic Portal Venous Gas Associated With Cocaine-Induced Intestinal Ischemia Hiren Patel, MD,1 Nihar Shah, MD,2 Hamid Shaaban, MD,2 Walid Baddoura, MD2. 1. St. Joseph’s Regional Medical Center, Paterson, NJ; 2. Seton Hall University School of Health and Medical Sciences, South Orange, NJ. Introduction: Air in the portal vein and liver was first described as hepatic portal venous gas (HPVG) in 1978 by Libman et al. It is a worrisome radiological sign that indicates an underlying serious gastrointestinal problem like bowel ischemia and inflammation of the gastrointestinal tract in the majority of patients, and they usually require surgical intervention to treat this potentially life-threatening condition. Our case report describes the unusual presentation of portal vein air, which resolved within a few hours. Case Report: A 51-year-old African American male with a past medical history of hypertension and cardiomyopathy (ejection fraction 15%) was brought to the emergency room with complaints of severe, stabbing abdominal pain located in the epigastric area, radiating to the right upper quadrant. The pain was precipitated after intravenous cocaine injection. The pain was associated with nausea, non-bloody vomiting, and diarrhea with non-bloody, liquid stools. A pertinent positive finding on physical exam was moderate abdominal tenderness in the epigastric area and right upper quadrant on deep palpation. On initial vitals, blood pressure was 188/95 and heart rate was 104. No significant changes in baseline laboratory studies were noted except a urine drug screen positive for cocaine. CT scan of the abdomen showed extensive portal venous gas and mesenteric venous gas throughout the abdomen. The patient was given a nitroglycerin patch for the elevated blood pressure. Empiric intravenous antibiotics and analgesics were administered. Before the patient was taken to the operating room for the diagnostic laparoscopy to find out the cause of portal vein air, CT scan of the abdomen was repeated and it was done 5 hours after the first CT abdomen, which revealed nearly complete resolution of the portal and mesenteric venous gas. Septic work-up including blood culture, urine culture, stool for C. difficile, HIV, and hepatitis A, B, and C was negative. HIDA scan was also negative for acute cholecystitis. After 4 days in the hospital, the patient’s clinical condition improved and he was subsequently discharged home. Conclusion: This is the first case report describing cocaine-induced mesenteric ischemia that resulted in HPVG, which spontaneously resolved within 5 hours. In our patient, the possible reason for the gas in the portal vein was impaired colonic mucosal barrier caused by transient mesenteric ischemia induced by cocaine-mediated vasoconstriction.

1200 Acute Massive Hepatic Enlargement in Sickle Cell Disease Minhaj Musa, MD, Kyaw Thein, MD, Bisrat Haile, MD, Rajat Mukherji, MD,FCCP, Harish Patel, MD,FCCP. Kingsbrook Jewish Medical Center, Brooklyn, NY. Introduction: Enlargement of the liver is a common condition in clinical practice and has multiple etiologies. Acute massive increase in liver size within a matter of 48 hrs is an unusual event. We report a case of a 25-year-old female patient with sickle cell disease who presented with right upper quadrant abdominal pain, fever, and leukocytosis of 36,000 mm3. A urine analysis suggested UTI and she was treated with antibiotics along with intravenous fluids. On the 2nd hospital day, the hemoglobin dropped to 6.8g/dl from 8.2g/dl on admission. The leukocytosis increased to 45,900 mm3 and the total bilirubin from a baseline of 9.0 mg/dl on admission, rose to 12.7 mg/dl two days later. A CT scan of the abdomen on admission showed a liver of normal size with mild intrahepatic biliary ductal dilatation. Two days later, with persistent right upper quadrant discomfort, worsening leukocytosis, and the rapid drop in hemoglobin, the patient underwent a repeat CT scan followed by MRI of the abdomen. In 2 days, the liver size had drastically increased from 17.5 cm to 20.5 cm in vertical length along the mid clavicular line. An infiltrative or cobble stone type pattern had appeared in the liver parenchyma. There was no intrahepatic or common duct dilatation. The hepatic and portal veins were patent. On subsequent vascular duplex study of the inferior vena cava (IVC), the hepatic and portal veins showed no evidence of thrombosis. Because of the patient’s deteriorating status, exchange transfusion was performed, following which, the liver function tests improved and liver size clinically diminished. This intriguing case illustrates the rare syndrome of hepatic sequestration in sickle cell disease. Our patient had an acute increase in liver size, which was not due to hepatic or portal vein thrombosis; nor was it due to cholestasis. Sickle cell disease may result in sequestration of red blood cells in the spleen or lungs. On occasion, the liver is the site of RBC sequestration. In addition to pain and a falling hematocrit, liver size increases rapidly. This sequence of events in the liver may be missed unless liver size is regularly measured. When hepatic sequestration occurs, prognosis is grave and exchange transfusion should be considered as a potentially life saving strategy. Our patient with sickle cell disease had a dramatic picture of an acutely enlarging liver, which with appropriate treatment rapidly returned to normal size.

1201 A Unique Case of Cirrhosis Due to Alagille Syndrome Edward Villa, MD, Natasha Von Roenn, MD. Internal Medicine, Loyola University of Chicago, Chicago, IL. Introduction: A 21-year-old undocumented Mexican male with no existing medical conditions presented with flank pain concerning for kidney stones. Of note, he also endorsed worsening jaundice and lower extremity swelling. He immigrated to this country from Mexico at age 3. Throughout his entire life, he has suffered from pruritus and has had knowledge of hepatomegaly. Presenting vitals


were unremarkable. On exam, he was small in stature, measuring 5 ft 5 in tall with weight of 125 pounds; he had deep set eyes, broad forehead with pointed chin (triangle facies), and scleral icterus; he had persistent S2 splitting on cardiac exam with a loud P2 as well as a systolic murmur loudest at left lower sternal border and increasing with inspiration; he had hepatosplenomegaly with distended abdomen positive for shifting dullness to percussion with fluid wave concerning for ascites. Ophthalmologic exam demonstrated a ring-like opacity at Schwalbe’s ring with thickening and anterior displacement of Schwalbe’s ring, consistent with posterior embryotoxon. Laboratory studies were remarkable for elevated transaminases (ALT of 146 and AST of 143), alkaline phosphatase of 397, and bilirubin of 5.1, which was suggestive of a cholestatic process. Serum albumin was 4.57 and total serum protein was 6.9. Viral hepatitis serologies were negative for hepatitis A, hepatitis B, and hepatitis C. Serum protein electrophoresis unremarkable. Liver biopsy demonstrated bile ductopenia as well as canalicular cholestasis without significant lobulation or steatosis; also present were grade1 periportal hepatitis with stage I periportal fibrosis. Esophagogastroduodenoscopy demonstrated grade III-IV non-bleeding esophageal varices that were banded, as well diffuse portal hypertensive gastropathy. Thoracic spinal x-ray revealed no spinal deformities or acute spinal processes. Echocardiogram demonstrated normal LV ejection fraction without diastolic dysfunction, as well as mild tricuspid regurgitation with estimated pulmonary artery systolic pressure of 29.2 mmHg; there was no evidence for septal defects.

1202 Idiopathic Non-cirrhotic Portal Hypertension: A Case Report in a White Female Cortni Tyson, MD. Internal Medicine, Howard University Hospital, Washington, DC. Case Report: A 63-year-old white female was seen in clinic for ascites. She had a recent paracentesis for fluid management and esophageal varices were noted on upper endoscopy 1 year prior. Her past medical history was significant for lupus, coronary artery disease, and upper GI bleed after banding of esophageal varices. Serologic evaluations were negative for chronic liver disease, including viral, auto-immune, or genetic etiologies. Liver biopsy was consistent with nodular regenerative hyperplasia, but negative for cirrhosis. On examination, her vital signs, physical exam, and review of systems were unremarkable. She had no further episodes of upper GI bleeding. Discussion: Idiopathic non-cirrhotic portal hypertension is a poorly understood disease, and many patients are initially incorrectly labeled as having liver cirrhosis. This entity has been reported in varying degrees in men in India and Japan, with few cases reported in Western populations. The most common reported cause of non-cirrhotic portal hypertension is schistosomiasis. An idiopathic diagnosis excludes chronic liver diseases, including parasitic infections and toxic exposures. In Western populations, a correlation has been seen between women and auto-immune disorders, such as lupus, sjogrens, and rheumatoid arthritis. Histologic findings include nodular regenerative hyperplasia, incomplete septal cirrhosis, and hepato-portal sclerosis. Clinical manifestations are similar to patients with cirrhosis, such as ascites and esophageal variceal bleeding. The prognosis of these patients is considerably better than those with underlying liver disease, and disease progression to cirrhosis and hepatocellular carcinoma is minimal to none. When variceal bleeding and ascites are controlled, life expectancy is near normal.

1203 A Rare Case of Peliosis Hepatis in a Young Female with End-Stage Renal Disease on Chronic Hemodialysis Vivek Reddy Garlapati, MD, Annu Gupta, MD, Hilary Hertan, MD. Gastroenterology & Hepatology, Montefiore Medical Center-Wakefield Campus, Bronx, NY. Case Report: A 22-year-old female with comorbidities of hypertension, ESRD on hemodialysis (since 2008) was referred for evaluation of abnormal liver chemistry. Mostly, her alkaline phosphatase was elevated (highest value was 339) with transient mild elevation in transaminases (highest AST and ALT were 38 and 52, respectively). Her bilirubin and liver synthetic function (PT/ INR, albumin) were normal. GGT was elevated (202). The patient was not taking any hepatotoxic agents. She denied any alcohol use. Anti-mitochondrial antibody, anti-smooth muscle antibody, anti-nuclear antibody, anti-LKM 1 antibody, hepatitis panel, and HIV were negative. MRI abdomen and MRCP revealed decreased signal intensity in the liver and spleen, which is due to iron deposition from previous blood transfusions, normal size, and morphology of liver and spleen, no liver lesions, normal intrahepatic, and extrahepatic bile ducts. Since the preliminary workup was inconclusive, percutaneous liver biopsy was performed. Histopathology revealed peliosis hepatis. Discussion: Peliosis hepatitis is a rare, benign condition characterized by the presence of multiple blood filled cystic areas of variable size randomly distributed within the liver parenchyma. It is associated with various conditions: drugs and chemicals including steroids, immunosuppressive drugs used in patients after renal and cardiac transplantation, infections like Bartonella henselae in HIV patients, endocarditis, monoclonal gammopathies, and malignancies like Hodgkin’s lymphoma. To our knowledge, this is the first case of peliosis hepatis associated with chronic hemodialysis. The clinical presentation is variable depending on the size of the cavity. It ranges from being asymptomatic to hepatomegaly, portal hypertension with esophageal varices and ascites, liver failure or as hemoperitoneum with shock secondary to intraperitoneal rupture. The definitive diagnosis is by liver biopsy. Diagnosis of Peliosis hepatis requires a high degree of suspicion. Hepatic ultrasound may show hyperechoic areas. MRI may show multiple peripheral lesions: hypointense on T1 and hyperintense on T2 images with bright foci suggestive of hemorrhage. Angiography may show multiple areas of accumulation of contrast media, most prominent during the parenchymal and venous phases.There is no definitive treatment for Peliosis hepatis. Treatment includes discontinuation of the offending agent, antibiotics for Bartonella henselae (erythromycin or doxycycline for 4 months), transarterial embolization in cases of intrabdominal bleeding due to rupture, and, rarely, liver transplantation in patients with irreversible liver injury.


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Abstracts 1204 Treatment of Hepatic Epithelioid Hemangioendothelioma: Finding New Uses for Thalidomide Matthew Soape, MD, Rashmi Verma, MD, Drew Payne, MD, Mitchell Wachtel, MD, Everardo Cobos, MD, Fred Hardwicke, MD. Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, TX. Introduction: Hepatic epithelioid hemangioendothelioma (HEH) is an extremely rare diagnosis with chemotherapy options not well-defined. Given its vascular nature, thalidomide has been used with success. Thalidomide-associated birth defects are well documented. Further investigation found a thalidomide and angiogenesis connection that has led it to become a viable chemotherapy option. We present a 49-year-old Hispanic female first seen for chest pain with cardiac etiology ruled out. She also complained of associated nausea, fatigue, and 30-pound weight loss. A prior computed tomography (CT) of the abdomen showed masses in the liver. The largest mass was lobulated and measured 6.7 cm x 5.5 cm. A repeat CT abdomen found enlargement of the hepatic masses and development of pulmonary nodules. Labs revealed normal liver function, negative Hepatitis B and C, and elevated cancer markers. Pathology from a liver biopsy revealed hepatic epithelioid hemangioendothelioma (HEH). Oncology was consulted and surgical resection was deferred. After developing a rash from the oral multi-kinase inhibitor sorafenib, thalidomide was started with the patient tolerating oral therapy. First described in 1982, HEH is extremely rare, occurring in 1 to 2 people per 100,000. Eighty-seven percent and 37% of patients present with multifocal disease and extrahepatic involvement, respectively. HEH is a low-grade malignant tumor with presentation usually asymptomatic. Risk factors include oral contraceptives, vinyl chloride, and hepatitis B. Histology is characterized as a vascular proliferation with cells having prominent cytoplasmic vacuoles in a signet ring formation. Immunohistochemical stains are positive for endothelial markers CD31, CD34, and factor VIIIrelated antigen. With a 75% 5-year survival rate, resection is preferable. However, resection is only an option in 10% of the cases. Chemotherapy agents tried have been doxyrubicin, vincristine, 5-FU, and thalidomide. Newer chemotherapy alternatives are targeting the vascular endothelial growth factor (VEGF), since malignant angiogenesis relies on the overproduction of VEGF. First released in 1957, thalidomide was used as an anti-emetic during pregnancy. Sadly, thalidomide was linked to a birth defect called phecomelia, or malformation of limbs. Proposed teratogenic mechanisms are the inhibition of VEGF and cereblon inactivation, which has a negative regulatory effect on FGF8 and disrupts limb formation. Thalidomide has shown good patient tolerance and control of disease progression over a long period of time. In conclusion, both the diagnosis of HEH and the use of thalidomide as chemotherapy are extremely rare. Given the mechanism of action against angiogenesis, thalidomide does show some benefit.

1205 An Unusual Cause of Elevated LFTs: Progressive Familial Intrahepatic Cholestasis Syed Amer, MBBS, Andrew Walker, PSM, MS, PA-C, Cuong Nguyen, MD. Mayo Clinic, Phoenix, AZ. Introduction: A 40-year-old otherwise healthy male presented to the GI clinic for follow-up of abnormal LFTs detected on a routine evaluation. The AST was 57 U/L, ALT 88 U/L, and ALP 214 U/L. There was no history of alcohol consumption or blood transfusion. Testing for hepatitis A, B, C, Wilson’s disease, autoimmune hepatitis, hemochromatosis, and alpha-1 antitrypsin deficiency was negative. Ultrasound and CT of the abdomen were unremarkable. MRCP with MR elastography revealed normal liver contour, with mild dilatation of a portion of the right intrahepatic biliary ducts and a mean liver stiffness value of 3.25 kPa. A liver biopsy showed evidence of disrupted hepatic architecture with micronodular cirrhosis. The histology findings were thought to be due to focal liver injury, possibly in or near the location of his prior cholecystectomy. One year later, his AST was 110 U/L, ALT 130 U/L, ALP 374 U/L, and total bilirubin 1.1 mg/dL. The mean stiffness on MR was 5.62 kPa. At that time, the patient revealed that his brother had just been diagnosed with esophageal varices. Given the abrupt change in liver stiff ness over 12 months and a family history of esophageal varices, congenital hepatic fibrosis was suspected. Both the patient and his brother then tested positive for a novel heterozygous mutation: c.3531_3533delACG variant that causes in-frame deletion of Glycine at position 1178 of the ABCB4 protein. Thus, the diagnosis of progressive familial intrahepatic cholestasis (PFIC) type 3 was confirmed. The patient was started on ursodeoxycholic acid (UDCA) and his subsequent LFTs gradually normalized. PFIC type 3 is an autosomal recessive disease caused by mutations in ABCB4 gene, which encodes the multidrug resistance - 3 (MDR3) gene, an ATP-binding cassette transporter. It acts as a phospholipid trans-locator involved in biliary phospholipid excretion. ABCB4 defects cause impaired excretion of phosphatidylcholine, an important component in formation of mixed micelles that protect the cell membrane of biliary epithelium from the detergent action of bile salts. Functional deficiency of ABCB4 solubilizes the cell membrane of the biliary epithelium inducing apoptosis. Diagnostic features include elevated serum bile salts, increased GGT, light microscopy findings of ductular proliferation, and inflammatory infiltrate in early stage, progressing to cirrhosis and cholestasis in later stages. Typically, PFIC type 3 is diagnosed in childhood or early adulthood. Rarely, it can also present much later in life, as in this patient. Manifestations are limited to the liver only. UDCA is helpful in about 50% and transplantation is required for hepatic failure.

1206 A Case of Zieve’s Syndrome Chukwuemeka Ezeoke, MD, Giao Vuong, MD, James Ampadu, MD, Christine Hachem, MD, FACG. Internal Medicine, Saint Louis University School of Medicine, St Louis, MO. Introduction: A 25-year-old African American man with a 10-year daily 8-oz vodka use presented with a 2-week history of jaundice, nausea, vomiting, and epigastric pain after symptoms did not improve with alcohol cessation. He denied a family history of liver disease. Exam revealed normal vitals, multiple tattoos, scleral icterus, diffusely tender abdomen, no hepatosplenomegaly, and negative rectal exam. Liver panel (LFTs) showed total bilirubin (TB) 3.2, conjugated bilirubin (CB)


1.2, unconjugated bilirubin (UCB) 2.0, AST 474, ALT 50, triglyceride 1093, cholesterol 300, alkaline phosphatase (AlkP) 231, gamma-glutamyl transpepetidase (GGT) 2034, albumin 2.2, negative amylase, lipase, autoimmune (ANA, ASMA, anti-mitochondrial, Anti-trypsin) antibodies, hepatitis/HIV serology, and normal coagulation markers. He developed hematochezia on hospital day 2, with a drop in Hgb from 11 to 8.3. Hemolysis labs showed reticulocyte count (3%), urobilinogen, and urine bilirubin, all elevated, LDH 260, with normal haptoglobin 137. Right upper quadrant ultrasound revealed a fatty liver. His Maddrey discriminant function (MDF) was -0.5. Triglycerides, AST, ALT, TB, CB, and UCB improved to 301, 77, 65, 1.2, 0.8,0.4, respectively, with supportive care in 4 days. Patient was discharged home. Our patient’s diagnosis was Zieve’s Syndrome. It is a rare syndrome affecting people 20 to 40 years old, and is characterized by transient jaundice, abnormal liver function tests, hemolytic anemia, and hyperlipidemia associated with alcoholism. Fatty infiltration of the liver occurs in up to 70% of patients. This syndrome is often misdiagnosed as alcoholic hepatitis, Gilbert’s syndrome or obstructive jaundice. Spontaneous resolution of hemolysis and LFTs within a week of stopping alcohol is the norm, with a longer duration of hyperlipidemia resolution. Our patient presented 14 days after alcohol cessation and symptoms onset; his hemolysis labs showed evidence of resolving hemolysis with normal LDH, but evidence of increased RBC turnover. It is important to recognize this syndrome in young alcoholics with concurrent anemia, without end-organ damage on ultrasound to avoid unnecessary interventions such as a liver biopsy or endoscopy given most lab abnormalities improve within 6 weeks from initial presentation. Hemolysis and hyperlipidemia are involved in erythrocyte membrane stability. Alcohol-induced hemolysis causes Vitamin E deficiency, which reduces polyunsaturated fatty acids. This induces oxidation of erythrocyte membrane glutathione, causing hemolysis and hepatocyte injury. In conclusion, Zieve’s syndrome should be suspected in young alcoholics presenting with rectal bleeding, abdominal symptoms, and jaundice.

1207 A Case of Sacromatoid Hepatocellular Carcinoma Without Prior Anticancer Therapy Hiren Patel, MD,1 Abhishek Kumar, MD,2 Sharon Peng, MD,1 Nihar Shah, MD,2 Hamid Shaaban, MD,2 Michael Maroules, MD2. 1. St. Joseph’s Regional Medical Center, Paterson, NJ; 2. Seton Hall University School of Health and Medical Sciences, South Orange, NJ. Introduction: Sarcomatoid hepatocelluar carcinoma (SHCC), also referred as spindle cell carcinoma, pseudosarcoma, or carcinosarcoma is a rare histological type of hepatocelluar carcinoma (HCC). Incidence of SHCC is 1.8% in surgically resected, and 3.9% to 9.4% in autopsy cases. Previous chemotherapy use is presumed to promote sarcomatous change. We report a case of SHCC without prior anticancer therapy. Case Report: A 66-year-old Hispanic male presented with complaint of abdominal distension. The patient had past medical history of cirrhosis due to hepatitis C infection, portal hypertension, esophageal varices, recurrent ascites s/p therapeutic paracentesis (last done 3 months prior), diabetes mellitus, and hypertension. The patient had a 20-pack a year smoking history, but quit 20 years ago and denied alcohol or illicit drug abuse. He had no family history of any cancer. Vital signs on presentation, blood pressure 105/58 mm hg, pulse 74 per minute, and regular, respirations rate 20 per minute, temperature 97.8 F, BMI 25.2. On physical exam, the patient was found to have distended abdomen, dull on percussion. Labs showed hemoglobin 12.5 gm/dL, white count 5700/ul, platelet count 134,000/ul, prothrombin time 15.8 seconds, INR 1.2, sodium 130 meq/L, potassium 4.1 meq/L, chloride 100 meq/ L, bicarbonate 28 meq/L, glucose 218 mg/dl, BUN 18 mg/dl, creatinine 0.9 mg/dl , calcium 8.2 mg/dl. albumin 2.6 G/DL, total protein 8.2 G/DL, bilirubin total 1.20 MG/DL, alkaline phosphatase 179 U/L, AST 34 U/L, ALT 20 U/L, and alfa-feto protein 4.3 ng/mL. CT abdomen showed a 4.3-cm rim-enhancing mass in the medial segment of the left lobe of the liver in periphery along the diaphragmatic crus. Biopsy of liver mass was done, which showed areas of moderately differentiated conventional HCC and other areas of high-grade spindle tumor. Immunohistochemical stains showed both components stained for keratin. The spindle component did not stain for desmin, CD31, CD34 but was positive for vimentin. The patient underwent upper and lower gastrointestinal endoscopy, which showed no evidence of malignancy. The patient refused any further treatment, and eventually died 8 months after diagnosis. Conclusion: SHCC, compared to ordinary HCC, has relative low serum AFP levels, higher incidence of intrahepatic and adjacent organ invasion, high tendency to large tumor size with central necrosis and hemorrhage in the tumor, delayed peripheral enhancement of the tumor on CT images, resistance to treatment, early recurrence after treatment, and a poorer prognosis, with approximate life expectancy less than 1 year after diagnosis. We should consider SHCC even when a patient has not undergone anticancer therapies.

1208 Cholestasis in AIDS: A Case of Disseminated Mycobacterium Avium Complex Nikhil Kapila, MD,1 Kunal Kapila, MD,2 Jonathan Wilmot, MD3. 1. Internal Medicine, University of Connecticut Health Center, Farmington, CT; 2. Goverment Medical College, Patiala, India; 3. University of Connecticut Health Center-Department of Gastroenterology/Hepatology, Farmington, CT. Objectives: 1.) Recognize the hepatic complications of AIDS. 2.) Consider mycobacterium avium complex (MAC) infection in those patients with AIDS and evidence of cholestasis. 3.) The incidence of MAC infection has decreased with the early initiation of anti-retroviral therapy and timely prophylaxis. Case Report: A 32-year-old male with a history of AIDS presented with an axillary abscess. The patient’s past medical history included AIDS, not being treated with highly active anti-retroviral therapy (HAART) due to non-compliance, and recurrent axillary abscesses. The patient denied tobacco or alcohol use; however, he was an active intravenous drug user. His vital signs were stable, and physical exam revealed a cachetic-appearing male with a soft, non-tender abdomen and hepatomegaly. Laboratory data included hemoglobin of 8.3, hematocrit of 24.6, platelets of 116, and a WBC of 1,900. His CD-4 count was 4. Liver function tests included an AST of 171, ALT of 79, total bilirubin of 0.5, and an alkaline phosphatase of 792. Computed tomography of the abdomen showed a grossly enlarged liver with no focal abnormalities and mesenteric lymphadenopathy. HIDA scan demon-


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strated findings consistent with infiltrative disease of the liver. Endoscopic ultrasound (EUS) revealed many abnormal lymph nodes in the celiac, perigastric, peripancreatic, and porta hepatis regions. Fine needle aspiration from the lymph nodes revealed epitheloid granulomas with abundant acid fast bacilli organisms. Blood cultures grew mycobacterium avium complex. The patient was started on azithromycin, ethambutol, and moxifloxacin, and after stabilization, he was discharged with close follow-up. Discussion: In recent times, with the advent and widespread use of HAART, the incidence of hepatic complications with AIDS has decreased. Hepatobiliary disease in patients with HIV/AIDS may be secondary to viral hepatitis, opportunistic infections, anti-retroviral therapy hepatotoxicity, and HIV cholangiopathy. Cholestasis, in the setting of AIDS, raises the suspicion for hepatic cholangiopathy and mycobacterium avium (MAC) infection of the liver. In the absence of biliary tree dilatation, a normal bilirubin, and evidence of infiltrative disease on imaging, we believed this presentation to be most consistent with disseminated MAC infection. The diagnosis was confirmed with positive blood cultures and cytology from intra-abdominal lymph nodes demonstrating multiple AFB positive organisms. Disseminated mycobacterium infection can be avoided by judicious use of prophylactic antibiotics and HAART; however, a high index of suspicion for MAC infection is necessary in those patients who are either intolerant to or non-compliant with medical therapy.

1209 Hepatotoxicity Associated With the Use of OxyELITE Pro: A Nutritional Supplement Patrick Koo, MD, Deepak Venkat, MD, Stanley Cohen, MD. Digestive Health Institute, University Hospital/Case Medical Center, Cleveland, OH. Introduction: Complimentary and alternative medical (CAM) therapies are commonly used in the United States. Several of these agents have been associated with hepatotoxicity. We present a case of severe cholestatic hepatitis attributed to the use of OxyELITE Pro, a new herbal weight loss remedy. Case Report: A previously healthy 33-year-old Laotian woman presented with acute onset of jaundice, nausea, and vomiting. She had been taking OxyELITE Pro for weight loss for approximately 3 months. On exam, she was jaundiced, but had no stigmata of chronic liver disease and no asterixis. Lab studies revealed a normal CBC, INR 1.7, alkaline phosphatase 194, AST 1008, ALT 1042, total bilirubin 12.2. Serologies were negative for evidence of acute viral hepatitis, autoimmune hepatitis, or metabolic causes of liver disease. Imaging studies were unremarkable. A transjugular biopsy revealed approximately 10% hepatocellular necrosis, and was read as most consistent with drug-induced hepatitis. Despite discontinuation of the supplement, her liver function tests worsened. She was started on prednisone and eventually had dramatic improvement in her LFTs. Conclusions: OxyELITE Pro is another herbal supplement that appears to have associated hepatotoxicity. At the same time that we saw this case, others were noted across the country. The majority were self-limited, but approximately 10% died or needed liver transplant. This entity should be suspected if both chronological and clinical criteria are met. Liver biopsy may be helpful to support the diagnosis, rule out other causes of hepatitis, and assist in prognostication. The mainstay of treatment is discontinuation of the supplement and supportive care. If liver function continues to worsen despite these actions, corticosteroids might be necessary. Clinicians should remember to question patients with unexplained hepatitis or jaundice about the use of medications as well as dietary and herbal supplements.

1210 Onset of Celiac Disease in a Patient Associated With Treatment of Chronic Hepatitis C Using Interferon-Based Triple Therapy Amandeep Singh, MD, Nayere Zaeri, MD, Immanuel Ho, MD, FACG. Crozer Chester Medical Center, Upland, PA. Introduction: Patients treated with interferon-based therapies for chronic HCV may develop exacerbation of autoimmune disease. We present the first case in the literature of a patient who developed celiac disease (CD) as a result of triple therapy (interferon, ribavirin, and boceprevir) for chronic HCV. Case Report: A 53-year-old white female with past medical history of IV drug abuse, previously treated with interferon monotherapy for HCV genotype 3a, was referred by her PCP for abnormal LFTs. Laboratory data on initial visit was positive for HCV RNA of 4,515,392 IU/mL, HCV genotype 1a, with normal CBC and LFTs. Liver biopsy showed Metavir grade 2 inflammatory activity and stage 1 fibrosis. Treatment was initiated with a 4-week lead-in phase of pegylated interferon alfa 2a plus ribavirin, followed by triple therapy using boceprevir (BOC) for a total of 28 weeks. HCV viral load obtained at week 4, 8, 12, and 21 were ALT). A day later, the labs started to trend down and transaminases began to improve. Eventually, the work-up was positive for HSV-1 IgG (>10.49) and IgM (1:40). ANA, AMA, anti-smooth muscle Ab, IGG subclass, Hep A-Ab , HepBsAg , Hep Bs Ab, Hep C Ab, LKMA were negative. The patient was observed in the hospital for 3 days more as the labs normalized and then discharged home on 2 weeks of acyclovir therapy. On follow-up exam, she had returned to baseline with no evident chronic liver disease. Conclusion: HSV 1 hepatitis is an extremely rare cause of acute liver injury in an immunocompetent patient. In a patient having acute liver injury, even in those with an apparently evident acetaminophen toxicity, it is important to look for other possible causes fulminant hepatitis and empirically start acyclovir therapy, especially when AST>ALT and LFTs worsen despite appropriate therapy on NAC. Strong consideration for liver biopsy should also be undertaken. It is also important to recognize that this patient did not have any signs of encephalopathy inspite of significant liver injury. This is an unusual presentation of acute liver injury from HSV 1 hepatitis along with concomitant Tylenol toxicity.

1213 A Case of Acute Liver Failure Associated With Synthetic Cannabis Use Presidential Poster Erin Spengler, MD, Douglas LaBrecque, MD. Internal Medicine, University of Iowa, Iowa City, IA. Introduction: A previously healthy 27-year-old man was transferred to our institution with concerns for acute liver failure. He presented after 2-3 days of fatigue, anorexia, nausea, and vomiting.



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Abstracts At the local hospital, he was found to have transaminases in the 10,000s, creatinine of 2.2, INR 6.5, and a lactic acid of >15, prompting transfer to our ICU. On arrival, the patient was alert but acutely ill-appearing. He denied use of any IV drugs, alcohol, or prescription medications. He admitted to current marijuana, synthetic cannabis, and tobacco use. He denied any OTC medications or supplements other than 35%) with no evidence of obstruction involving the cystic duct or the common bile duct. The Maria and Victorino diagnostic scale of hepatotoxicity score was 10. Three days after the last dose of Plavix, the liver enzymes started to trend down, along with resolution of symptoms. The patient improved remarkably and was discharged on day 3, in a stable condition. At the 2-week follow up, the patient had complete normalization of liver enzymes. After an informed discussion with the patient, she was subjected to a drug re-challenge with a single dose of 75 mg of clopidogrel. Her liver function tests were serially measured on the days 0, 2, and 7, which suggested a worsening pattern of liver enzymes on day 2, followed by a normalizing trend by day 4, confirming our diagnosis of druginduced hepatotoxicity.

1225 Portal Hypertensive Gastric Polyps Presenting as Iron Deficiency Anemia in a Cirrhotic Patient Sajan Jiv Singh Nagpal, MD, Carole Macaron, MD, Naim Alkhouri, MD. Cleveland Clinic, Cleveland, OH. Introduction: A 64-year-old white female with a past medical history of diabetes mellitus type II, hypertension, hyperlipidemia, obesity (BMI 33 kg/m2), and compensated NASH cirrhosis presented to the outpatient clinic for evaluation of new onset iron-deficiency anemia, unresponsive to oral and IV iron therapy and requiring almost monthly blood transfusions. The patient did not have a prior history of gastrointestinal bleed. Her review of symptoms was significant only for generalized fatigue and shortness of breath. Current medications included pantoprazole, atorvastatin, sitagliptin, metformin, glyburide, lisinopril, and aspirin. Her outside hospital work-up for anemia included an EGD, a colonoscopy, and a capsule endoscopy, which were significant for mild portal hypertensive gastropathy without esophageal or gastric varices. The patient’s labs were significant for a microcytic anemia (MCV 70.3 fL), nadir hemoglobin of 7.3g/dL, and a ferritin of 17.9 ng/ml. Her liver function tests revealed an AST of 183 U/L, ALT of 153 U/L, total bilirubin of 0.8 mg/dL, and alkaline phosphatase of 73 U/L; these values remained stable throughout the course of her follow-up. Her BUN and creatinine were 15mg/dL and 0.70mg/dL, respectively, and her INR was 1.1. Her calculated MELD score was 7. A repeat EGD at our institution showed multiple bleeding gastric polyps and severe portal hypertensive gastropathy (Figure 1). The largest polyps were removed with a hot snare, and histopathologic examination demonstrated the presence of a hyperplastic epithelium and an edematous lamina propria containing prominent ectatic blood vessels consistent with portal hypertensive gastric polyps. The unique histology showing prominent capillary ectasia in the lamina propria strongly points to the possibility that the formation of gastric polyps was a direct consequence of the patient’s portal hypertension. It is unclear whether these polyps have underlying malignant potential or if they eventually regress with the reduction of portal pressures after the placement of a transjugular intrahepatic portosystemic shunt (TIPS).


[1225A] Figure 1. Gastric antrum showing multiple bleeding polyps and severe portal hypertensive gastropathy.

1226 Hypervitaminosis A Presenting With Decompensated Liver Disease in the Absence of Cirrhosis Shivali Berera, MD, Fernando Calmet, MD, Leopoldo Arosemena, MD, Marcelo Larsen, MD, Monica Garcia-Buitrago, MD. Jackson Memorial Hospital/University of Miami, Miami, FL. Introduction: Hypervitaminosis A is a known, yet rare, cause of postsinusoidal portal hypertension. We describe a case of a man who presented with anasarca after vitamin A megadosing. A 47-year-old man without prior medical history presented with 3 weeks of increasing abdominal girth, lower extremity edema, dyspnea, and orthopnea. He was taking high doses of multiple nutritional supplements for 5 years, including 120,000 IU of vitamin A per day, but no medications. He denied tobacco, alcohol, or recreational drugs. He appeared cachectic. Right-sided breath sounds were decreased with dullness to percussion. He had a distended abdomen with shifting dullness and an indurated liver edge palpable 5 cm below the costal margin. His spleen was not palpable. He had lower extremity edema, but no other stigmata of chronic liver disease. On presentation, laboratory data showed abnormal liver tests (protein 6.0 g/dL, albumin 2.9 g/dL, total bilirubin 1.3 mg/dL, AST 49 u/L, ALT 31 u/L, alkaline phosphatase 136 u/L, INR 1.2, creatinine 0.81 mg/dL, and platelets 357,000/mm3). Hepatitis A, B, and C serologies and markers for autoimmune hepatitis and PBC were negative. There was no evidence of genetic or metabolic diseases. Abdominal ultrasound showed ascites, hepatomegaly, and patent suprahepatic veins. Paracentesis revealed a total protein of 4.4 g/dL and serum ascites albumin gradient of 1.7 g/dL. Echocardiogram was normal except for a mild pericardial effusion. A liver biopsy showed parenchyma with glycogenated nuclei, centrilobular lipofuscin, prominent stellate cells with vacuolization, mild lymphocytic portal inflammation, and centrilobular sinusoidal dilation with perivenular fibrosis. Trichrome stain showed periportal, centrilobular, and perisinuosidal fibrosis. Smooth muscle actin immunostain highlighted the vacuolated stellate cells. These findings suggested hypervitaminosis A. The patient discontinued vitamin A 2 months after presentation, but continued to deteriorate with worsening ascites, hepatic hydrothorax, encephalopathy, and SBP. He died 8 months after presentation. Vitamin A is known to cause peri- and postsinusoidal fibrosis after prolonged daily doses >25,000 IU. Literature regarding chronic ingestion in adults is scant. Most cases are potentially reversible, although some progress relentlessly despite cessation of vitamin A. Patients with decompensated liver disease tend to have a worse prognosis, and portal hypertension may occur in the absence of cirrhosis. Continued deterioration after cessation may be due to bioaccumulation and slow tissue turnover (half-life: 58-286 days). Hypervitaminosis A should be considered in the differential diagnosis of portal hypertension of obscure origin.

1227 Porto-Pulmonary Venous Anastomosis (PPVA) and Its Clinical Significance: A Case Report and Literature Review Muhannad Al Hanayneh, MD,1 Deborah Majchel-Koss, MD,1 Eric Walser, MD,2 Richard Goodgame, MD1. 1. Internal Medicine, University of Texas Medical Branch, Galveston, TX; 2. University of Texas Medical Branch, Galveston, TX. Introduction: As many have suggested, 15% of patients with cirrhosis of the liver and severe portal hypertension may develop a porto-pulmonary venous anastomosis (PPVA). PPVA is a direct vascular connection between the esophageal veins and the pulmonary veins, close to the left atrium. Cirrhotic patients who do not develop a gastro-renal shunt (a decompressing vascular connection between the portal venous system and the renal vein) are most likely to develop a PPVA. Modern imaging methods can demonstrate a PPVA when severe hepatic cirrhosis is investigated. A PPVA is a right-to-left


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Abstracts 1229 A “Q”uizzical Cause of Abnormal LFTs Katherine Chen, BS, Margaret Adamcewicz, DO, Donald Tsynman, MD, Christine Granato, MD, Erik Olson, DO, Ashok Shah, MD, MACG, Benedict Maliakkal, MD. Gastroenterology, University of Rochester Medical Center, Rochester, NY.

[1227A]

Figure 1. Coronal view. Arrow to PPVA.

shunt that, theoretically, could be associated with clinically significant systemic arterial hypoxemia or emboli. We describe a patient with moderately severe hepato-pulmonary syndrome (HPS) and a PPVA. He presented a clinical dilemma as this connection (PPVA) could have contributed to his hypoxia. A detailed literature review was performed of all reported PPVA cases using the PubMed database and searching all cited references for similar cases; a total of 38 reported cases were found in the literature. Embolization of this shunt was performed by a trans-septal approach with the help of cardiology and interventional radiology with no significant improvement in hypoxia. There is little evidence that PPVA causes clinically significant hypoxemia. PPVA is likely a risk factor for systemic emboli when needle or catheter techniques are used to treat or prevent bleeding from gastro-esophageal varices. The published medical literature and our experience suggest that PPVA has very little clinical significance.

1228 Systemic Mastocytosis: A Confounder of Refractory Pruritus in a Liver Disease Patient Creating Management Dilemma Jagpal Klair, MD, Mohit Girotra, MD, Johnny Jones III, MD, Aneet Kaur, MD, Farshad Aduli, MD, FACG. University of Arkansas for Medical Sciences, Little Rock, AR. Introduction: Systemic mastocytosis (SM) results from a clonal, neoplastic proliferation of abnormal mast cells (MC) in 1 or more organ systems. Patients become susceptible to itching, urticaria, and anaphylactic shock, which occur due to histamine release from mast cells. SM manifestations may co-exist in the presence of other systemic disease, thus confounding the overall clinical presentation. Case Report: A 27-year-old white woman with a history of Crohn’s disease with primary sclerosing cholangitis (PSC) had refractory diarrhea (since Crohn’s diagnosis 15 years ago) and refractory pruritus of 8 years’ duration. She developed intense pruritus in 2005, followed by a diff use erythematous macular rash, and was seen by dermatology with skin biopsies failing to provide any clear etiology. Concurrently, abnormally elevated liver enzymes (especially alkaline phosphatase) were noted and further work-up with MRCP and liver biopsy suggested a diagnosis of PSC. Her pruritus management consisted of ursodiol, antihistamines, cholestyramine, rifampin, and sertraline, with minimal improvement. The patient was referred for consideration for a liver transplant, in view of her refractory pruritus. She was seen by orthopedics for bilateral knee joint pain and swelling, and orthopedics did a bone scan that revealed increased uptake around the distal right femur, where a bone biopsy was performed and histopathology on the biopsy revealed multifocal aggregates of CD117+/ tryptase+ mast cells (MC) with >25% showing abnormal morphology and co-expression of CD25. Pathology findings were suggestive of indolent systemic mastocytosis. Discussion: SM is diagnosed by 1 major criterion plus 1 minor criterion or 3 minor criteria. The major criterion is defined as multifocal clusters of MC (>15) in the bone marrow. Minor diagnostic criteria include elevated serum tryptase level, presence of KITD816V, abnormal MC expression of CD25, and/or CD2. SM classification into indolent (SM), aggressive (ASM), associated with a clonal nonMC lineage disease (SM-AHNMD), and mast cell leukemia (MCL) subgroups is a useful first step in establishing prognosis. SM treatment is generally palliative. Interferon-α and corticosteroids are used for symptomatic management in ASM patients. Imatinib has a therapeutic role in the presence of an imatinib-sensitive KIT mutation or in KITD816-unmutated patients. Treatment of SM-AHNMD is based primarily on a non-MC neoplasm with hydroxyurea having some therapeutic benefit. Through our case, we want the gastroenterologist to remain cognizant of this rare entity and to have a greater suspicion when encountered with patient with refractory pruritus in a setting of biliary disorder (PBC, PSC), for adequate diagnosis and management.


Introduction: Q fever is a rare cause of abnormal liver function tests (LFT) in an urban population. The disease is characterized by sudden onset of fevers, chills, headaches, myalgia, and pneumonitis or hepatitis. In North America, acute Q fever usually presents as atypical pneumonia. We present a case of Q fever in a patient who presented with jaundice, anorexia, and intermittent fevers. Case Report: A 62-year-old Nepalese man with past medical history of diabetes presented with fatigue and 3 weeks of fevers. On admission, he was febrile to 102°F and found to have ALT 81U/L, AST 103U/L, alkaline phosphatase 298U/L, and total bilirubin 7.7mg/dL with direct component 6.1mg/dL. Synthetic function was preserved with INR 1.2 and platelets of 246THOU/uL. Albumin of 2.8g/dL and pre-albumin of 3mg/dL signified severe malnutrition. The patient denied abdominal pain or change in bowel pattern, but reported nausea and vomiting for 2 days. He denied recent foreign travel, sick contacts, or new medications. Imaging studies revealed fatty liver with an edematous gallbladder and splenomegaly, but no pancreatic mass or biliary obstruction. Urine drug test, acetaminophen, alcohol, and salicylate levels were normal. Viral hepatitis panel was negative, including HIV, CMV, EBV, and HSV. Autoimmune work-up was unremarkable, and he was previously treated for latent TB. There was no leukocytosis, but his fevers persisted despite negative infectious work-up, including brucellosis. Subsequently, the patient underwent liver biopsy, which revealed non-necrotizing granulomas in the background of mild steatohepatitis. Special stains were negative for iron, copper, acid-fast bacilli, and fungal organisms. Finally, after a prolonged hospitalization, the patient was found to have positive Coxiella burnetti serologies confirmed by PCR. He was started on doxycycline, and his fevers and LFT improved. Upon further review, the family admitted to recently consuming freshly slaughtered and skinned goat meat from their local goat farm. Discussion: Acute Q fever is a worldwide zoonosis caused by a Gram-negative bacterium Coxiella burnetti, and is spread by inhalation of bacteria from air contaminated by cattle, sheep, or goat feces, urine, or placenta. It is endemic in the Netherlands and Middle East, and less commonly seen in the United States. Given the nonspecific nature of clinical manifestations of acute Q fever, its diagnosis requires a high index of suspicion. It is usually self-limited, and in most cases, diagnosed retrospectively. Treatment with doxycycline of symptomatic patients has been shown to shorten illness and reduce risk of progression to chronic disease.

1230 A Blakemore for the Bile Duct Konika Bose, MD, Moshe Rubin, MD, FACG, Syed Hussain, MD. Gastroenterology, New York Hospital Queens, Flushing, NY. Case Report: An 86-year-old woman presented with 1 day of epigastric pain, vomiting, and chills. On exam, she was normotensive, afebrile, and had epigastric tenderness. Laboratory findings demonstrated: TBili 3.4 mg/dL, DBili 2.6 mg/dL, SGOT 410, SGPT 316, WBC 9.3 K/uL (90% neutrophils). Ultrasound showed gallstones, gallbladder wall thickening, and a common bile duct (CBD) measuring 8-9 mm. CT revealed gallbladder wall thickening. Choledocholithiasis was suspected and ERCP was performed. Cholangiogram revealed dilated CBD with a small stone, and sphincterotomy was performed without bleeding. With multiple balloon sweeps, 1 gallstone was extracted from the CBD. During extraction, fluoroscopy revealed extravasation of dye outside the distal CBD. Shortly thereafter, copious blood was seen in the duodenum. A 10 x 60-mm Boston Scientific® Wallflex fully covered stent (SEMS) was then deployed into the CBD under fluoroscopic and wire guidance. No source of bleeding was identified with either duodenoscope or gastroscope. After resuscitation, an emergency CTA was performed and showed portal venous gas, portal vein thrombus, and biliary varices. No further bleeding episodes occurred this hospitalization. No attempt was made to remove the SEMS out of concern of rupturing additional varices. Discussion: Choledochal varices form from venous dilation in the setting of increased extrahepatic portal pressures. The extrahepatic bile duct is surrounded by 2 different venous systems. Dilation of the paracholedochal veins of Petren, which run parallel to the bile duct, usually causes extrinsic compression of the bile duct wall. With dilation of the epicholedochal venous plexus of Saint, which line the outer surface of the CBD, bleeding and mechanical obstruction may occur1. Although choledochal varices are uncommon, they can lead to life-threatening consequences during endoscopy or surgery. The proposed mechanism is squeezing of the dilated vascular channels proximally resulting in rupture of distal channels2,3. Jacobson et al first described rupture of a choledochal varix following balloon extraction of a stone, resulting in massive bleeding, and subsequently placing a plastic stent.1 Sharma et al described 3 similar cases 3. While choledochal variceal rupture following balloon extraction has been described (4-7), this is the first reported case of choledochal variceal bleeding secondary to balloon extraction and successful treatment with the placement of a fully covered SEMS. The proposed mechanism is tamponade of the choledochal varices, similar to the effect of a Blakemore tube on esophageal varices. Future prospective randomized trials are required to explore the use of SEMS for bleeding choledochal varices.

1231 Rare Complication of Simple Liver Cyst Necessitating Prompt Management Jagpal Klair, MD, Gaurav Syal, MD, Farshad Aduli, MD, FACG. University of Arkansas for Medical Sciences, Little Rock, AR. Introduction: Hepatic cyst usually refers to solitary nonparasitic cysts of the liver, also known as simple liver cysts (SLC). Although mostly asymptomatic, they can lead to extrinsic compression of inferior vena cava (IVC), leading IVC thrombosis and necessitating the need for increased awareness and prompt management.


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Case Report: A 72-year-old white woman presented to the hospital with progressively worsening lower extremity swelling for 1 week. She did not complain of abdominal pain, distension, shortness of breath, or chest pain. She was not on hormone replacement therapy, and had no prior history of deep vein thrombosis (DVT). Physical examination showed 2+ pitting pedal edema with tenderness and minimal erythema of left lower extremity. Abdominal exam was unremarkable. Laboratory tests showed INR 1.3, total bilirubin 1.4, alkaline phosphatase 279, and normal aminotransferases. Left LE duplex ultrasound revealed DVT of femoral vein. CT abdomen with contrast showed multiple simple liver cysts with a large cyst (12.2 x 11.4 x 13.1 cm) causing extrinsic compression of IVC with extensive venous thrombsis extending from left ileo-femoral veins to IVC. She was started on therapeutic anticoagulation with enoxaparin. Vascular surgery performed successful thrombolysis of IVC and left ileofemoral thrombus with t-PA, followed by placement of infrarenal IVC filter. The next day, open deroofing of large liver cysts was performed. The patient did well post-operatively, and was discharged 5 days later on warfarin. Discussion: Differential diagnosis of hepatic cysts includes SLC, polycystic hepatic cyst, hydatid cyst, hepatic abscess, and neoplastic cysts. SLCs are congenital malformations estimated to occur in approximately 5% of the population. Most SLCs are asymptomatic, diagnosed incidentally, and do not carry malignant potential. Complications of SLC include torsion, infection, rupture, intracystic hemorrhage, and compression of adjacent structures like IVC. External compression of IVC lumen leads to decreased flow caudally, which predisposes to thrombus formation, as seen in our patient. Lower extremity swelling in the absence of cardiac disease and vascular collateral formation in the absence of known liver disease points towards the possibility of IVC obstruction. CT scan and LE ultrasound with duplex are the best initial tests for the evaluation of suspected IVC thrombosis and LE DVT respectively; CT scan can also identify the etiology of extrinsic IVC compression. SLC do not require treatment unless symptomatic or causing complication. Large symptomatic SLCs are managed surgically with removal or deroofing.

1232 A Rare Case of Acute Liver Failure From an Adverse Drug Reaction Muhammad Baig, MBBS, MD, Mohsen Hasanin, MD, Sanam Anwer, MBBS, MD. UAB Montgomery Internal Medicine Residency Program, Montgomery, AL. Introduction: Acute liver failure is a rare, but potentially fatal complication of intravenous amiodarone. While oral amiodarone is not known to cause acute liver failure, we present a case of fatal acute liver failure after an increase in oral amiodarone dose. An 89-year-old woman was discharged after treatment for acute systolic congestive heart failure (CHF) secondary to atrial fibrillation (AF) with rapid ventricular response. She had coronary artery disease, hypertension, tachy-brady syndrome status post pacemaker placement, and hypothyroidism. Medications include aspirin, clopidogrel, beta blocker, statin, digoxin, furosemide, and levothyroxine. She was on amiodarone 200 mg daily for 3 years, which caused a mild intermittent subclinical transaminitis. CHF and AF resolved with diuresis and increasing amiodarone dose to 400 mg daily, on which she was discharged. One week later, she presented to the emergency department with generalized, dull abdominal pain for one day. Vital signs were normal. Physical examination revealed scleral icterus, bibasilar crepitation, and hepatomegaly. Investigations revealed leukocytosis, thrombocytopenia, anemia, elevated creatinine, elevated alanine aminotransferase and aspartate aminotransferase levels (4000 mg/dL and 9000 mg/dL, respectively), elevated alkaline phosphatase, bilirubin, ammonia, and INR, normal autoimmune panel, normal acetaminophen and alcohol levels, and negative viral hepatitis serology. Abdominal ultrasound was normal. CT of abdomen without contrast revealed hepatomegaly and mild ascites. She developed grade III hepatic encephalopathy within 24 hours of admission. Amiodarone-induced fulminant hepatic failure was diagnosed. Amiodarone was discontinued and she was medically managed. Highly elevated transaminase levels started to decline. Her mental status and renal function continued to deteriorate. She became hemodynamically unstable, requiring vasopressors. According to Naranjo algorithm (a tool to determine the likelihood of a drug being responsible for an adverse reaction), it was highly probable that her condition was due to amiodarone. Amiodarone is an anti-arrhythmic drug commonly used for tachy-arrhythmias. Severe acute liver failure has been reported as a complication of intravenous amiodarone, thought to be due to the solubilizer polysorbate 80, which is the vehicle in intravenous amiodarone. Acute liver failure caused by oral amiodarone raises the possibility of a mechanism other than polysorbate 80. When patients who are elderly, critically ill, or have pre-existing transaminitis are started on oral amiodarone or have their dose increased, providers should be vigilant to detect acute liver disease to prevent fatal consequences.

bolic activity compared to the normal liver parenchyma. Two small (0.7 cm in size), stable subpleural nodules in the right lower lobe of the lung were also detected, which were suspected to be due to granulomatous changes and not metastatic disease. Work-up for common causes of chronic liver disease, including viral serologies, was negative. Prothrombin time, INR, albumin, tumor markers including alpha-fetoprotein, CA-19, and carcinoembryonic antigen were within normal limits. The patient was referred to surgery for resection of the mass and underwent right hepatectomy. The surgical pathology revealed well-differentiated hepatocellular carcinoma. Interestingly, no cirrhosis or even fibrosis was seen in the surrounding hepatic parenchyma. The patient had an uncomplicated postoperative course. He remains asymptomatic and continues to have mild elevation in serum transaminases 1 year after his surgery. (AST, ALT, ALP, and total bilirubin were 102, 133, 136 IU/L, and 0.5 mg/dL, respectively). Conclusion: Our patient with metabolic syndrome developed hepatocellular carcinoma without pre-existing cirrhosis or advanced fibrosis. Metabolic syndrome may be a risk factor not only for chronic non-alcoholic liver disease, but also HCC, even in the absence of nonalcoholic steatohepatitis or advanced fibrosis. Further studies are required to identify a subset of metabolic syndrome patients at a higher risk for development of HCC, who may benefit from HCC screening.

1234 Cholestatic Hepatitis: An Unusual Presentation of Lisinopril-Mediated Hepatotoxicity GURPINDER SINGH, MD, MBBS, Amit Kachalia, MD, MBBS, Jaspreet Kaur, MBBS, Kinjal Kachalia, MBBS, Vincent Rizzo, MD, MBA, FACP. Icahn School of MEdicine at Mount Sinai Queens, Fresh Meadows, NY. Case Report: A 47-year-old female with diabetes mellitus and hypertension presented with jaundice and dark urine for 1 week. She had no history of alcohol use, liver disease, sick contacts, fever, or travel. She received enalapril for 5 months before switching to lisinopril 2 years before admission. Exam showed icteric sclera and jaundice. Labs showed ALP 750 U/L, AST 169 U/L, ALT 210 U/L, GGT 813 U/L, total bilirubin 13.4mg/dL with conjugated 7.7 mg/dL. Before initiation of lisinopril, liver enzymes were normal. Hepatitis serologies, ANA, anti- mitochondrial, anti-smooth muscle, c-ANCA, and pANCA were negative. Ceruloplasmin, Tylenol, and alpha-1antitrypsin levels were normal. MRI showed hepatomegaly; no fatty infiltration, cirrhosis, or dilation of biliary tree. Liver biopsy showed portal hepatitis with lymphocytic infiltration, cholestasis, mild portal fibrosis (Figure 1); no bile duct damage, cytoplasmic inclusion, or amyloid. Impression was drug-induced hepatitis. Lisinopril was discontinued and the patient improved clinically and biochemically. The patient was discharged uneventfully, and 6 months later, she had normal liver enzymes. Discussion: We report the first case of lisinopril-induced cholestasis mediated hepatotoxicity as opposed to previous reports of direct hepatocellular injury. In our case, extensive work-up ruled out other causes of hepatitis. Earlier cases have shown similar latency to onset and histopathological findings of portal inflammation by lymphocytes without centrilobular necrosis. Similarity in histopathological findings along with a strong temporal relationship between lisinopril withdrawal and improved biochemical and clinical scenario, with absence of other constitutional symptoms and eosinophilia, strongly point toward lisinopril-induced hepatotoxicity. This case highlights controversy as to whether this patient could have been safely continued on other ACE-I except lisinopril, or would have developed hepatotoxicity if enalapril was continued. Conclusion: Discontinuation of ACE-I usually leads to normalization of liver enzymes; however, continuation can be potentially fatal, and there is need for further research guiding monitoring of liver enzymes with use of ACE-I.

1233 An Unusual Case of Hepatocellular Carcinoma Without Pre-existing Liver Cirrhosis or Fibrosis in a Patient With Metabolic Syndrome Gouri Sreepati, M.B.B.S, Ashish Aggarwal, M.B.B.S, Craig Lammert, MD. Medicine, Indiana University School of Medicine, Indianapolis, IN. Introduction: Hepatocellular carcinoma (HCC) is a rare, but well-recognized outcome among patients with advanced fibrosis. Metabolic syndrome is a risk factor for nonalcoholic fatty liver disease, as well as cirrhosis. We present a case report of isolated hepatocellular carcinoma without pre-existing liver fibrosis or cirrhosis occurring in a patient with metabolic syndrome. Case Report: A 63-year-old male with metabolic syndrome, defined by hypertension, type 2 diabetes mellitus, dyslipidemia with elevated triglyceride levels, and BMI of 32.5 had mild elevation in liver enzymes (AST, ALT, ALP, total bilirubin were 57, 82, 87IU/L, and 0.3mg/dl, respectively), which was attributed to nonalcoholic fatty liver disease. He had a symptomatic umbilical hernia and underwent further evaluation. The clinical work-up included an abdominal CT scan with IV contrast that revealed an incidental hepatic mass. A follow-up MRI of the abdomen revealed a mass in the dome of the liver. A PET scan, ordered to look for any metastatic disease and possible primary sources of tumor, revealed a 3.4 x 2.9-cm hypervascular hepatic mass in the right hepatic lobe with hypermeta-


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Figure 1. Trichome stain showing portal tract fibrosis.


| OCTOBER 2014

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Figure 1.

1235 Successful Treatment of Fibrosing Cholestatic Hepatitis C With Sofosbuvir and Simeprevir Meghan NeSmith, MD,1 Atif Zaman, MD, FACG,1 Jennifer Urquhart, MD,2 Jody Hooper, MD,1 Joseph Ahn, MD, FACG1. 1. Oregon Health & Science University, Portland, OR; 2. Kaiser Permanente, Portland, OR. Case Report: A 62-year-old female with HCV (GT 1a, nonresponder to pegylated interferon-alfa [PEG] and ribavirin [RBV]) who had been doing well on tacrolimus and mycophenolate presented with jaundice 3 years after liver transplantation (LT). Labs were significant for AST 391 u/L, ALT 324 u/L, AP 184 u/L, TB 1.3 mg/dL, and DB 0.4 mg/dL. An ultrasound showed a patent portal vein and hepatic artery. A liver biopsy showed moderate acute cellular rejection (ACR), also with cholestasis and portal fibrosis. The patient was treated with 3 doses of methylprednisolone 500 mg IV followed by a prednisone taper. Repeat liver biopsies 12 and 26 days later were interpreted as resolving ACR, but still showed moderate cholestasis, raising concern for fibrosing cholestatic HCV (FCH). Labs showed AST 193, ALT 334, AP 334, GGT 1054 u/L, TB 19.7, DB 11.4, HCV RNA 4,009,783 IU/mL. PCR for CMV and EBV was negative. When the patient’s labs worsened with a TB of 39.1 and HCV RNA 1,076,167 IU/mL after a second course of methylprednisolone, a fourth liver biopsy done 7 weeks after initial presentation revealed marked cholestasis, numerous damaged bile ducts, mixed inflammation, and stage 2 fibrosis. FCH could not be ruled out histologically, and clinical suspicion was high, thus treatment was begun with a combination of sofosbuvir (SOF), simeprevir (SIM), and RBV. The patient’s liver tests markedly improved and after 6 weeks; her HCV RNA level was undetectable. RBV was discontinued at week 6 due to anemia. The patient is doing well at week 16 with normalization of her labs (Figure 1), with a plan to complete a 24-week course of SOF/SIM. Discussion: FCH is an aggressive form of HCV that can occur in up to 14% of patients transplanted for HCV, and can lead to graft loss and death. Differentiating FCH from ACR can be challenging, and can lead to a delay in diagnosis. Treatment of presumptive ACR with high-dose steroids can exacerbate FCH. With the advent of safer and more effective HCV regimens, the histologic criteria for FCH may need to be broadened in order to identify patients who may benefit from earlier HCV treatment.

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Figure 1. Atypical infiltrative plasma cells-FNA.

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than that are diagnosed as a primary lesion (SEP). Most patients with SEP present with symptoms related to the location of the mass. Less common sites of involvement include the gastrointestinal tract, liver, lymph nodes, testes, skin, and central nervous system. When the liver is affected, a direct diffuse neoplastic plasma cell infiltration results with symptomatic features such as extrahepatic biliary obstruction, jaundice, or ascites. Our case proves that EUS can be an important modality in diagnosing SEP.

Endoscopic Ultrasound Fine Needle Aspiration: A Novel Way to Diagnose a Solitary Extramedullary Plasmacytoma of the Liver

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Steven Guttmann, MD, Jack Husney, MD, Nnaemeka Anyadike, MD, Ira Mayer, MD, Rabin Rahmani, MD. Gastroenterology, Maimonides Medical Center, Brooklyn, NY.

Bosentan-Induced Autoimmune Hepatitis

Introduction: Plasmacytoma is a neoplastic production of a single line of plasma cells, usually forming monoclonal immunoglobulin. These tumors most often originate in the bone marrow, but extramedullary proliferation can occur in 3% of cases. Wheras upper respiratory involvemt is common, GI-associated solitary extramedullary plasmacytomas (SEP) are rare, accounting for 10% of cases. SEP refers to a solitary non-osseous plasma cell neoplasm in the absence of any other sign of multiple myeloma, and often presents a diagnostic challenge. We present a rare SEP diagnosed by EUS-FNA. A 77-year-old female presented with abdominal fullness and bilious vomiting. Lab results showed increased total and direct bilirubin with elevated transaminases. CT of the liver showed gallbladder wall thickening. Management with IV fluids and antibiotics were initiated for acute cholecystitis. LFTs continued to increase despite therapy, and EUS was performed, which revealed a 1.7 x 1.8-cm hypoechoic heterogeneous lesion noted in the liver and FNA was performed. Cytology revealed infiltrative plasma cells consistent with solitary extramedullary plasmacytosis of the liver. The patient was started on radiation therapy. Plasma cell neoplasm is essentially a clonal disease of differentiated B-cells, which can encompass a broad spectrum and present as asymptomatic monoclonal gammopathy of undetermined significance to multiple myeloma. Five percent of patients with multiple myelomas are diagnosed with extramedullary plasmacytomas, and even less


Amir Taefi, MD, Suzan Ebrahimi, MD, Farzin Rashti, MD, Grishma Joy, MD, Mitesh Patel, MD, Won Cho, MD. Washington Hospital Center, Silver Spring, MD. Introduction: Bosentan is an endothelin receptor antagonist used for pulmonary arterial hypertension (PAH). Drug-induced liver injury (DILI) is 1 of the reported side effects. However, the mechanism of the injury is not well understood. A 56-year-old female with PAH on bosentan from 2 months ago was found to have an INR of 12.8 in the lab work. She was started on Coumadin from 2 weeks prior to admission for DVT. Inpatient lab works showed AST: 592, ALT: 194, and Alk-P: 273. Total protein was 7.7, albumin 2.6, globulin 5.1, and total bilirubin 16.1. She also had of dark urine, pruritus, and yellowing of the eyes and skin. She denied abdominal pain, nausea, or vomiting. PMH: sickle cell disease, PAH, pulmonary embolism, and migraine. Home medications were bosentan, ASA, tramadol, synthroid, Lasix, folic acid, and hydroxyurea. She denied any tobacco, ETOH, or illicit drug use. Physical exam was significant for icteric sclera. There was no abdominal tenderness and the bowel sounds were present. LFTs from 1 month ago were normal. Further labs showed normal LDH, AMA, DIC panel, and hepatitis panel. CMV PCR, EBV serology, and HSV PCR were negative too. IgG was 2,600 and ASMA was positive. Imaging showed cholelithiasis without evidence of choledocholithiasis or biliary dilatation. Liver biopsy showed mild diffuse portal lobular chronic inflammation composed of lymphocytes, plasma cells, and rare eosinophils. Focal


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[1237A] Figure 1. Liver biopsy showing hepatic necrosis, cholestasis, and ballooning degeneration without significant steatosis or portal fibrosis.

are still poorly understood. We hereby report the first case of nimesulide leading to ascites in the presence of bilateral pleural effusions in the absence of fulminate hepatic failure. Case Report: A 44-year-old Brazilian woman with no remarkable past medical history presented with sharp right upper quadrant epigastric pain following a recent 2-week trip to Brazil. She was visiting her family, who lived in a mountainous region and owned a farm that housed cows and pigs, but she did not have any direct contact with animals during her visit. However, she did drink local, unfiltered tap water. Prior to travel, she had sustained an ankle sprain and in Brazil; she was prescribed nimesulide 200 mg 3 tablets a day for 5 days. On presentation, she reported nausea with episodes of non-bloody emesis with body aches, chills, and weakness. On exam, she was afebrile with no scleral icterus. Abdomen was tender to palpation in the right upper quadrant, with positive Murphy’s sign. Her lungs exhibited absent to decreased breath sounds in the bilateral bases. Her white blood cell count was 7,600 per μL. Liver tests showed an AST 327 U/L and ALT 518 U/L. CT abdomen revealed large-volume ascites, periportal edema, and bilateral pleural effusions. Hepatitis A IgM antibody, hepatitis B core IgM antibody, hepatitis B surface antigen, hepatitis B surface antibody, hepatitis C, and hepatitis E antibodies were all negative. Anti-smooth muscle antibodies, antinuclear antibodies, antineutrophil cytoplasmic antibodies, and antimitochondrial antibodies were also negative. She subsequently underwent a transjugular liver biopsy, which was noted for acute lobular hepatitis with prominent zone 3 necrosis and a trans-sinusoidal gradient of 5 mm Hg. Additionally, a simultaneous diagnostic paracentesis was also obtained, which was significant for a SAAG gradient of 1.1. Further infectious work-up revealed a negative HIV, HSV, EBV, and CMV. Yellow fever, Strongyloides, Dengue fever, Leptospira, Schistosoma, and Brucella antibodies were also negative. Conclusion: There have been reports associating nimuselide with fulminant hepatic failure, but none involving nimuselide with pleural effusions and ascites without frank hepatic failure. Although the exact mechanism remains unclear, a clinician still needs to be aware of nimesulide as a possible cause of ascites and pleural effusion in spite of the absence of fulminant liver failure, as documented in our patient, and a thorough drug history is very pivotal.

1240 hepatic necrosis, cholestasis, and ballooning degeneration without significant steatosis or portal fibrosis was observed (Image 1). Bosentan was discontinued for this patient, and after 1 month, LFTs normalized. Mechanism of DILI in bosentan is not clear. In the presented case, the positive ASMA and the pathology findings indicating the dominance of plasma cells and lymphocytes and scarcity of eosinophils represent an autoimmune-induced mechanism. This autoimmune-induced hepatitis was most likely secondary to bosentan, and less likely AIH, given the age and also the fact that liver function improved when the patient stopped taking bosentan.

1238 Focal Fatty Infiltration of the Liver Mimicking Malignancy in High-Risk Patients Vinay Yalamanchi, DO, Wallace Wang, MD, Moshe Rubin, MD, FACG, Ari Bunim, MD, FACG. New York Hospital of Queens, New York, NY. Introduction: A 54-year-old male with a history of alcohol abuse was hospitalized for progressively worsening abdominal pain for 5 months. The patient noticed increased abdominal girth without any weight changes. Blood tests revealed an elevation of total bilirubin (9.1 mg/dL), alkaline phosphatase (243 U/L), aspartate aminotransferase (135 U/L), and alanine aminotransferase (34 U/L). Coagulation studies revealed an elevated prothrombin time (22.7 s) and INR (2.00). An alpha-feto protein level was normal at 5.4 ng/mL. Contrast-enhanced computed tomography (CT) of the abdomen and pelvis showed moderate ascites, a nodular liver consistent with cirrhosis, and focal lesions. For further evaluation, contrast-enhanced magnetic resonance imaging (MRI) with contrast was performed, and a 5.7-cm mass with heterogenous contrast enhancement at the periphery of segment 4A was seen. The differential for this lesion included a metastatic lesion, abscess, hemangioma, or atypical hepatocellular carcinoma (HCC). A biopsy of this lesion revealed hepatic steatosis with bridging fibrosis. Immunochemistry staining was negative for any primary or secondary malignancy. Focal fatty infiltration can appear as nodular areas mimicking metastasis or primary tumors in cirrhotics. Cirrhosis secondary to viral hepatitis or alcoholism carries the highest risk for the development of HCC. Current guidelines state that nodules greater than 1 cm for patients at risk for HCC require a 4-phase multidetector CT (MDCT) or dynamic contrast-enhanced MRI. Biopsy is the next step to diagnosis if imaging studies are inconclusive; however, if negative, surveillance through ultrasound (US) is performed at 3-6 month intervals until the lesion disappears, increases in size, or is diagnostic for HCC. Ten-20% of HCC tumors do not enhance during contrast imaging due to hypovascularity, and are hard to distinguish between dysplastic nodules, also further complicating the diagnosis. Noncirrhotic patients with primary liver malignancies or metastasis may also present with peritumoral sparing of fatty infiltration. Opposed-phase gradient-echo MRI is the test of choice under these circumstances. In the case of a patient with existing hepatic hemangioma or HCC, the portal phase will create hyperechogenicity due to a lack of portal flow through the tumors. This case posed a diagnostic dilemma because the patient had risk factors for HCC such as alcohol-related cirrhosis, but he had a hepatic lesion with an atypical enhancement pattern. As a result, a biopsy was obtained revealing a benign condition. Subsequently, the patient stopped drinking, his ascites resolved, and this lesion disappeared on follow-up interval imaging.

1239 Pleural Effusion, Ascites, and Periportal Edema in the Absence of Fulminant Hepatic Failure Secondary to Nimesulide Justin Lui, MD, Bilal Gondal, MD MRCSI, Joan Kheder, MD, Curtis Barry, MD. Department of Medicine, University of Massachusetts Medical School, Worcester, MA. Introduction: Nimesulide is a non-steroidal antinflammatory drug that has been associated with hepatoxicity leading to acute hepatitis, as well as fulminant hepatic failure. The mechanisms have been studied, but


Primary Hepatic T-cell Lymphoma Causing Acute Liver Failure and Hemophagocytic Lymphohistiocytosis Daniel Eshtiaghpour, MD, Sharareh Shahangian, MD, Ariana Cornejo, RN, Sofiya Reicher, MD, Anuj Datta, MD, Viktor eysselein, MD. Harbor UCLA, Torrance, CA. Introduction: A 58-year-old woman presented with fever, malaise, and decreased appetite for 3 weeks. She denied nausea, vomiting, diarrhea, dysuria, headache, or night sweats. Her temperature was 39.4 degrees Celsius, and heart rate was 105 beats per minute. Examination was notable for mild epigastric tenderness. Laboratory tests showed an AST 695 of IU/L, an ALT of 477 IU/L, and an alkaline phosphatase of 363 IU/L. Her total bilirubin was normal. Peripheral blood smear was notable for toxic granulation and Döhle bodies and 59% bands. Ultrasonography of the liver was unremarkable. Computed tomograhy of the abdomen showed numerous subcentimeter lesions throughout the liver. She had persistent fevers and developed progressive pancytopenia accompanied by rapid increase in hepatic transaminases and alkaline phosphatase. Her total bilirubin increased to 4.3 mg/ dL, and her INR increased to 1.6. Her ferritin was markedly increased at 21,892 ng/mL. A bone marrow aspirate and biopsy were obtained to evaluate potential infectious and malignant etiologies for her constellation of fevers and hematologic abnormalities. On hospital day 4, she underwent a percutaneous liver biopsy. After the biopsy, she developed hemorrhagic shock. Despite aggressive resuscitative efforts, the patient expired. Histologic specimens from the patient’s liver and bone marrow revealed involvement by an abnormal population of lymphoid cells of T-cell origin positive for CD8 and CD30. Her autopsy confirmed a diagnosis of primary T-cell lymphoma of the liver, along with findings consistent with hemophagocytic lymphohistiocytosis and disseminated intravascular coagulation. Our case represents primary hepatic T-cell lymphoma complicated by hemophagocytic lymphohistiocytosis, disseminated intravascular coagulation, and acute liver failure. While secondary hepatic involvement is a common occurrence in advanced NHL, primary hepatic lymphoma (defined as confined to the liver or with predominantly hepatic involvement) is exceedingly rare. The majority of reported cases are B-cell in origin. The most common presenting clinical features are abdominal pain, fever, night sweats, weight loss, and hepatomegaly. Laboratory features include elevated transaminase and lactate dehydrogenase levels. Hepatic involvement may vary from a solitary lesion to multiple distinct lesions, to diffuse infiltration. As other malignancies such as hepatocellular carcinoma and metastatic colorectal cancer may present similarly, histopathology is mandatory to establishing a diagnosis. On rare occasions, t-cell lymphomas may present with acute liver failure (encephalopathy and coagulopathy in the absence of a preexisting liver condition), which confers a dismal prognosis.

1241 A Multifactorial and Simultaneous Presentation of Acute Pancreatitis and Acute Hepatitis Nasir Akhtar, DO, Alicia Kovach, BS, Kimberly Fairley, MS, DO, Nina Ahuja, MD, Michael Komar, MD. Geisinger Medical Center, Danville, PA. Introduction: Acute pancreatitis and alcoholic hepatitis are ailments with significant morbidity and mortality. The incidence of acute pancreatitis is 35 cases/100,000 individuals, with 1.4% of cases due to drug-induced pancreatic injury. The incidence of alcoholic hepatitis is unknown, as patients are often asymptomatic or undiagnosed; however, the prevalence is estimated to be 5 million cases. Druginduced liver injury accounts for 10% of acute hepatitis cases. We present a case of simultaneous presentation of acute pancreatitis and acute hepatitis due to drug-induced injury and concomitant alcohol use. Case Report: A 49-year-old male with a history of previously compensated alcohol-induced cirrhosis and seizures managed with carbamazepine had a physical exam significant for icterus, with upper right quadrant and epigastric pain. Laboratory investigations demonstrated a lipase of 174 U/L, AST of 215 U/L, ALT of 97 U/L, ALP of 218 U/L, total bilirubin of 8.9 mg/dL, creatinine of 0.8


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Abstracts mg/dL, and INR of 1.14. Maddrey’s discriminant function (MDF) was 19 and MELD score was 16. A CT of the abdomen demonstrated acute pancreatitis, cirrhotic liver, and an absence of gall stones. Over his hospital course, the MDF increased to 31 and the MELD to 19. Acute pancreatitis resolved with cessation of carbamazepine and bowel rest. Liver biopsy showed moderate mixed steatosis, mild cholestasis, ballooning hepatocytes, neutrophils consistent with acute pericholangitis in the background of bridging, and pericellular fibrosis. The patient recovered with the above conservative management. Discussion: Although it is rare for acute pancreatic and liver disease to present simultaneously, the liver and pancreas are developmentally related in structure and function. Disease in each organ occurs via activation of stellate cells, parenchymal damage, and fibrosis. This patient’s low MDF score on admission supported that a second insult complicated his presentation of liver disease. Carbamazepine can cause pancreatitis and cholestatic hepatitis. Carbamazepine-induced hepatitis is rare, occurring in 16 cases/10,000 treatment years, usually within 6 weeks of treatment, but can occur up to 6 years after. Carbamazepine-induced pancreatitis is also rare, as causality has been reported via medication re-challenge. Our patient had resolution of pancreatitis and improvement in liver function with cessation of carbamazepine and alcohol. Although rare, a simultaneous presentation of pancreatic and liver disease due to a multifactorial etiology must remain in the differential for patients with use of alcohol and antiepileptics.

1242 Treatment of Duodenal Variceal Hemorrhage With Endoscopic Band Ligation Tripti Chopade, MD, Dina Halegoua-De Marzio, MD, Ali Siddiqui, MD, Jesse Civan, MD, Jonathan Fenkel, MD. Department of Medicine, Division of Gastroenterology and Hepatology, Thomas Jefferson University, Philadelphia, PA. Introduction: Duodenal varices (DV) are a rare but potentially serious complication of portal hypertension due to high risk of massive gastrointestinal bleeding. Case Report: A 52-year-old male with a past medical history of idiopathic non-cirrhotic portal hypertension since childhood was transferred to our hospital for management hematemesis and melena. His medical history was significant for recurrent gastric and esophageal variceal bleeds, which were treated with sclerotherapy. He underwent splenorenal shunt surgery and splenectomy approximately 23 years ago with good response. Abdominal contrast tomography demonstrated evidence of thrombosis of main portal vein and right hepatic vein, precluding the management with trans-jugular intrahepatic porto systemic shunt (TIPS). The patient’s hemoglobin was 7.4 at admission, despite receiving 5 units of packed red blood cells (RBCs) at another hospital. He underwent esophagogastroduodenoscopy (EGD) with visualization of spurting DV in the second part of duodenum (Figure 1). Endoscopic band ligation (EBL) of DV with 1 band was performed and hemostasis achieved. Post-EBL patient was hemodynamically stable, and his melena resolved. Follow-up EGD 2 weeks later showed of obliteration of the banded DV. Surveillance EGD 5 months later showed complete regression of banded DV with scarring at the site and non-bleeding varices on the opposite duodenal wall. Discussion: EBL is widely accepted as a primary therapy for esophageal variceal bleeding; however, there is no widely accepted treatment modality for duodenal varices. Blood flow in duodenal varices is frequently high, and results in profuse bleeding. Prognosis is poor, with mortality rates as high as 40%. With this case, we share our experience of successful EBL as a treatment for DV hemorrhage in a patient where other modalities, such as TIPS, are impossible or contraindicated. However, one must monitor for the formation of additional varices in other intestinal sites after EBL with surveillance endoscopy or capsule endoscopy.

1243 Glyburide-Induced Cholestatic Hepatitis Jennifer Phemister, MD, Aaysha Kapila, MD, Pranav Patel, MD, Jason Mckinney, DO, Mark Young, MD. East Tennessee State University, Johnson City, TN. Introduction: Glyburide is a second generation sulfonylurea commonly used in the treatment of type 2 diabetes mellitus. The most common side effects include hypoglycemia, gastrointestinal disturbances, rashes, and nocturia with rare reports of hepatotoxic effects of glyburide - hepatic cholestasis, granulomatous hepatitis, and liver failure. Approximately 1% of drug-induced liver disease is caused by sulfonylurea derivatives, which are either predominately parenchymal or cholestatic in nature. Early recognition of an idiosyncratic drug reaction to glyburide is essential to prevent the reversible hepatic injury. We hereby present a case of a 35-year-old female with a past medial history significant for polycystic ovarian syndrome who presented to the primary care clinic with fever and malaise for 10 days, which was unrelieved by a 1-week course of Keflex. She was also found to have elevated blood glucose levels of 319 mg/dL and A1c of 10.2%. She was started on glyburide. After the first dose, the patient developed nausea and vomiting. Lab work done at the urgent care was significant for deranged liver function tests, prompting the admission to the hospital. On initial exam, the vitals were significant for pulse 112/min, blood pressure 103/60 mm Hg, and temperature 100.8 F. Physical exam was significant for mild abdominal distention with no tenderness to palpation. Labs revealed WBC-15.3 K/uL, hemoglobin/Hematocrit 12.5 g/dL/35.8 %, a cholestatic pattern with total bilirubin 1.9 mg/dL, alkaline phosphatase 286 U/L, AST 56 U/L, and ALT 73U/L. Viral hepatitis panel and HIV markers were unremarkable. Anti-mitochondrial antibody, smooth muscle antibody, myeloperoxidase antibody, and anti-neutrophilic antibody were negative. Ultrasound and computed tomography scan ruled out any evidence of obstruction. Hepatobiliary iminodiacetic acid scan was also negative for any signs of cholecystitis or obstruction. Based on imaging and clinical presentation, diagnosis of an idiosyncratic reaction to glyburide resulting in cholestasis was established. The patient stopped glyburide and initiated insulin for glucose control, leading to resolution of symptoms and improvement of the liver functions. On 2 weeks’ follow-up, there was normalization of liver enzymes. After the detailed discussion, the patient was agreeable to take the drug re-challenge, which confirmed the glyburide-induced cholestatic pattern of liver injury on re-exposure.

1244 The Wrong Side: A Rare Case of “Wandering Liver” Srinivas Guptha Gunturu, MD, Dipti Sagar, MD, Hilary Hertan, MD, FACG. Albert Einstein University/ Montefiore Medical Center, Bronx, NY. Introduction: A 78-year-old male presented with abdominal pain and diarrhea of 2 days’ duration. His PMH included congestive heart failure, alcohol abuse, hypertension, and psychosis. Abdominal examination was significant for right upper quadrant (RUQ) and rebound tenderness with no guarding or rigidity. Labs: total bilirubin 2.3 mg/dl (normal: 0.2-0.1mg/dl), direct bilirubin 2.2 mg/dl (normal: 20.0 mg/dL. Viral hepatitis serologies, antimitochondrial antibody, anti-liver-kidney microsomal antibody, antinuclear antibody, and anti-smooth muscle antibody were negative. IgG level normalized. Her thyroid stimulating hormone (TSH) was 20,000 U/L), ALT (4,516 U/L), ALP (1,120 U/L), total bilirubin (12.8 mg/dL), PT/INR (26.2/2.41), lipase (11,981 U/L), lactic acid (18.1 mg/dL), LDH (>6,000 U/L), and uric acid (14.8 mg/dL). Toxicology was negative for alcohol, acetaminophen, and aspirin. Serology was negative for HAV, HBV, HCV, HIV, EBV, CMV, ANA, Anti-Sm, AMA, RPR, and leptospirosis. Abdominal ultrasound and CT abdomen showed marked hepatosplenomegaly, thickened gallbladder wall, and intra-abdominal lymphadenopathy. Within 24 hours after transfer, she went into PEA arrest and resuscitation efforts fell short. Autopsy revealed a pulmonary embolism as the immediate cause of death. There was widespread infiltration of the liver, spleen, lymph nodes, lungs, kidneys, and bone marrow by sheets of large atypical lymphocytes with irregular nuclear folds. Immunohistochemical stained positive for CD 45, CD 10, CD 79a, BCL-2, and CD 20, leading to a diagnosis of DLBCL of germinal center type. Conclusion: This case illustrates a rare presentation of ALF secondary to malignant infiltration. This diagnosis is often overlooked because of low incidence and nonspecific clinical, laboratory, and imaging findings. Most patients are diagnosed on autopsy. A high index of suspicion can provide early diagnosis and treatment, and thus improve survival in aggressive hematological malignancies.


1251 Two Diseases, One Treatment: The Challenges Faced When Treating an Overlap Syndrome Mervin Figueroa-Pinto, MD, Ivan Antúnez, MD, Rafael Pastrana, MD, Carmen González-Keelan, MD, Esther Torres, MD, FACG. University of Puerto Rico School of Medicine, San Juan. Introduction: A 53-year-old female with arterial hypertension and bronchial asthma complained of abdominal pain for the past 4 months. The pain was epigastric, stabbing, 10/10, irradiating to the lower abdomen, lasting hours to days, not associated to food, and without any improving or worsening factors. This was accompanied by nausea and 2-3 episodes of vomiting per day, of gastric content without blood or bile. She had anorexia with an 8-pounds loss in 6 months, general malaise, weakness, fatigue, itching, joint pain (wrist, elbow, and knee), dry mouth and eyes, and occasional swelling of her legs. She also complained of a red rash throughout the body, and hyperpigmentation of the arms. She used alcohol daily for 30 years and smoked 10-15 cigarettes each day, but quit both 5 years ago. Physical exam showed an overweight patient with a body mass Index of 28.7 kg/m2. Scattered bilateral forearm hyperpigmented areas and erythematous blanching papules were present in the chest and extremities. The abdomen showed no distention, normal bowel sounds, diffuse tenderness to deep palpation, no rebound tenderness, no palpable spleen, resonant percussion, a liver span of 11 cm, and no shifting dullness. Laboratories showed normal CBC, prothrombin time, and partial thromboplastin time. Aspartate and alanine aminotransferases were 308 and 407 IU/L respectively, alkaline phosphatase was 467 IU/L, total bilirubin was 1.25 mg/dL, and globulins were 8.3 g/dL. Hepatitis serology, lipid panel, iron studies, and anti-nuclear antibody were normal. Anti-mitochondrial antibody titers were 1:640 and immunoglobulin M was 425 mg/dL. Abdominal sonogram showed a liver normal in size, echotexture, and echogenicity without any focal mass. Liver biopsy showed chronic portal inflammation (confluent necrosis) with lymphocytes and plasma cells suggestive of autoimmune hepatitis, and bile duct destruction and loss suggestive of primary biliary cirrhosis. The diagnosis of overlap syndrome was made. On follow-up, improvement of liver enzymes without any therapy was noted. It was decided to start the patient only on ursodiol 15 mg/kg. After 4 months, there was a complete normalization of all liver chemistry. Deciding whether to target the autoimmune hepatitis or the biliary component is a challenging decision for the clinician. Individual features usually guide the decision, and close observation of the response is necessary. Adequate response to therapy is not always obtained, even when combined therapy is given. Randomized clinical trials comparing single versus combined therapy for both diseases are necessary to define therapeutic guidelines for the overlap syndrome. Disclosure - Dr. Torres - Advisory board: AbbVie.

1252 Gastrointestinal Involvement of Systemic Amyloidosis Brijesh Patel, MD,1 Thure Caire, MD,2 Chris Nobo, MD,2 Patrick Brady, MD,2 Christopher Albers, MD,3 Jennifer Horkan, PA3. 1. Internal Medicine, University of South Florida, Tampa, FL; 2. University of South Florida Division of Digestive Disease, Tampa, FL; 3. Tampa General Hospital Department of Hepatology, Tampa, FL. Introduction: Amyloidosis presents with multiple organ system involvement at an annual incidence of approximately 3,000 cases in the U.S. It usually involves multiple organ systems, with the most common being renal and cardiac manifestations. Gastrointestinal (GI) system involvement is rare, occurring in approximately 3% of cases. Presentation may include hepatomegaly with or without splenomegaly and GI bleed; however, patients rarely present with GI bleed as the primary or sole symptom. We present a case of a patient who presented with symptoms of upper GI bleeding leading to esophagogastroduodenoscopy (EGD) and resultant biopsy diagnostic for amyloidosis. Case Report: A 72-year-old white male with PMH significant for peptic ulcer disease and coronary artery disease presented with 2 weeks of melena, fatigue, lower extremity edema, and increasing abdominal girth. In the emergency department, fecal occult blood testing was positive and the patient was admitted for suspected GI bleeding. EGD with biopsy was done, which revealed gastritis and polyps in fundus and body of stomach. Symptoms progressed to include acute renal failure with creatinine peaking at 1.6 mg/dL. Urinalysis showed nephrotic range proteinuria (>500 mg/dL). Pertinent labs included: AST 111 IU/L (5.0-34 IU/L), alkaline phosphatase 645 IU/L (40-150 U/L), serum albumin 1.5 g/dL (3.5-5.0 g/dL), and INR 1.3. Abdominal ultrasound showed ascites with a normal-appearing liver and normal-sized spleen. Ascitic fluid analysis resulted in a SAAG of 1.5 and protein of 0.8 g/dL, suggestive of portal hypertension. Gastric biopsy revealed amyloid deposits, positive for Congo red stain with apple green birefringence by polarized light. The patient underwent trans-jugular liver biopsy, which revealed near complete replacement of hepatic parenchyma with amyloid deposition confirming the diagnosis. The patient is currently being evaluated for further characterization, and pending studies include SPEP, UPEP, flow cytometry, skeletal survey, and bone marrow biopsy, which will dictate mode of treatment. Discussion: Amyloidosis is a systemic disease that may present with a constellation of symptoms. GI tract involvement with amyloid may result in occult bleeding in 45-75% of patients, which may be from ulceration, erosions, vascular fragility, and lack of vasomotor response. When present in the liver, amyloid may lead to portal hypertension and liver failure. In an infiltrative process such as amyloid, the elevation of alkaline phosphatase is most prominent. This is a rare case in which the presenting symptom of amyloidosis was GI bleeding and diagnosis was initially made by endoscopic biopsy.

1253 Unusual Liver Tumor in a Patient With Chronic Hepatitis C Shaina Lynch, DO. University of Connecticut, Farmington, CT. Introduction: Hepatoid adenocarcinoma is a rare alpha-feta protein-producing extrahepatic adenocarcinoma with morphologic characteristics closely resembling those of hepatocellular carcinoma. We present a case of hepatoid adenocarcinoma with an unknown primary tumor in a


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patient with a known history of chronic hepatitis C. A 57-year-old African American male with a past medical history of chronic hepatitis C presented to his primary care clinic for a routine visit. Elevated liver enzymes were noted on routine laboratory testing, and upon further investigation, the patient was found to have a large hepatic mass. Liver biopsy was performed, and pathology demonstrated an immunohistochemical staining pattern with CD34 consistent with hepatocellular carcinoma-like features, as well as an immunohistochemical staining for AE1 AE3, CD20, and CDX2 consistent with metastatic adenocarcinoma. These pathology results were consistent with a diagnosis of metastatic adenocarcinoma with “hepatoid” adenocarcinoma features. Before the patient was able to undergo further work-up, he presented to the emergency department with acutely worsening abdominal pain. He was found to have a large intraperitoneal bleed secondary to rupture of the hepatic capsule, requiring almost complete embolization of the hepatic artery. Although rare, due to the aggressive nature and poor prognosis, hepatoid adenocarcinoma should be considered in patients with pathology not consistent with hepatocellular carcinoma, regardless of underlying chronic liver disease.

1254 Testicular Acute Hepatitis B-Related Polyarteritis Nodosa Emely Eid, MD, Juan Blum Guzman, MD, GI. UF Health Jacksonville, Jacksonville, FL. Introduction: Polyarteritis nodosa (PAN) is a necrotizing focal segmental vasculitis that affects medium-sized muscular arteries. Less than 1% of patients with hepatitis B virus (HBV) develop PAN. Survival rate at 1 year is worse in HBV-related PAN due to lethal GI complications. We describe a case of acute hepatitis B-associated PAN presenting with testicular pain. A 35-year-old African American male presented to the emergency department with a chief complaint of testicular pain for 2 months. He was previously treated for suspected epididymitis as an outpatient with a course of doxycycline. On physical examination, the patient was found to be afebrile, with a blood pressure of 169/104 mmHg and a heart rate of 94 bpm. He was anicteric, with a benign abdominal exam and right testicular pain elicited on palpation. On admission, labs showed: white blood cell count 14.7 thou/mm3, hemoglobin 11.4 g/dl, MCV 66.7, Cr 1.74 mg/dl, AST 202, ALT 188, alkaline phosphatasel, total bilirubin 0.9, urinalysis: protein 50. Testicular ultrasound with Doppler was ordered, showing a 0.3-cm x 0.4 cm x 0.4 cm ill-defined heterogeneous irregular mixed hypoechoic focus on the medial aspect of the right testicle, with a target/bull’s eye appearance, exquisitely tender to sonographic examination. Doppler images demonstrated increased vascularity. Urology was consulted for evaluation of testicular pain and abnormal testicular ultrasound. Pt tested negative for gonorrhea and Chlamydia; he was started on IV Ceftriaxone for empiric coverage; scrotal support/elevation was provided. The patient was admitted to medicine for workup of transaminitis and acute kidney injury concerning for possible vasculitis. Gastroenterology was consulted for evaluation of anemia and transaminitis. The patient tested positive for hepatitis B surface antigen and hepatitis B core antibody IgM, positive HBe antigen, and a HBV DNA viral load of 113,392.000 IU/mL. He had EGD and colonoscopy for work-up of anemia that showed a small hiatal hernia, gastric erosion, and erythema in fundus and body; 2-mm rectal polyp. Pathology revealed mild chronic gastritis. Urology performed right testicular biopsy, revealing vasculitis with associated thrombosis involving medium-sized muscular arteries most consistent with polyarteritis nodosa located on the superior medial region of the right testicle. The patient was then started on treatment for hepatitis B with tenofovir adjusted to his creatinine clearance. Rheumatology was consulted and recommended IV steroids, and later the patient was started on cyclophosphamide. After few days of treatment, there was a significant improvement on the patients liver enzymes. The patient will be followed in GI clinic to confirm viral suppression and conversion of HBeAg.

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Discussion: This case is an example as to how laboratory data in the right clinical setting can cause significant confusion among clinicians when dealing with a patient with Gilbert’s syndrome. The initial assumption was that the patient’s bleeding was secondary to portal hypertension and that TIPS would be necessary, when in fact, this would have provided no benefit to the patient. Given its high prevalence in the general population, it is important to always consider the possibility of Gilbert syndrome when dealing with a patient with hyperbilirubinemia without a clear etiology of cirrhosis.

1256 Mycoplasma Pneumonia: The Cause of an Obscure Cholestatic Hepatitis Arnaldo Freire, MD, MPH, Antonio Soto, MD, Rafael Tirado, MD, Maria Dueno, MD, Doris Toro, MD, FACG. Internal Medicine, Caribbean VA Healthcare System, San Juan. Introduction: Mycoplasma pneumonia (M. pneumonia) is one of the most common pathogens affecting the respiratory system. Extra-pulmonary manifestations including the cardiovascular, hematological, gastrointestinal, integumentary, and central nervous system had been reported. Only a few cases of M. pneumonia hepatitis are found on the literature. Being a rare condition, the exact pathogenesis of this manifestation is not well understood. M. pneumonia hematogenous liver invasion is implied as the putative cause. Here, we present a 32-year-old Puerto Rican man, previously healthy, who came for evaluation due to a 5-day history of intermittent stabbing-like right upper quadrant abdominal pain. He also complained of unquantified fever, generalized malaise, arthralgias, anorexia, and dark-colored urine. He denied sick contacts, recent travel, alcohol, or drug abuse. On physical exam, he was febrile, with generalized jaundice and a truncal macular rash. Upon lung auscultation, there were bibasilar ronchi; the liver was palpable and tender. Laboratory studies were remarkable for leukocytosis with shift to the left and cholestasis (total bilirubin 6.2 mg/dL, alkaline phosphatase 227 U/L, aspartate aminotransaminase 117 U/L, alanine aminotransferase 187 U/L, gamma glutamyl transferase 176 U/L). Chest x-Ray showed left basilar interstitial infiltrates and bilateral pleural effusions. Abdominal ultrasound demonstrated hepatomegaly without biliary tree dilation. Common causes of viral hepatitis, such as HAV, HBV, and HCV were excluded. Serology for EBV and CMV were negative for acute infection. Acetaminophen levels, anti-smooth muscle, and anti-mitochondrial antibodies were negative. Ceruloplasmin and alfa-1-antitrypsin were normal. Mycoplasma IgM and IgG titers were 7,314 u/mL and 1,372 u/mL, respectively. The patient was initially treated with broad spectrum antibiotics, which were later deescalated to levofloxacin, completing 28 days of therapy. He responded very well to therapy, with complete resolution of jaundice and normalization of liver enzymes. To the best of our knowledge, this is the second case reporting M. pneumonia cholestatic hepatitis with lung involvement in the adult. Furthermore, our patient’s presentation included a macular rash, which was not present in the previous case report. Having a positive serology for M. pneumonia in the absence of all common causes of acute hepatitis makes our diagnosis very likely. The rapid improvement after proper antibiotic therapy also supports our diagnostic impression. This case illustrates a rare cause of cholestatic hepatitis that may be overlooked. For this reason, it is of utmost importance that we increase physicians’ awareness of the hepatic manifestations of M. pneumonia.

1257 Small Bowel Variceal Bleeding Secondary to Gyno-Enteric Shunt Kasra Adham, MD,1 Meho Jasarevic, MD,1 Michael Bern, BS,2 Jesse Davidson, MD,1 Vishal Patel, MD,1 M. Jonathan Bern, MD1. 1. medicine-GI, Virginia Tech Carilion School of Medicine, Roanoke, VA; 2. Washington University School of Medicine, St. Louis, MO. Introduction: A 70-year-old woman with a history of cirrhosis secondary to hemochromatosis and prior alcohol abuse (with long-term abstinence) was admitted for large-volume hematochezia. She had a history of esophageal variceal bleeding in the past, which was effectively treated with esophageal variceal

Previously Undiagnosed Gilbert Syndrome Causing Confusion in a Case of Hematemesis Secondary to Gastric Varices Neil Marya, MD, Joseph Charpentier, DO. Internal Medicine, University of Massachusetts-Worcester, Northborough, MA. Introduction: Gilbert syndrome is a relatively common condition affecting an estimated 4-16% of the population. It is mostly seen in males and diagnosed after adolescence. Gilbert syndrome is characterized by unconjugated hyperbilirubinemia without any pathologic abnormalities of the liver parenchyma. Patients with undiagnosed Gilbert syndrome can present with acute jaundice and may be subjected to needless interventions directed at the liver. We present a case of a 36-year old male with significant hematemesis with an associated hyperbilirubinemia. The clinical course illustrates how undiagnosed Gilbert syndrome can result in confusion leading to potentially needless invasive interventions. Case Report: A 36-year-old incarcerated male with a history prior heavy alcohol use (incarcerated 7 years ago) transferred to our institution for hematemesis and hypovolemic shock. At the outside hospital, the patient had 2 endoscopies demonstrating clot in the gastric fundus and findings suggestive of gastric varices. Given the history of alcohol use and findings of hyperbilirubinemia, the concern was that the patient’s variceal bleeding was secondary to chronic liver disease with decompensated portal hypertension and that the patient would require an emergent TIPS procedure. On arrival to our facility, lab work demonstrated an albumin 2.6 g/dL, total bilirubin 3.0 mg/dL, direct bilirubin 0.5 mg/dL, alkaline phosphatase 23 IU/L, AST 12 IU/L, ALT 10 IU/L, HGB 10.1 g/dL , INR 1.2, and a platelet count 69 th/mm3. The patient was started on medical therapy including continuous octreotide and pantoprazole infusions. Following a gastroenterology consult, a 4-phase CT scan of the abdomen was recommended. This demonstrated no focal or diffuse hepatic abnormalities or evidence of portal hypertension. It did demonstrate evidence of a main splenic vein thrombosis with significant large splenic varicosities and gastric mucosa varices. Following this finding, the patient was consulted by general surgery who performed a splenectomy. The patient’s unconjugated hyperbilirubinemia was attributed to a new diagnosis of Gilbert’s syndrome.


[1257A] Figure 1. Small bowel varices with communication to the superior mesenteric vein and parametrial veins.


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Abstracts band ligation. Her last EGD and banding was performed 4 years prior to presentation with obliteration of esophageal varices. Two years prior to admission, she had a negative surveillance colonoscopy for a personal history of colon polyps. A bleeding scan was performed shortly after admission. Accumulation of radiotracer was noted in the right lower quadrant, suggesting active hemorrhage from the distal small bowel or right colon. Mesenteric angiography was performed with the intention of hemostasis following the positive bleeding scan. A clear bleeding site was not identified. At this point, the patient had received 20 units of red blood cells, several units of FFP, and vitamin K. The platelet count remained above 60 K/μL. She did not receive platelet transfusion. Her fibrinogen level was normal. As the site of bleeding remained unclear, a colonoscopy was performed to the distal 30 cm of ileum. This demonstrated blood clots and fresh blood to the proximal extent of the exam. EGD was performed using a pediatric colonoscope. The proximal 80 cm of small bowel was examined. EGD-enteroscopy did not demonstrate a clear bleeding source. No esophageal or gastric varices were seen. To further define the bleeding site, abdominal and pelvic CT angiography was performed. A portosystemic shunt between the parametrial veins and the superior mesenteric vein was identified (Figure 1). A partial portal venous thrombosis was also seen. The patient was taken to the operating room for exploratory laparatomy. The involved segment of small bowel was resected and suture ligation of the shunt was performed. Following surgery, there was no further hematochezia.

1258 Acute Liver Injury of Rare Etiology: Hemophagocytic Lymphohistiocytosis Amit Mori, MD,1 Dipendra Chaudhry, MD2 1. Transplant Hepatology, Carolinas Medical Center, Charlotte, NC; 2. Wake Forest School of Medicine, Winston-Salem, NC. Introduction: A 40-year-old man presented with jaundice, malaise, and myalgias. About 2 weeks prior to presentation, he was exposed to sheet rock dust at work, leading to symptoms of sinusitis, and he was prescribed augmentin. His symptoms persisted and gradually worsened to severe jaundice, anorexia. There was no history of alcohol use, IV drug use, recent travel, or sick contacts. On exam, he had fever of 103.8°F, jaundice, hepatosplenomegaly, and faint pink skin rash on both ankles. His pertinent laboratory findings included bilirubin of 10 (direct bilirubin 3.4), alkaline phosphatase 218, AST-905, ALT-1654, INR-1.8, ANC of 900, platelets 44,000, and Hb 7.9. An abdomen US showed mild hepatosplenomegaly without evidence of biliary obstruction and a chest x-ray showed hazy right lower lobe nonspecific opacity. Further work-up with pertinent findings included elevated LDH (997), positive ANA with titers >1280, elevated ACE level of 154, ferritin of 24,680, and triglycerides of 358. A peripheral smear showed mild lymphocytosis raising concerns for HLH, and the patient underwent bone marrow biopsy that showed trilineage hematopoiesis with histiocytic proliferation and hemophagocytosis (Figure 1) confirming diagnosis of HLH. As a work-up for possible underlying trigger of HLH, further laboratory findings included a negative hepatitis panel including HBV DNA, HIV, CMV,HSV,EBV, parvovirus B19, negative CSF findings, RMSF serology, and negative findings for other tick borne diseases. Autoimmune work-up was negative (except positive ANA and ACE level, as above) that included anti-smooth muscle antibody, anti-mitochondrial antibody, quantitative immunoglobulin levels, C-ANCA, and P-ANCA. He was empirically treated with doxycycline for his possible pneumonia, underlying tick-borne disease. His liver functions gradually improved along with cytopenia, and thus he did not undergo liver biopsy. A primary diagnosis of HLH is made with possible autoimmune trigger, but unfortunately the specific underlying disorder remains uncertain. The patient was treated with doxycycline and prednisone, and clincally improved gradually over next few weeks with normalization of his liver functions.

1259 Hepatolithiasis: A Cause for Persistent Abdominal Pain That Escaped MRCP Frank Senatore, MD,1 Ankeet Bhatt, BS,1 Houman Rezaizadeh, MD,1 Murali Dharan, MD, FACG2 1. University of Connecticut School of Medicine, Farmington, CT; 2. St. Francis Medical Center, Hartford, CT. Introduction: We report a case of a 37-year-old female with a past medical history of open cholecystectomy in 2004, ERCP with drain placement for biliary stones in 2005, and hepaticojejunostomy via Roux-en-Y for a severely strictured common bile duct in 2006, who presented to the ED with a 2-day history of right upper quadrant abdominal pain. Her recurrent chronic pain that predated surgery had recently worsened. Her symptoms were worse with deep inspiration and were associated with nausea and non-bloody emesis, though she denied fevers, dark colored urine, acholic stools, or changes in bowel habits. On exam, she was hemodynamically stable with right upper quadrant tenderness, hepatomegaly, and a positive Murphy’s sign. Laboratory investigation demonstrated normal AST, ALT, ALP, and bilirubin levels. Initial imaging with ultrasound and CT scan revealed distended intrahepatic biliary ducts in the right lobe without an identifiable cause. Upper endoscopy showed a normal esophagus, stomach, and duodenum; further evaluation with ERCP was limited due to her prior hepaticojejunostomy. Her pain continued to progressively worsen. Due to persistent progressive pain, MRCP was performed with findings of right hepatic lobe intrahepatic ductal dilatation, right lobe atrophy, and left lobe hypertrophy, without evidence of filling defect, mass, or stricture. Despite the negative MRCP, the patient’s persistent symptoms lead to further investigation with an IR guided percutanous cholangiogram. This revealed dilated right hepatic ducts were multiple filling defects consistent with hepatolithiasis. An internal/external biliary drain was placed for decompression. Due to the persistence of the intrahepatic stones, the patient was scheduled for biliary endoscopy with lithotripsy. At 2-week follow-up, after the lithotripsy, the patient was pain free. This case illustrates a relatively rare cause of a common complaint: hepatolithiasis causing right upper quadrant abdominal pain. While the established sensitivities and specificities for MRCP detecting hepatolithiasis and biliary strictures are 97% and 99% respectively, the identification of hepatic stones on percutanous cholangiogram in this patient illustrates the importance of clinical judgment over investigative results in pursuing further management, especially in patients with ongoing symptoms of unclear etiology and a complex surgical history.

1260 The Cat Is Out of the Bag: A Case of Disseminated Bartonella henselae Mimicking Post-Transplant Lymphoproliverative Disorder David Chascsa, MD, Darryn Potosky, MD. University of Maryland, Baltimore, MD. Introduction: A 61-year-old man status post orthotopic liver transplant in 2008 for hepatitis C cirrhosis, requiring redo transplantation that same year for hepatic artery thrombosis, presented in November of 2013 with a newly elevated alkaline phosphatase level. His post-transplant course had been complicated by fibrosing cholestatic hepatitis C, treated with pegylated interferon and ribavirin, resulting in a sustained virologic response. Despite successful treatment, mild abnormalities in his liver tests persisted. Subsequent work-up included a complete serologic evaluation for other causes of liver disease, ERCP without obstruction, and liver biopsy showing non-specific hepatitis. Upon presentation to clinic, the patient complained of malaise and poor appetite. He was found to have a markedly elevated alkaline phosphatase level of 854 units/L; his prior baseline had been between 150 units/L and 200 units/L. He was admitted to the hospital, where a liver transplant ultrasound revealed a splenic lesion. Follow-up MRI confirmed a 2 cm x 1 cm splenic lesion and also found periportal lymphadenopathy, raising concern for post-transplant lymphoproliferative disorder (PTLD). His Epstein Barr (EBV) PCR was found to be 6,000 copies/mL; previously, it had been negative. Positron emission tomography scan found hypermetabolic lesions within the spleen and adjacent to the liver along with metabolically active lymphadenopathy. The lesions were not amenable to endoscopic ultrasound-guided fine needle aspiration. Biopsy of the spleen showed acute inflammation and focal granuloma suggestive of an infectious pathology. EBV-encoded small nuclear RNA staining was negative. Further history discovered that the patient lives on a farm and takes care of feral cats. Given this, the specimen was sent for Steiner staining, which revealed coccoid organisms concentrated in the granulomatous area suspicious for bacillary angiomatosis. Serum bartonella IgG titer was greater than 1:2560. The patient was started on doxycycline, as azithromycin was contraindicated in the setting of his prolonged QT interval. His immunosuppression goals were decreased. The patient‘s alkaline phosphatase levels normalized with treatment. Elevated alkaline phosphatase levels are common after liver transplantation and require thorough evaluation. Potential etiologies include acute cellular rejection, cholangiopathy, malignancy, and infection. In the setting of an elevated serum, EBV, PCR, and lymphadenopathy, PTLD must be considered. This case points to the importance of considering infectious etiologies of abnormal liver function tests in post-transplant patients, as well as the need for a tissue diagnosis when evaluating a patient for PTLD.

1261 Sofosbuvir Plus Simeprevir for the Treatment of Recurrent Hepatitis C With Fibrosing Cholestatic Hepatitis After Liver Transplantation

[1258A]

Figure 1. An RBC and platelets within histiocytes.

ACG Clinical Vignette Award Presidential Poster Danny Issa, MD,1 Bijan Eghtesad, MD,2 Nizar Zein, MD, FACG,2 Naim Alkhouri, MD, FACG,2 Richard Adams, RN,2 Ibrahim Hanouneh, MD, FACG2. 1. Cleveland Clinic, Department of Internal Medicine Fairview Hospital, Cleveland, OH; 2. Cleveland Clinic, Digestive Disease Institute, Cleveland, OH. Introduction: Fibrosing cholestatic hepatitis (FCH) is an aggressive form of hepatitis C virus (HCV) recurrence after liver transplantation (LT), which frequently results in graft failure and death. Treatment of FCH remains challenging, and the optimal antiviral therapy for this particular pattern of HCV is yet to be determined.



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Case Report: We report 3 cases of recurrent HCV with FCH in LT recipients treated with a combination of 2 direct-acting antiviral drugs. All 3 patients had genotype 1 HCV, and received the same treatment (Rx) regimen of sofosbuvir (400 mg/day) and simeprevir (150 mg/day), co-administered for 24 weeks. The first patient was a 68-year-old female previously a non-responder to interferon and ribavirin, who developed recurrent HCV with severe FCH at 2 months post-LT. A pre- Rx HCV viral load of >40,000,000 IU/mL decreased to 596 IU/mL at week 4, and then to 58 IU/mL at week 6 of Rx, then became undetectable at week 12 and remained undetectable at week 24 of Rx. The patient had a delayed but remarkable biochemical improvement with bilirubin decreasing from 40.8 mg/dL pre- Rx to 2.1 mg/dL at week 12 of Rx. At week 4 of Rx, the patient had an episode of allograft acute cellular rejection and responded well to high doses of steroids. A course of Rx was complicated by self-limiting acute pancreatitis of uncertain etiology and refractory pruritus. The second patient was a 56-year-old female who received LT for HCV and developed FCH at 9 months post-LT. The HCV viral load improved from >9,120,000 IU/mL pre- Rx to 43 IU/mL at week 4, then became undetectable at week 6 and remained undetectable at week 24. The patient had complete normalization of liver enzymes at week 2 of Rx and has experienced no adverse events. The third patient was a 62-year-old male with multiple co-morbidities who had LT for HCV complicated by FCH at 4 months post-LT. Pre- Rx HCV viral load of >69,000,000 IU/mL decreased to 3,200 IU/mL at week 2 and became undetectable at week 6 of Rx. His liver biochemistries improved markedly at week 6 of Rx with pre-treatment bilirubin of 21 mg/dL decreased to 6.7 mg/dL. However, the patient developed hepatic artery thrombosis complicated by sepsis. He was admitted to ICU and died of multiorgan failure. Conclusions: The combination of sofosbuvir and simeprevir is an efficacious oral regimen in LT recipient with recurrent hepatitis C and FCH. However, safety profile needs to be carefully evaluated. Further studies are needed to better address the optimal treatment in this patient population.

embolization contrast study demonstrated elimination of fistula. The procedure was without complications and well tolerated. Discussion: Liver biopsy plays an important role in managing patients with chronic liver diseases. Type 2 hepatoportal fistula is a rare but serious complication from liver biopsy. This case demonstrated the importance of color Doppler ultrasonography in detection of hepatoportal fistula. Furthermore, preemptive treatment with radiological guided embolization can prevent development of portal hypertension and its complications.

1262 Blue Cell Tumor of Liver Bhavtosh Dedania, MBBS,1 Shounak Majumder, MBBS,1 Murali Dharan, MD2. 1. University of Connecticut Health Center, Farmington, CT; 2. Saint Francis Hospital, Hartford, CT. Introduction: Liver is a common extra nodal site of involvement in lymphomas. However, primary hepatic lymphoma (PHL) is a rare tumor, representing less than 0.05% of all cases of non-Hodgkin’s lymphoma (NHL). Case Report: An 84-year-old woman with history of coronary artery disease, hypothyroidism, internal hemorrhoids, and colon cancer status post partial bowel resection presented to the ER with complaints of abdominal discomfort, constipation, and significant weight loss. She was a former smoker, but denied any alcohol abuse. Physical examination revealed conjunctival pallor and non-tender hepatomegaly. Laboratory studies revealed normal liver function tests, negative hepatitis serology, and normal levels of alpha-feto protein and carcino-embryonic antigen. Contrast-enhanced CT scan of abdomen showed a 10 x 5.1 x 7.5 cm mass in the right hepatic lobe. Subsequent liver biopsy showed a high-grade c-Myc-positive NHL of liver. The microscopic findings included diffuse proliferation of small and medium-sized “blue cells” showing round to indented nuclear contours, delicate chromatin, inconspicuous basophilic nuclear material, and scant clear pink cytoplasm. The majority of the small blue cells in the neoplasm expressed CD20 and CD5 consistent with a B cell lymphoproliferative process. Ki67 index was more than 95%. Fluoroscopic in-situ hybridization (FISH) analysis for cMyc gene arrangement was consistent with high-grade B cell lymphoma of Burkitt’s type. The patient underwent staging positron emission tomography (PET) scan and bone-marrow biopsy were negative for extra hepatic disease. The patient was treated with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) immuno-chemotherapy for 6 cycles. A follow-up PET scan done at 6 months showed marked interval improvement and no abnormal foci of increased FDG uptake in the liver. Discussion: PHLs are rare. Of all PHLs, primary diffuse large B-cell lymphoma (DLBCL) is the most common variant, found predominantly in middle-aged white males. Pre-existing chronic hepatitis B or C infection is a known risk factor. A high Ki-67 index is considered a poor prognostic marker. Although c-Myc positivity is classically associated with Burkitt’s lymphoma, a few cases of c-Myc positive DLBCL have been reported. There is very limited data to guide management in patients with PHL, especially in cases with atypical features, like our patient. Although more aggressive chemotherapy regimens were considered, she was treated with R-CHOP in view of her age and limited extent of disease. This case highlights the importance of reporting treatment outcomes in patients with PHL in an attempt to develop an evidence-based approach to the management of these rare tumors.

1263 Pre-emptive Embolization for Post-liver Biopsy Asymptomatic Type 2 Hepatoportal Fistula Youran Gao, MD, Craig Greben, MD, Anupama Duddempudi, MD, FACG, Tai-Ping Lee, MD, FACG. North Shore- LIJ, Manhasset, NY. Introduction: Hepatoportal fistula is an arteriovenous communication between the splanchnic artery and the portal vein that can be either congenital (type 3) or acquired (type 1 small peripheral and type 2 large central). Type 1 is usually transient and asymptomatic, whereas type 2 can cause portal hypertension and its complications of variceal bleed or ascites. Herein, we present a case of type 2 hepatoportal fistula developing after liver biopsy and its management. Case Report: A 75-year-old woman with autoimmune hepatitis with overlap syndrome was seen at a follow-up visit. She underwent an ultrasound-guided left lobe liver biopsy 1 year ago for worsening liver enzymes. The biopsy was without complications. A routine ultrasound of the abdomen with color Doppler at this follow-up showed a moderate to large communication of the left hepatic artery with the left portal vein with reverse flow on color Doppler ultrasonography. Although the patient was asymptomatic, she was referred to interventional radiology for embolization due to the size of the fistula. Segment 2 of the left hepatic artery was successfully embolized using 0.3 cc 40% n-butyl-2-cyanoacrylate. A post-


[1263A] Figure 1. Hepatoportal fistula post embolization with n-butyl-2-cyanoacrylate.

1264 Management of Massive Parastomal Variceal Bleed by Minimally Invasive Percutaneous N-butyl-2cyanoacrylate Embolization Youran Gao, MD, Tai-Ping Lee, MD, FACG. North Shore- LIJ, Manhasset, NY. Introduction: Parastomal variceal bleed is a serious problem in patients with surgical stomas and portal hypertension. They are difficult to manage due to challenges in hemorrhage control and tendency to rebleed. We present a case of massive parastomal variceal bleed successfully treated using fluoroscopic guidance injection of N-butyl-2-cyanoacrylate (NBCA). Case Report: A 56-year-old man presented to the emergency department with profuse bleeding from colostomy site. The patient had significant history for alcoholic cirrhosis and post-colostomy from Hartmann’s procedure for diverticular bleed 10 years ago. He failed 2 previous attempted closure of colostomy due to bleeding diathesis. He had numerous recurrent parastomal bleed requiring multiple blood transfusions, treated by silver nitrate cauterization and suture ligation. On admission, Hb was 4.6. Parastomal bleeding was severe, requiring 14 units of PRBC despite topical surgical ligation and cauterization. A CT angiogram to assess for parastomal variceal bleed was requested by the liver team, which showed an extensive network of varices adjacent to the left lower quadrant ostomy draining into an enlarged inferior mesenteric vein. Transjugular intrahepatic portosystemic shunt (TIPS) was considered, but the patient was deemed not a candidate due to moderate aortic stenosis, mild pulmonary hypertension, and MELD of 17. Instead, he underwent radiology-guided embolization by using sonographic guidance. Varices were confirmed and venography revealed a network of varices overlying the ostomy. Under fluoroscopy, 2 cc NBCA was injected percutaneously into the varicose veins at 2 locations, respectively. The embolization was successful without complication. Hemoglobin remained stable at 8.6 over the next 3 days. He was discharged and had no parastomal bleeding over the past 4 months. Discussion: Parastomal variceal bleed should be highly suspected in patients with cirrhosis and portal hypertension. TIPS has been recommended for control of stomal variceal bleeding. However, our case demonstrated that percutaneous fluoroscopic embolization with NBCA is a simple, safe, and effective procedure in control of parastomal variceal bleed when TIPS was infeasible.

1265 Hepatic Adenomatosis Presenting With Transaminitis and New Onset Diabetes Mellitus Sara Ancello, DO, Ellen Kurkowski, DO, Alan Shienbaum, DO. Rowan University School of Osteopathic Medicine, Stratford, NJ. Introduction: Hepatic adenomatosis (HA) is a rare, benign, hepatic neoplasm consisting of greater than 10 hepatic adenomas in an otherwise normal parenchyma. Incidence is unknown, as HA is


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Abstracts mainly documented in case reports. Patients may be asymptomatic or present with a number of complications, such as hepatic necrosis or intra-peritoneal hemorrhage from lesions >4 cm. Etiology is poorly understood, and some sources suggest a genetic link, supported by a possible association with maturity onset diabetes of the young (MODY). Treatment may require conservative surgical management for larger lesions or transplant in rare cases, as HA carries with it a 10% risk of malignant transformation to hepatocellular carcinoma. Patients should follow with a specialist and obtain regular imagining studies to monitor for complications and malignant transformation. Family members should undergo genetic screening. Further data must be compiled to better understand the genetic basis of HA, as well as the role of endogenous and exogenous steroids. We present the case of a 21year-old Vietnamese female found to have elevated transaminases and blood glucose during her stay, who was ultimately diagnosed with HA and new onset diabetes mellitus. This case provides evidence in support of a genetic etiology of HA, as well as the association between HA and glucose intolerance. Adequate follow-up and cancer surveillance will likely result in improved clinical outcomes for patients with HA.

1266 De Novo Primary Sclerosing Cholangitis (PSC) Post Liver Transplantation for Alcoholic Cirrhosis Presidential Poster Shiva Kumar, MD, FACG. Liver Transplant Program, Aurora St. Luke’s Medical Center, Milwaukee, WI. Introduction: Primary sclerosing cholangitis (PSC) is a well-established indication for orthotopic liver transplantation (OLT). Recurrence of PSC has been well documented post OLT and can lead to allograft loss and the need for consideration of re-transplantation. However, de novo PSC in patients transplanted for other indications has never been reported before. We describe the first case of de novo PSC in a patient who had undergone OLT for alcoholic cirrhosis. A 54-year-old male underwent OLT in June 2010 for end-stage liver disease secondary to alcoholic cirrhosis. The patient had no history of PSC or inflammatory bowel disease (IBD) prior to OLT. Careful examination of the explant revealed evidence of cirrhosis with no histological features suggestive of PSC. He was noted to have elevation in his liver tests 2 years post OLT and underwent an extensive evaluation, including doppler ultrasound and serologic tests, all of which were negative. He was on a stable immunosuppressive regimen with adequate trough levels of tacrolimus. Liver biopsy revealed bile ductular proliferation, mild peri cholangitis, and moderate concentric peri-ductal fibrosis. He subsequently developed severe diarrhea with blood, work-up of which confirmed a diagnosis of ulcerative pan colitis (UC) and a non-healing skin ulcer on his right leg above the medial malleolus. Work-up, including skin biopsy, confirmed a diagnosis of pyoderma gangrenosum (PG). Since his liver tests continued to remain elevated in a cholestatic pattern, ERCP was performed. This is an irregular stricturing of the intra-hepatic ducts with a ‘beaded’ appearance, radiographically diagnostic of PSC. This report described the first ever case of de novo PSC post-OLT in a patient transplanted for another indication. The diagnosis was based on a compatible liver profile, typical findings on cholangiography, and corroborative findings on liver histology. The natural history of de novo PSC OLT and the impact of immunosuppression on disease progression is unclear. Re-transplantation for allograft dysfunction due to de novo PSC post OLT has never been reported. Remarkably, this patient also developed UC and PG post-OLT, known extra-hepatic associations of PSC.

[1265A] Figure 1. Sagittal view of the liver on MRI showing multiple well-circumscribed hepatic lesions.

[1266A]

Figure 1.

1267 Oral Contraceptive-Induced Hepatic Sinusoidal Dilatation Shiva Kumar, MD, FACG. Liver Transplant Program, Aurora St. Luke’s Medical Center, Milwaukee, WI.

[1265B] lesion.

Figure 2. Transverse section during CT-guided needle biopsy of a hepatic


Introduction: Hepatic sinusoidal dilatation (HSD) is characterized by widening of hepatic capillaries that may involve the entire lobule or predominantly the central or periportal areas. Dilatation of the hepatic sinusoids is associated with several conditions, the most important being venous outflow obstruction. They have been reported to occur in association with medications. However, oral contraceptive (OCP)-induced hepatic sinusoidal dilation is exceptionally rare. A 39-year-old female who had been on OCP for more than a decade was referred for evaluation of mild right upper abdominal pain, hepatomegaly, and abnormal liver tests, specifically mild isolated elevation of alkaline phosphatase. Serological tests for other etiologies of chronic liver disease were all negative. Ultrasonography with Doppler analysis revealed hepatomegaly and normal appearing hepatic vasculature. MRI revealed hepatomegaly and post-gadolinium scans demonstrated heterogeneous enhancement of the liver, with greater enhancement in the periphery of the liver than in the more central portions, especially on the earlier phase scans. Liver biopsy showed prominent mid and centrizonal sinusoidal dilatation with accompanying atrophy of the hepatocytes (Figure 1) and mild peri-sinusoidal fibro-


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sis. Transjugular hepatic venogram was unremarkable, with no evidence of hepatic venous outflow obstruction. At follow-up 1 year after discontinuation of OCP, the patient remains asymptomatic with normal liver tests and normal contrast-enhanced MRI with reversal of changes noted on prior MRI scans. Repeat liver biopsy showed normal-appearing hepatic parenchyma with complete regression of hepatic sinusoidal dilatation. Hepatic sinusoidal dilatation in the absence of hepatic venous outflow obstruction has been reported in patients with tumors or granulomas, antiphospholipid syndrome portal-vein thrombosis, and rarely, medications. HSD is an exceptionally rare and often under-recognized manifestation of hepatotoxicity secondary to OCP. Although the natural history of HSD related to OCP is not clear, the presence of perisinusoidal fibrosis suggests risk of progressive liver disease with continuation of OCP. HSD appears to regress completely with prompt discontinuation of OCP.

[1268B]

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Figure 1.

Figure 2.

with a median survival of less than a year. Sorafenib, a multi-target tyrosine kinase inhibitor, is the only systemic treatment option known to prolong survival in advanced HCC and improve median survival from 7.9 to 10.7 months and time to progression from 2.8 to 5.5 months. Complete regression of locally advanced HCC with sorafenib monotherapy is exceptionally rare. Identification of tumor biomarkers may enable a more targeted approach to patients most likely to benefit from systemic therapy for HCC.

1269 Hepatocellular Carcinoma Secondary to Metabolic Syndrome: A Morbid Association of Concern

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Dovid Moradi, MD, Alfred Burger, MD, Faraj Faour, MD. Mount Sinai Beth Israel, New York, NY.

Complete Regression of Locally Advanced Hepatocellular Carcinoma (HCC) Following Sorafenib Monotherapy

Introduction: An 82-year-old Greek-born female who had been out of contact with an MD for 15 years but previously diagnosed with hypertension, hyperlipidemia, and obesity (BMI>30), was admitted after sustaining a slow fall to the ground. Physical exam was significant only for multiple ecchymosis on the right hip and elbows bilaterally. Labs showed a positive urinalysis, a T bili 3.3 mg/dL, alk phos 334 U/L, AST 138 U/L, and ALT 102 U/L. A right upper quadrant ultrasound was ordered to evaluate the abnormal liver function tests, and revealed multiple masses in the left hepatic lobe. A CT of the abdomen/pelvis confirmed masses extending from left to right hepatic lobes with portal vein occlusion. Testing was negative for hepatitis A, B, and C. INR was 1.1, alpha-Fetoprotein 48800 ng/mL, and CA19-9 77 U/mL. Liver biopsy showed carcinoma with clear cell features, favoring primary hepatocellular carcinoma (HCC) as the diagnosis. The patient was discharged to sub-acute rehab for her physical therapy and followed up as an outpatient with oncology. It was determined she was not a candidate for chemotherapy due to ongoing poor functional performance; she was then referred to home hospice and passed away 7 weeks after diagnosis. Her initial fall was attributed to a sensitive E. Coli UTI treated with a beta-lactam. We present a case of HCC in a patient with nonalcoholic fatty liver disease (NAFLD) and the metabolic syndrome without other traditional high-risk factors of HCC. Liver cancer is the fifth most common cancer in the United States and causes the third most cancer related deaths. Recently, hepatology research has begun focusing on causes of HCC other than viral hepatitis and alcoholic cirrhosis. NAFLD is reported to be associated with up to 27% of HCC cases in the United States. The prevalence of NAFLD is as high as 30% in the general population and 90% of those with morbid obesity (BMI>40). NAFLD is the direct result of chronic liver damage due to metabolic syndrome. According to the CDC, the prevalence of metabolic syndrome was 34% in the United States from 2003-2006, affecting up to 100 million people. Metabolic syndrome increases the risk of developing NAFLD 4-11 times compared to the general public. NAFLD increases the risk of developing HCC by 2.8%. As gastroenterologists, we must educate our physician colleagues who routinely manage the epidemic of obesity and the metabolic syndrome on a daily basis; this emerging and relatively newly described risk factor for HCC must be considered with abnormal labs. Although screening guidelines have not yet been implemented for this high-risk population, practitioners should use this information while educating patients in hopes of reducing future complications.

Shiva Kumar, MD, FACG. Liver Transplant Program, Aurora St. Luke’s Medical Center, Milwaukee, WI. Introduction: A 53-year-old male with chronic hepatitis C presented with abdominal pain and weight loss. Triple phase CT scan showed a nodular liver with hepatomegaly and arterial phase enhancement, suggesting significant hepatic tumor burden with an infiltrating lesion involving the entire left lobe, medial right lobe with a satellite subcapsular lesion, and left portal vein thrombosis (Figure 1). Serum alpha fetoprotein (AFP) was markedly elevated at 44,000 U/mL. Based on imaging characteristics and the degree of AFP elevation in the setting of cirrhosis secondary to HCV, a diagnosis of multifocal hepatocellular carcinoma (HCC) was made. The patient was not considered a candidate for liver transplant evaluation because of the degree of hepatic tumor burden with evidence of macro vascular invasion. Systemic therapy was initiated with sorafenib. He was also referred for consideration of radio-embolization (Yttrium-90), but refused. Sorafenib dosage was optimized at 400 mg by mouth twice daily. Follow-up imaging performed 8 months after initiation of systemic therapy revealed complete regression of the tumor, including the sub-capsular lesion and complete resolution of portal vein thrombosis (Figures 2). Laboratory studies showed a dramatic interval decrease in AFP level to 2 U/mL. Most patients with HCC present with advanced and multifocal disease at the time of diagnosis,

1270 Cholestatic Jaundice Due to Renal Cell Carcinoma: A Variant of Stauffer’s Syndrome Aaysha Kapila, MD, Pranav Patel, MD, Mark Young, MD. East Tennessee state university, Johnson City, TN.

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Figure 1.


Introduction: Renal cell carcinoma is associated with a wide spectrum of para-neoplastic syndromes, which may be precursors of primary or recurrent disease. Non-metastatic hepatic dysfunction in patients suffering from renal cell carcinoma is known as Stauffer’s syndrome, first described by Stauffer in 1961. Hepatic dysfunction without jaundice is commonly described in the literature, but paraneoplastic cholestatic jaundice is rare. A 65-year-old male with past medical history significant for end-stage renal disease on hemodialysis, diabetes, coronary artery disease, and congestive


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Abstracts heart failure presented to the hospital with jaundice, malaise, fatigue, poor appetite and abdominal discomfort for the last 2 weeks. The patient was a non-smoker and non-alcoholic with no family history of malignancy or liver diseases. Vitals were unremarkable on initial presentation. Physical examination was significant for mild tenderness in the right upper quadrant. Blood work demonstrated blood glucose 240 mg/dL, BUN-28 mg/dL, creatinine 1.91 mg/dL, total bilirubin 8 mg/dL, direct bilirubin-4.5 mg/dL, alkaline phosphatase-353 U/L, AST-45 U/L, and ALT-26 U/L. Complete blood count revealed white count-6.0 K/uL, hemoglobin-11.7 mg/dL, hematocrit-34%, and platelets182000 /μL. Initial urinalysis was significant for protein, glucose, trace ketones, 4+ urobilinogen, a large amount of bilirubin, and a small amount of blood. Ultrasound of the liver demonstrated thick-walled gallbladder with cholelithiasis and intraluminal sludge. Computed tomography of the abdomen with oral contrast demonstrated a 1.5-cm enhancing exophytic lesion in the lower pole of the right kidney (Figure 1). Thus, the radiological evaluation confirmed the diagnosis of renal cell cancer. The patient underwent surgery for RCC that resolved the hepatic dysfunction in 2-3 weeks post-surgery. Stauffer’s syndrome is associated with the production of cytokines by the tumor and several biochemical abnormalities, including elevated serum alkaline phosphatase. Hepatic dysfunction, in the absence of liver metastases, occurs in 10-15% of RCC and is attributed to the production of cytokines from the tumor, including interleukin-6. It is associated with fever, weight loss, and an unfavorable prognosis.

[1271A]

Figure 1.

1272 A Rare but Sinister Cause of Leukemoid Reaction: Alcoholic Hepatitis

[1270A] Figure 1. CT abdomen demonstrated a 1.5-cm enhancing exophytic lesion in the lower pole of the right kidney (marked by an arrow).

1271 Gas Forming Infection of the Spleen Charles Maltz, MD, PhD. Weill Cornell Medical College, New York, NY. Introduction: Air in the spleen has been well reported following splenic embolization. The incidence of infection in these patients has been reported to approach 50%. An emphysematous infection of the spleen without manipulation or trauma is quite rare, with only 1 case report in the literature. Here, we report a case of a man with air within the parenchyma of the spleen caused by a gas-forming bacterial infection. There was no preceding instrumentation or trauma. Case Report: A 38-year-old man with poorly controlled diabetes and obesity (BMI = 50) presented to the emergency department with fever and malaise. A CT scan of the abdomen and pelvis revealed hepatosplenomegaly and his blood count showed an atypical lymphocytosis. Serology for CMV was positive for IgM and he was discharged with the diagnosis of CMV mononucleosis. He gradually improved, but after several days, he developed the sudden onset of LUQ pain and fever to 39.5. A repeat CT scan again demonstrated hepatosplenomegaly, but with the new finding of a gas containing defect within the anterior tip of the spleen. This was associated with capsular and free intraperitoneal foci of gas, consistent with gas forming a splenic infection and subsequent rupture. He was treated with antibiotics, with subsequent blood cultures growing Clostridum perfringins. He eventually underwent splenectomy with the pathology of the spleen showing an abscess cavity involving the splenic parenchyma. Discussion: Infection of the spleen with a gas-forming organism has been reported once before in a patient who, like our patient, was a massively obese diabetic. Certainly poorly controlled diabetics are prone to life-threatening infections, yet there is only 1 report of such a gas forming infection of the spleen. The added risk factor here may be the massive splenomegaly, which appeared to be the result of an acute CMV infection. Reference: Landen S, Closset J . Gas-Producing Infection of the Spleen in a Super-Super-Obese Patient. Obesity Surgery 2007;17:1418-18.


Raman Khehra, MD,1 Cristina Strahotin, MD,1 Jose Oliva, MD,1 Jan Silverman, MD2. 1. Division of Gastroenterology, Allegheny General Hospital, Pittsburgh, PA; 2. Department of Pathology, Allegheny General Hospital, Pittsburgh, PA. Introduction: We are reporting a case of alcoholic hepatitis that presented with marked leukocytosis. A 41-year-old female with PMHx heavy alcohol abuse and depression presented with new onset jaundice, abdominal pain, and fever. Physical exam revealed RUQ tenderness and anasarca. She had marked leukocytosis; 51,150/mcl with 90% neutrophils (see table for other labs). Work-up revealed no source of infection. RUQ sonogram revealed cirrhotic morphology of liver and moderate ascites. Maddrey’s discriminant function was 44.1. She was started on prednisolone 40 mg orally, daily. Paracentesis revealed high SAAG and low protein ascites, but no SBP. MRCP showed no biliary pathology. Liver biopsy showed moderate to severe steatohepatitis with neutrophilic infiltration and bridging fibrosis. Lille model score was 0.85. There was minimal improvement in hyperbilirubinemia and leukocytosis with 28 days of prednisolone therapy. She was evaluated for liver transplant, but deemed to be a poor candidate. Her course was further complicated by recurrent episodes of hepatic encephalopathy. At 7 weeks, she developed terminal HRS and she was eventually placed on hospice care. Mild leukocytosis is common in alcoholic hepatitis (AH), but leukemoid reaction (LR) is extremely rare. Leukocytosis is mediated by TNF pathways. LR in AH predicts a grave prognosis. On review of

[1272]

Table 1. Trend of liver panel, CBC, and renal function Day 1

Day 29

WBC (/mcL)

51,150

42,930

Day 55 37,660

Platelets (/mcL)

434,000

198,000

107,000 2.9

INR

1.6

1.9

BUN (mg/dL)

30

50

87

Creatinine (mg/dL)

1.0

1.2

2.4

T. Protein (g/dL)

4.5

4.9

5.5

Albumin (g/dL)

2.6

3.1

3.3

T. Bili (mg/dl)

17.9

10.4

14.8

D. Bili (mg/dL)

12.6

6.4

9.5

Alk Phos (U/L)

197

97

129

ALT (U/L)

73

31

10

AST (U/L)

245

96

79


S375

S376

Abstracts

and erythrocytosis (18k). His medical history included HTN and a major vehicular accident (1978) that required left nephrectomy, splenectomy, and partial bowel resection. As part of the evaluation, an abdominal CT revealed changes of prior splenectomy and nephrectomy and a large (13 cm) heterogeneous, centrally necrotic enhancing mass lesion in the left upper quadrant, which was suggestive of a GIST. The CT also revealed a subtle 5.7-cm mass lesion in the dome of the liver, suspicious for possible metastatic lesion. Percutaneous biopsy of the liver lesion revealed intra-hepatic splenosis with aggregates of atypical B-cells. Flow cytometry was positive for clonal population of lambda light chain restricted B-cells, and B-cell clonality was positive by PCR, thus confirming the diagnosis of low-grade B-cell lymphoma, likely marginal zone, within intrahepatic splenosis. The LUQ mass lesion was biopsied via EUS-FNA and confirmed to be a GIST based on cytological features and immunohistochemistry profile. The patient was referred for surgical management of the GIST and chemotherapy for the lymphoma. Intra-hepatic splenosis itself is rare, but needs to be considered in the differential of hepatic masses, particularly in the setting of traumatic splenectomy. Lymphomatous transformation of intra-hepatic splenosis is extremely rare, with only 2 cases previously reported in the literature. The establishment of the correct diagnosis in our case avoided an uncessary surgical procedure for the liver lesion. Moreover, the finding of a large GIST caused an additional diagnostic challenge, but judicious sequential use of a percutaneous biopsy of the liver lesion followed by EUS-FNA of the GIST proved critical in establishing the correct diagnoses of 2 concurrent but distinct malignancies.

[1272A]

Figure 1. Steatohepatitis with Mallory body.

literature, AH associated with LR was fatal in 13 out of 14 reported cases. Given the extremely poor prognosis in this subgroup of patients, a special consideration should be given to liver transplant in carefully selected patients.

1273 Hepatic Epithelioid Hemangioendothelioma: A Rare Cause of Acute Liver Failure Danny Avalos, MD,1 Yanelba Toribio, MD,2 Julio Gutierrez, MD2. 1. University of Miami Regional Campus, Atlantis, FL; 2. University of Miami/Jackson Memorial Hospital, Miami, FL. Introduction: A 59-year-old previously healthy white female with a family history of hyper-homocysteinemia in a daughter presented with 4 weeks of worsening abdominal distention with ascites and lower extremity edema. Shortly after admission, she developed severe hepatic encephalopathy with respiratory and renal failure. The patient was icteric with a total bilirubin 25.9, AST 743, ALT 339, ALP 1,357, total protein 7.3, serum albumin-ascites gradient >1.1, and ascites total protein 5 cm) with good outcome and avoiding a surgical intervention.

1277 Glycogenic Hepatopathy: A Differential Diagnosis of Acute Hepatitis in Diabetes Mellitus Marco Silva, MD,1 Helder Cardoso, MD,1 Susana Rodrigues, MD,1 Joana Oliveira, MD,2 Joana Pardal, MD,3 Joanne Lopes, MD,3 Guilherme Macedo, MD, PhD, FACG1. 1. Gastroenterology department, Centro Hospitalar São João, Porto, Portugal; 2. Endocrinology department, Centro Hospitalar São João, Porto, Portugal; 3. Pathology department, Centro Hospitalar São João, Porto, Portugal. Introduction: Acute hepatitis is always a diagnostic challenge. In the setting of a young adult with type 1 diabetes mellitus (T1DM), the differential diagnosis usually includes viral hepatitis, autoimmune, and metabolic liver diseases such as juvenile hemochromatosis. Liver biopsy (LB) may have a key role in establishing the correct diagnosis. Case Report: A female patient, 29 years old, presented with a 2-month history of asthenia, anorexia, peripheral edema, and epigastric pain, more intense in the last 2 weeks. The patient had poorly controlled T1DM (HbA1c 10.9%, normal range 4-6) diagnosed at the age of 4. She denied the use of drugs, except sporadic alcohol intake and Indian tobacco smoking 6 months before. Physical examination revealed hepatomegaly and peripheral edema without jaundice or altered consciousness. Laboratory analysis revealed acute hepatitis with increased aspartate aminotransferase (991 U/L, normal 5000 IU/ L, international normalized ratio 5.1, and model for end-stage liver disease (MELD) score 34; he was transferred to our center’s intensive care unit for evaluation for liver transplant. He became encephalopathic within 24 hours of arrival. HCV antibody (Ab) was negative, and HCV RNA was 455,000 IU/mL. Hepatits B virus IgG core Ab was positive with a negative surface antigen and DNA. HIV Ab was positive with HIV RNA of 94,569 copies/mL. An absolute CD4 count was indeterminate due to high background, but CD4 lymphocyte percentage was 11%, corresponding to an absolute count of 1:16384. Results: The patient’s encephalopathy, serum aminotransferases, and INR improved over the next 48 hours with supportive care, and sofosbuvir and ribavirin were initiated on day 5. Given the positive RPR discovered on day 10, intramuscular penicillin G 2.4 million units was administered. He was discharged with a declining HCV viral load of 569 IU/mL. Ten days later, he presented to an outside hospital with new renal failure, bilirubin >30, and MELD score of 31. He was started on antiretroviral therapy for HIV and broad spectrum antibiotics. Unfortunately, his condition continued to worsen and the family elected to pursue hospice. Conclusion: This is a unique presentation of fulminant liver failure in a patient with acute HCV and advanced AIDS. Typically, acute HCV presents with minimal symptoms; however, immunosuppression and HIV infection impact the natural history of disease. Historically, HCV and HIV co-infection occurred in the setting of intravenous drug use, in which HCV was acquired first. Recently, an epidemic of acute HCV has been recognized in HIV-infected men who have sex with men. In this context, acute HCV is more often symptomatic, presents with higher elevations in transaminases with more rapid progression to fibrosis and liver failure. Our case suggests that fulminant hepatitis may also be more common when acute HCV infection occurs in the background of advanced HIV infection.

1319 Levofloxacin as a Cause of Vanishing Bile Duct Syndrome Katherine Shaffer, MD, Ram Subramanian, MD. Internal Medicine, Emory University, Atlanta, GA. Introduction: Vanishing bile duct syndrome (VBD) is a rare, poorly understood grouping of acquired liver disorders presenting with progressive ductopenia and cholestasis. Many drugs have been implicated in VBD, including ciprofloxacin and moxifloxacin, but levofloxacin has not yet been connected to VBD. We present a case of VBD that would be the first attributed to levofloxacin. Case Report: A previously healthy 30-year-old female presented with jaundice and recurrent vaginal bleeding after an episode of Stevens-Johnson syndrome attributed to levofloxacin. Laboratory studies were significant for bilirubin of 35 mg/dl, ALT 237 IU/L, AST 603 IU/L, alkaline phosphatase 609 IU/L, and INR 2.19. Liver biopsy demonstrated absence of appreciable bile ducts in half of the portal tracts, suggestive of vanishing bile duct syndrome (Image). Due to progressive hepatic failure, the patient underwent successful orthotopic liver transplantation and remains clinically stable.

[1320]

[1319A] Figure 1. Explanted liver showing a portal tract without bile ducts, and cholestasis involving the entire lobule.

Conclusion: This case demonstrates the importance of maintaining a high level of suspicion for fluoroquinolone-induced liver injury or VBD in a patient presenting with jaundice and liver injury of unclear etiology. Its pathogenesis is related to both direct insult to the biliary tract and autoimmune injury occurring when pathogens and pharmaceuticals act as haptens for the biliary ductal epithelium. These processes stimulate biliary apoptosis to outpace cellular regeneration, resulting in ductopenia. The treatment of VBD is not standardized, but includes discontinuation of the causative etiology and ursodeoxycholic acid to stimulate biliary excretion and bile duct cell growth. Avoidance of re-exposure of the causative etiology is key.

1320 Successful Renal Transplant in Epstein Syndrome: A Rare Cause of Thrombocytopenia Diagnosed During Pre-transplant Evaluation Shivali Berera, MD, Fernando Calmet, MD, Kalyan Bhamidimarri, MD, MPH, Jackson Memorial Hospital/University of Miami, Miami, FL. Introduction: Hepatology evaluation is often required in patients prior to renal transplant. Epstein syndrome (EPTS) is a rare cause of ESRD, and transplantation data is limited. We describe the case of a man with EPTS who was initially deemed a poor transplant candidate due to severe thrombocytopenia, but subsequently underwent uneventful renal transplant. A 29-year-old man with hearing loss and ESRD on hemodialysis was referred to our hepatology clinic for elevated liver enzymes and thrombocytopenia prior to renal transplant. The patient denied a history of bleeding diathesis. He had a splenectomy at age 4 due to presumed ITP. Physical exam was unremarkable, except for an abdominal surgical scar. Laboratory tests revealed hemoglobin 12 g/dL, WBC 4,500/mm3, platelet count 5,000/mm3, albumin 4.4 g/dL, total bilirubin 0.5 mg/dL, AST 131 u/L, ALT 336 u/L, alkaline phosphatase 182 u/L, and PT 10.4 s. Hepatitis A, B, and C serologies and markers for autoimmune hepatitis and PBC were negative. There was no evidence of genetic or metabolic diseases. Ultrasound showed a hyperechogenic liver, and a liver biopsy showed mild portal inflammation and focal ballooning degeneration, but no fibrosis or steatosis. He was found to have an MYH9 mutation and diagnosed with EPTS. He underwent kidney transplant with preoperative transfusion of platelets. During the procedure, he received platelets and packed RBCs, and had an estimated blood loss of 200 mL. Two days later, he received additional platelets prophylactically. His platelet count then remained near his baseline of 5-17,000/mm3 without additional transfusions or bleeding complications. EPTS is an

Table 1. Reported Cases of Renal Transplantation in MYH9-RD Patients

Case #

Patient

Platelet count

Perioperativemanagement

Complications

Author, Year

1

39 y/o M with FTNS

Baseline 96K/mm3

Unknown

Hematoma of rectus abdominus muscle, upper GI bleed

Peterson, et al., 1985

2

21 y/o F with MYH9-RD

Unknown

Unknown

Unknown

Sekine et al., 2010

3

20 y/o M with MYH9-RD

Unknown

Unknown

Unknown

Sekine et al., 2010 Sekine et al., 2010

4

32 y/o F with MYH9-RD

Unknown

Unknown

Unknown

5

17 y/o F with FTNS

Baseline 48K/mm3; maintained > 50K/mm3

Preoperative platelets

Intracranial hemorrhage, surgical wound hematoma

Min et al., 2014

6

23 y/o M with FTNS

Baseline 9K/mm3; maintained > 100K/mm3

Perioperative platelets

None

Min et al., 2014

7

29 y/o M with EPTS

Baseline 5-17K/mm3; maintained > 40K/mm3

Perioperative platelets

None

Berera et al., 2014

FTNS: Fechtner syndrome (another subtype of MYH9-RD)



| OCTOBER 2014

www.amjgastro.com

Abstracts autosomal dominant disorder characterized by hearing loss, nephritis, and macrothrombocytopenia included in the spectrum of MYH9-related disorders (MYH9-RD). Assessment of liver function is a vital component of pre-renal transplant evaluation. There are 6 cases reported in the literature of renal transplantation in patients with MYH9-RD (Table 1). Bleeding is a common perioperative complication, which may be preventable with aggressive platelet transfusions. To our knowledge, this is the second case reported to undergo renal transplant without bleeding complications.

1321 A Case of Subacute Liver Failure Associated With Black Cohosh Use Hyuntae Kim, MPH, Constantine Fisher, MD, Marci Laudenslager, MD, Manish Thapar, MD. Drexel College of Medicine, Philadelphia, PA. Introduction: Black cohosh is a herbal medication for the treatment of postmenopausal vasomotor symptoms. We report a case of subacute liver failure associated with black cohosh use. A 50-year-old female with a history of hypertension, uterine fibroids, and a recent hospitalization with acute hepatitis secondary to black cohosh use presented with asterixis and confusion. Two months prior, she started black cohosh to treat hot flashes. Within 1 week of use, she developed yellowing of eyes, abdominal pain, nausea, and vomiting, requiring a hospitalization. She had no underlying liver or autoimmune disease. Medications included hydrochlorothiazide and metoprolol. Family history was significant for hypertension, coronary artery disease, and autoimmune hepatitis. She had a 4-pack-year smoking history and endorsed having 1 alcoholic drink daily for 10 years, but quit 2 months ago. Physical exam on initial presentation was remarkable for jaundice. Her liver function tests (LFTs) were: AST 3,007 IU/mL, ALT 2,072 IU/mL, total bilirubin 16.9 mg/dL, direct bilirubin 10.3 mg/dL, ALP 155 IU/mL, GGT 203 μU/mL, but no coagulopathy. Serum ammonia was mildly elevated at 54 μmol/L. Hepatitis panel and liver autoimmune serology along with serum levels of ceruloplasmin and alpha-1-antitrypsin were all within normal limits. RUQ ultrasound suggested mild hepatic steatosis. Liver biopsy revealed severe acute hepatitis with submassive hepatic necrosis. The patient was discharged on day 9 of hospitalization with improved LFTs (AST 1,279 IU/mL, ALT 1,003 IU/mL) on prednisone. One month after discharge, the patient presented with an acute onset of asterixis and confusion. Laboratory studies revealed worsening jaundice: AST 644 IU/mL, ALT 501 IU/mL, total bilirubin 26.54 mg/dL, direct bilirubin 17.88 mg/dL, ALP 496 IU/mL, PT 21.5 s, and INR 2.01. Serum ammonia was elevated at 159 μmol/L. Anti-smooth muscle antibody was tested positive, but ANA was negative. The presence of mixed hepatocellular/cholestatic liver injury, coagulopathy, and hepatic encephalopathy rendered a clinical diagnosis of subacute liver failure. The patient scored 5 on the Roussel UCLAF causality assessment method (RUCAM), suggesting black cohosh as a probable cause of her liver injury. The patient was subsequently evaluated for transplantation. At the time of this report, she has improved on her own. In conclusion, patients and healthcare professionals should be aware that black cohosh can result in liver failure. This case underscores the urgent need for federal regulations on herbal preparations.

1322 Fulminant Hepatic Failure After Consumption of Wild Mushrooms Soujanya Sodavarapu, MD, Satbir Singh, MD, Stephen Hosea, MD. Santa Barbara Cottage Hospital, Goleta, CA. Introduction: Fulminant hepatic failure is a life-threatening condition and needs early recognition. A rare cause includes the consumption of Amanita-containing wild mushrooms. In this case report, we present a 70-year old male found to be in fulminant hepatic failure secondary to wild mushroom consumption. This is a 70-year-old male with no known past medical history found unconscious outside of his parked RV for an unknown amount of time. The patient was brought to the emergency room by emergency medical services. Initial vital signs showed hypotension, tachycardia, tachypea, and low saturation. Glucose was 30. The patient received 1 amp of dextrose-50 (D-50), raising his blood sugar to 70. At this time, the patient became minimally arousable, but still confused and incoherent. The patient had to be intubated for airway protection. Initial labs: ABG showed pH 20, AST 4197 U/L, ALT 3497 U/L, total bilirubin 3.2 mg/dL, INR 9.08, maekedly elevated LDH, and continued hypoglycemia; ammonia >500. The patient was anuric. Creatinine was 4.70 and creatinine phosphokinase 4,000. Blood alcohol level, acetaminophen level, hepatits panel, and ANA were negative. The patient remained hypotensive even with aggressive fluid resuscitation, and required pressor support and D10 drip for hypoglycemia. The patient was also initiated on N-acetylcysteine and dialysis. Abdominal ultrasound revealed no portal or venous thrombosis and normal kidneys. Several hours after admission, the patient was more alert, responsive, followed commands appropriately, and was able to answer questions. After specific query, the patient reported ingesting wild mushrooms while hiking in the hills a few days prior to presentation. A few mushrooms were recovered from the patient’s trailer and sent for analysis. The patient was transferred to a transplant center. Due to lack of social support, transplantation was not performed; the patient was made comfortable and later passed away. Only 3% of wild mushrooms are considered poisonous. Amanita phalloides, also known as the “death cap” mushroom, is of this poisonous mushroom variety involved in causing fulminant hepatic failure. Early recognition and prompt transfer to transplant center is critical. Local community awareness and early clinical recognition is of utmost importance.

1323 Rare Case of Acute Liver Failure Caused by Diffuse Liver Metastases in a Patient With Non-Muscle Invasive Transitional Cell Carcinoma of the Bladder Ashish Zalawadia, MD, Rishi Sharma, MD, Stuart Gordon, MD. Henry Ford Hospital, Detroit, MI. Introduction: Acute liver failure (ALF) secondary to infiltration of the liver by malignant cells is unusual, and hematological malignancies are the most common underlying etiology. ALF secondary to liver infiltration from transitional cell bladder cancer is extremely rare.


Case Report: A 70-year-old woman with a 2008 history of non-muscle invasive (Stage T1) transitional cell cancer of bladder, treated with transurethral resection of the bladder tumor, presented to the hospital with right upper quadrant pain, fever, and vomiting. Labs showed WBC 12,000, lactate 6.2 mmol/L, and abnormal liver parameters (AST, 416 U/L; ALT, 147 U/L, total/direct bilirubin, 6.1/4 mg%, alkaline phosphatase, 268 U/L, INR, 1.5). Abdominal ultrasound showed multiple gallstones and non-dilated CBD. ERCP showed no CBD stone or evidence of cholangitis. Viral hepatitis, autoimmune serologies, and other laboratory studies for other causes of acute liver failure were negative or non-reactive. A CT scan showed numerous low attenuation masses in the liver and enlarged retroperitoneal lymph nodes, and the bladder appeared normal. A liver biopsy showed sheets of malignant cells. P63 stain was positive, suggestive of metastatic carcinoma of urothelial origin. The patient’s liver synthetic parameters continued to worsen. She developed hepatic coma and expired 6 days after presentation. Discussion: ALF secondary to infiltration of the liver by malignant cells is a well-described entity, with hematological malignancies, including lymphoma and leukemias, being the most common causes. Other metastatic malignancies that rarely can cause ALF include adenocarcinomas and melanoma. ALF secondary to liver infiltration from transitional cell bladder cancer is extremely rare, with only 3 previous cases reported, all with documented muscle invasive (Stage T2) disease. Conclusion: To our knowledge, we report the first case of ALF secondary to non-muscle invasive (Stage T1) transitional cell bladder cancer occurring 5 years after original presentation and presumptive cure.

1324 Fatal Isoniazid Hepatotoxicity in a Patient With Rheumatoid Arthritis Treated for Latent Tuberculosis Radu Butuc, MD, Adriana Abrudescu, MD, Ricardo Lopez, MD, Leelavathi Kasturi, MD, FACG, Sabiha Bandagi, MD. Icahn School Of Medicine at Mount Sinai, Queens Hospital Center, Jamaica, NY. Introduction: To present a case of fatal Isoniazid (INH) hepatotoxicity in a patient with rheumatoid arthritis treated for latent tuberculosis infection, therefore to increase the awareness among physicians of this potentially lethal drug side effect. Methods: A 59-year-old female with past medical history of rheumatoid arthritis was tested positive for latent tuberculosis as part of work-up before initiation of anti-TNF-alpha therapy. The patient was started on INH therapy with monthly follow-ups in pulmonary clinic. During the first 6 months, she was noncompliant with her follow-ups and INH therapy. Liver tests were checked before and after starting the INH, and were normal. After she started to take INH consistently, she presented to ER complaining of cough, general weakness, and subjective fevers. She was diagnosed with URI, was given Tylenol, and was discharged home. INH therapy was continued. Eleven days later, the patient presented to the emergency room with general weakness, jaundice, abdominal pain, and vomiting. She had scleral icterus and generalized jaundice on exam. Labs were significant for markedly deranged liver enzyme and elevated INR. She was admitted with the impression of drug induced liver injury and then transferred to a tertiary facility where a liver biopsy was performed. The biopsy was compatible with drug-induced liver injury with submassive hepatic necrosis, with underlying chronic liver injury from steatohepatitis. The patient was placed on the transplant list, but while awaiting transplantation, her condition progressively worsened and she expired within 2 months. Results: INH hepatotoxicity is a common complication of antituberculosis therapy, ranging in severity from asymptomatic elevation of serum transaminases to hepatic failure necessitating liver transplantation. Its features are generally indistinguishable from viral hepatitis. All patients who receive INH therapy should be counseled about the risk of severe hepatitis and the harmful effects of overdose. The most important factor in the management of isoniazid-associated hepatitis is the early recognition and early discontinuation of INH and other potential hepatotoxins. In the setting of fulminant hepatic injury, considering early GI referral and liver transplantation is important. Survival rates depend on the severity of the hepatitis and on how early it is detected. If drug therapy is discontinued promptly, mortality should be negligible. If INH is continued after symptoms develop, mortality due to hepatic failure may exceed 50% unless liver transplantation is performed. Conclusion: Hepatotoxicity should be considered in all patients receiving INH and presenting with a viral syndrome. Mortality and morbidity from INH hepatotoxicity can be significantly reduced by early recognition and discontinuation of INH.

1325 “Black Ant”-Induced Autoimmune Hepatitis Phoenix Fung, MD. Rutgers New Jersey Medical School, Newark, NJ. Introduction: It has been reported that medications and herbs may induce immune-mediated liver disease, indistinguishable from autoimmune hepatitis. The diagnosis of drug-induced autoimmune hepatitis (DIAH) remains a challenge for clinicians, as most of the available data are case reports and series. We present a case of DIAH triggered by “Black Ant”. A 50-year-old man presented to the emergency department with nausea, vomiting, and jaundice over a 2-day period. The patient had no significant medical history. The only supplement taken was “Black Ant,” used for sexual dysfunction during the last 6 months. The physical examination revealed jaundice and hepatomegaly 2 cm below the right costal margin. Pertinent laboratory findings included: AST/ALT 1839/1593, total/direct bilirubin 16.4/11.9, and INR 1.4. ANA was 1:640, and ASMA 49.4. The ultrasound of the abdomen was normal. The liver biopsy showed interface hepatitis, portal inflammation, lymphoid aggregates with plasma cells (no eosinophils) with stage 1 fibrosis. The patient received corticosteroids as an inpatient; however, he did not continue the medications or follow-up in the office. He returned to ED 3 months later with elevated liver enzymes. He was admitted, and steroids with azathioprine were administered. Improvement of aminotransferases and INR was noted. Recent laboratory evaluation revealed significant improvement of the aminotransferases (AST/ALT 26/26), total bilirubin (1.3), and autoimmune markers (ANA 1:160, ASMA 10.3), lending support to the diagnosis of drug-induced auto-immune


S389

S390

Abstracts

hepatitis. DIAH is a difficult entity to diagnose. The past medical history reveals the etiology of the disease. Clinical presentation includes non-specific symptoms such as jaundice, fatigue, and malaise presenting at approximately 1.5 months from the exposure to the offending drug. The liver biopsy findings can be variable, including lymphoplasmacytic infiltrates, portal inflammation, interface hepatitis, zone 3 necrosis, confluent necrosis, hepatocellular cholestasis, and rosette formation. The hallmark of the disease is the presence of autoimmune markers, including ANA and ASMA, reported as high as 83% of the cases. The mainstay of treatment is discontinuing the offending agent. Steroids can be used in severe cases where there is no improvement. Relapse after corticosteroid withdrawal is less common in DIAH compared to classic auto-immune hepatitis. Black Ant is an herbal sexual enhancement drug that was recently recalled by the FDA after being noted to contain high doses of sildenafil. Clinicians should be aware of the presentation of DIAH and keep it within their differentials when evaluating patients with acute liver injury. Disclosure - I authorize my co-authors to dislose their financial relationships.

mild hepatomegaly, and normal flow within the portal and hepatic veins, with no intrahepatic ductal dilatation. These were all consistent with an ultrasound done about 7 years ago, and were felt to be due to his polycystic kidney disease. Coincidentally, his FK506 level at admission reached the highest peak it had in almost 9 months and his tacrolimus dosage was reduced prior to discharge. His other immunosuppressants at the time were methylprednisolone and mycophenolate mofetil. He was ultimately diagnosed with reactivated latent hepB and entecavir was initiated prior to discharge. He has not yet returned to our clinic for follow-up. Literature regarding reactivation of HBV has demonstrated a variety of cases where a positive HBsAg was noted in the setting of a previously positive antiHBsAb. This has been reported in a variety of immunocompromised hosts, including cases of solid organ transplant, AIDS patients, and those undergoing various chemotherapeutic regimens such as rituximab. Our case occurred in a similar setting; however, it was unique because of the re-emergence of HBVsAg positivity despite the presence of a positive antiHBsAb. It is generally accepted that one cannot demonstrate HBVsAg positivity, and that the infection is considered cleared with appearance of HBVsAb. It is difficult to assess the prevalence of such cases because no other reports have been published at this time.

1326 Hepatitis B Flare Preceding Unexpected Fetal Demise in a Pregnant Woman With Inactive Hepatitis B: A Case for Estrogen Withdrawal-Induced Viral Rebound Presidential Poster 2

1

2

1

Ana Petrova, MD, Yetian Zhang, MD, PhD, Meira Abramowitz, MD, Cherif El Younis, MD, FACG . 1. Brookdale University Hospital, Brooklyn, NY; 2. SUNY Downstate Medical Center, Brooklyn, NY. Introduction: Estrogens have been shown to up-regulate certain estrogen receptors (ER-α), thereby reducing hepatitis B transcription. We report a pregnant patient with documented non-replicative hepatitis B, who presented with flare of hepatitis B followed by spontaneous termination of pregnancy with fetal demise. Case Report: A 28-year-old female, G6P3, 30th week of gestation, with history of hepatitis B (healthy carrier), with normal liver enzymes and undetectable hepatitis B DNA, presented with 1 week of anorexia, nausea, vomiting, and abdominal discomfort. No fever or chills. Her ROS was unremarkable. Examination revealed icteric sclera and findings consistent with pregnancy; otherwise unremarkable. Labs revealed : AST 1329 U/L , ALT 950 U/L, bilirubin 5.9 mg/dL, alkaline phosphatase 219 U/L. She tested positive for hepatitis Bs Ag, HBV c Ab IgG, HBV cAb IgM, and hepatitis B DNA was 133,232 IU/ml. She tested negative for hepatitis A and hepatitis C serology. Liver appeared normal on ultrasound. The rest of liver disease work-up was negative. Three days after discharge, the patient presented with stillbirth. Over the following 3 weeks, liver enzymes normalized and HBV DNA declined to lower levels (Table). Discussion: It has been known that women with hepatitis B (HBV) infection generally have lower viral loads than men. This was attributed, at least in part, to the increase in hepatic expression of estrogen receptor (ER)-α in response to estrogen exposure. As a result, up-regulation of ER-α induces regression of HBV transcription through binding to hepatocyte nuclear factor 4α. During normal pregnancy, the exposure to high estrogenic milieu predictably up-regulates ER-α and suppresses the transcription of hepatitis B DNA. In our case, with the abrupt decline in estrogen as would be the case in premature termination of pregnancy, this up-regulation of ER-α receptors ceases with subsequent rebound transcription of hepatitis B DNA, resulting in a replicative viraemic state of hepatitis B. The documentation of hepatitis B cAb IgM was consistent with reactivation. Conclusion: The observation depicted in this case emphasizes the effect of fluctuating level of estrogens on the course of hepatitis B during pregnancy, and might further contribute to our understanding of the effect of sex hormones on the pathogenesis of HBV-induced liver disease and the impact of therapeutic exogenous estrogenic treatment in the setting of hepatitis B infection.

[1326]

Baseline

1328 Acute Deep Venous Thrombosis Unmasking Underlying Wilson’s Disease: Case Report FNU Jaydev, MD,1 Eyad Baghal, MD, FACG,2 Amara Nidimusili, MD,1 Marwan Saad, MD1. 1. Internal Medicine, Trinitas Regional Medical Center, Elizabeth, NJ; 2. Seton Hall University School of Health and Medical Sciences., Elizabeth, NJ. Introduction: Wilson’s disease (WD), also known as hepato-lenticular disease, is an autosomal recessive disorder of copper excretion and can clinically present with hepatic, neurological, and psychiatric manifestations, which makes the diagnosis challenging in most of the cases. We present a case whose atypical presentation led to the unmasking of his underlying WD. Case Report: A 32-year-old male, recently diagnosed with type II diabetes mellitus, presented with pain and swelling of right lower extremity. On detailed history, the patient mentioned having a 3month history of intention tremors, sialorrhea, hypophonia, progressive micrographia, and family history of a second-degree relative having WD. He had advanced intension tremors, cogwheel rigidity in the upper extremities, and olfactory dysfunction. His laboratory investigations showed D-dimer of 4,335 units, elevated PT (16.5 sec) and INR (1.8), and low albumin level (3.0 gm/dl) with normal liver enzymes. Right popliteal acute deep venous thrombosis (DVT) was confirmed by Doppler US. MRI brain showed cortical and cerebellar atrophy. MRI abdomen showed liver cirrhosis, mild splenomegaly, and small esophageal varices. Extensive work-up proved the diagnosis of WD by low serum copper level of 60 mcg/dL, low serum ceruloplasmin level of 15 mg/dL, and high 24-hour urine copper of 211 mcg. Liver biopsy showed macrovascular steatosis less than 5%, grade 3 portal and periportal chronic inflammation, grade 1-2 lobular inflammation, and stage 2 portal fibrosis with intact architecture and negative iron stain. Chemical quantification of copper in the liver biopsy was 219 ug/g drywt. Discussion: WD is caused by mutation of ATP7B gene on long arm of chromosome 13, which codes for a protein responsible for incorporating excess copper into ceruloplasmin to be excreted from the body. Subsequently, this leads to accumulation of copper in several organs, mainly the liver, brain, and cornea, and inevitably leads to progressive liver and neurological dysfunction. Hepatic manifestations range from asymptomatic biochemical abnormalities to acute hepatitis or chronic hepatitis and cirrhosis. Neurological manifestations include dysarthria, dystonia, tremors, or Parkinson’s-like manifestations. Less commonly, WD may present with cerebellar manifestations. Our patient had manifestations of cerebellar involvement as well as Parkinsonian features. This case presents a unique initial presentation of WD in the form of unprovoked DVT secondary to the hypercoagulable state, complicating chronic liver disease. As far as we know, DVT has not been reported to be one of the presenting complications of WD especially in patients without advanced liver cirrhosis.

Table 1. Lab Data AST

ALT

AP

BILI

HBV DNA IU/ml

HBcAb IgM

31

21

100

0.1

Undetect

−Ve

1329

133232

+ Ve

Wandering Liver in a 60-Year-Old: Diagnosis and Significance

Day 1

1329

950

219

5.9

Day 5

94

190

109

1.7

Week 4

35

36

89

0.9

Presidential Poster 472

1327 A Rare Case of Reactivated Hepatits B in the Setting of Hepatitis B Surface Antibody Positivity Sadra Azizi, MD, Emory Manten, MD, Jesse Green, MD. Albany Medical Center, Albany, NY. Introduction: A 57-year-old male presented with abnormal liver chemistries in the setting of routine lab testing for his renal transplant follow-up. He underwent post-cadaveric renal transplant in 2011 secondary to polycystic kidney disease. Of note, he was involved in a recent motor vehicle accident about a month prior and had since been taking about 1.5 g of acetaminophen for pain control. He denied jaundice, diarrhea, abdominal pain, fever, or nausea/vomiting. He had an elevated total bilirubin (3.7mg/dL on admission, 4.7 peak during his hospital stay), alkaline phosphatase (160 IU/L on admission), aspartate aminotransferase (325 IU/L on admission, 364 peak), and alanine aminotransferase (486 IU/L on admission, 491 pek). Of note, he did have a history of prior hepatitis B infection, with documented negative HBsAg and positive antiHBsAb in 2011. He was initiated on NAC therapy despite a negative acetaminophen level. On repeat serologic testing, it was discovered that he now had a positive HBsAg, which was solidified by confirmation testing, as well as a positive antiHBsAb. His HBcoreAb-IgG was positive while his HBcoreAb-IgM was negative. HAV and HCV testing were both negative. Abdominal ultrasound revealed cysts of varying sizes infiltrating throughout the liver,


Annu Gupta, MD, T s Dharmarajan, MD. Montefiore Medical Center, Bronx, NY. Introduction: A wandering liver is a rare entity, but more common than we realize. The rise in incidence is secondary to higher utilization of imaging of patients with abdominal disorders, typically diagnosed during evaluation of colonic volvulus or intestinal obstruction. We present a case of a 60-year-old male with choledocholithiasis and a wandering liver. Case Report: A 60-year-old male hospitalized with acute cholecystitis and choledocholithiasis. CT abdomen done at admission confirmed gallstones in the biliary tract with normal position of the liver and gallbladder. MRI cholangiopancreatography (suggested by gastroenterologist) revealed liver and gallbladder on the left side with pancreas, duodenum, and spleen in normal anatomical position. The liver pedicle was distorted, with dilated common bile duct (CBD) lying parallel to pancreatic duct. The anatomy posed challenges to perform ERCP and place a CBD stent with multiple failed attempts. Pancreatic duct stent was placed to avoid post ERCP acute pancreatitis. Eventually, a CBD stent was placed and the patient was scheduled for elective cholecystectomy. Discussion: Wandering liver is a phenomenon where the liver moves freely from the right side of the abdomen to the left, and is associated with a persistent ventral mesentery. Operative findings describe lax or absent suspensory hepatic ligaments and a long colonic mesentery. In our case, the patient had choledocholithiasis with gallstones in the CBD. The benefits of procedures such as ERCP are challenged by risk of complications in such patients, with increased risk of complications related to pancreatobiliary instrumentation. Complications include pancreatitis, retroperitoneal duodenal perforation, hemorrhage, and sepsis, as also hepatic pedicle torsion and bowel obstruction. Wandering liver is usually associated with wandering gall bladder and gall bladder torsion, requiring laparoscopic cholecystectomy. Wandering liver is a typical imaging-related diagnosis, and made incidentally in the younger population. Most patients are generally left alone.


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Abstracts nisone was initiated. Our case demonstrates a unique presentation of sulfasalazine-induced DRESS mimicking small duct PSC on liver biopsy. Sulfasalazine has been implicated in approximately 6% of reported cases of DRESS. It has been shown to cause hepatosplenomegaly, hepatotocellular injury, peripheral lymphadenopathy, and phototoxicity. Our patient developed a cholestatic hepatitis with liver biopsy changes that can also be seen with small duct PSC, which has not been reported in the literature. Since sulfasalazine may be used in patients with UC, a disease which carries a 4-fold increased risk of PSC, it is important to consider alternative causes of cholestatic hepatitis in this patient population.

1332 A Unique Symptomatic Presentation of Type II Cryoglobulinemia Syndrome With Chronic Hepatitis C Virus Infection Dominic Colella, DO, Bruce Le, DO, Juan Sarol, MD, Javier Sobrado, MD, FACG. Nova Southeastern University - Larkin Community Hospital, South Miami, FL.

[1329A]

Figure 1. Wandering liver: liver migrated on the left side.

1330 Acalculous Cholecystitis Associated With Acute Q Fever Infection Nisha Shah, MD, John Bassett, MD, FACG, Thomas Mellor, MD. Walter Reed, Bethesda, MD. Introduction: Q Fever is a worldwide zoonotic infection caused by the bacterium Coxiella burnetii (C. burnetii). Human infection is due to inhalation of air contaminated with excretions from infected farm animals. Because of its high infectivity and low inoculum requirement, C. burnetii is considered a category B bioterrorism agent by the Center for Disease Control. The antigenic variations of its capsule separates acute from chronic infection with presentation ranging from flu-like illness to cholestasis. Case Report: A 52-year-old male presented with a 3-week history of fevers, night sweats, headaches, and early satiety, which began 48 hours after returning from the Netherlands. Exam showed right upper quadrant tenderness, and lab work revealed elevated liver associated enzymes in a cholestatic pattern with decreased synthetic function, elevated inflammatory markers, and normocytic anemia, but no leukocytosis. Imaging showed gallbladder wall thickening and progressive fatty infiltration of the liver. During his hospitalization, he had persistent fevers despite broad spectrum antibiotic therapy, worsening anemia, and continued cholestasis with an alkaline phosphatase up to 235 U/L and total bilirubin up to 2.0 mg/dL. Repeat imaging showed acalculous cholecystitis, prompting a cholecystectomy, which was confirmed by histology. A liver biopsy was significant for steatohepatitis with non-caseating granulomas involving both the parenchyma and portal areas. Positive C. burnetii titers were consistent with acute Q fever infection. The patient was treated with doxycycline and had subsequent clinical improvement and resolution of the cholestasis. Discussion: Q fever is an uncommon infection in the United States. Acalculous cholecystitis related to Q fever is rare, with only a dozen case reports in the published literature. Because of its variable presentation, it should be considered in a patient with fevers, right upper quadrant pain, and cholestasis, often with a lack of leukocytosis.

1331 All About the Medication Reconciliation: A Case of DRESS Syndrome Appearing as Primary Sclerosing Cholangitis Xiao Jing Wang, MD,1 Christian Mustroph, BS,2 Parit Mekaroonkamol, MD,3 Ryan Ford, MD3. 1. Internal Medicine, Emory University School of Medicine, Atlanta, GA; 2. Emory University School of Medicine, Atlanta, GA; 3. Emory University School of Medicine, Digestive Disease Department, Atlanta, GA. Introduction: Drug reaction with eosinophilia and systemic symptom (DRESS) is a rare type IVb, delayed drug-induced hypersensitivity reaction with a multitude of systemic manifestations. Numerous drugs can cause DRESS, leading to diffuse rash, fever, eosinophilia, and organ damage. DRESS can mimic a variety of other illnesses, requiring high suspicion and careful history taking for accurate diagnosis. Here, we report an unusual case of DRESS mimicking small duct primary sclerosing cholangitis (PSC). A 65-year-old female with known ulcerative colitis (UC) presented with an 11day history of nausea, vomiting, abdominal pain, diffuse pruritus, and jaundice. Medication reconciliation revealed that she had been initiated on sulfasalazine 5 weeks prior to symptoms. Physical exam revealed right flank tenderness and a coalescing erythematous maculopapular rash on her face, trunk, and distal extremities. Her liver function tests showed an alanine aminotransferase of 265 IU/L, aspartate aminotransferase of 163 IU/L, alkaline phosphatase of 500 IU/L, total bilirubin of 6.1 mg/dL, direct bilirubin of 3.2 mg/dL, and an international normalized ratio of 1.2. Her white blood cell count was 18,500 cells/mm3, including 20% eosinophils and 7% atypical lymphocytes. Viral hepatitis serologies and autoimmune markers were negative. An MRI of the abdomen did not show any disease of the large bile ducts. A bone marrow biopsy showed an eosinophilic infiltration without evidence of leukemia or lymphoma. A liver biopsy showed a mixed portal inflammation with eosinophil predominance and focal cholestasis of small bile ducts with a ductular reaction. Her RegiSCAR score was 7, supporting a diagnosis of DRESS. Sulfasalazine was stopped and pred-


Introduction: Cryoglobulinemia refers to the presence of blood protein precipitates, known as cryoglobulins, in an individual’s serum and plasma. The prevalence of clinically significant cryoglobulinemia is estimated to be 1 in 100,000 individuals. The disease can be classified into 3 types with the Brouet classification scheme, which is based on the immunological analysis of cryoglobulins. Type I consists of an isolated monoclonal immunoglobulin. Type II or mixed cryoglobulinemia is a combination of polyclonal immunoglobulins with a monoclonal immunoglobulin and rheumatoid factor activity. Type II is associated with chronic viral infections as well, such as hepatitis C infection. Type III contains multiple polyclonal immunoglobulins. A 59-year-old female patient with a medical history of chronic hepatitis C virus infection, hepatic cirrhosis, gastroesophageal reflux disease, and hypertension presented with the complaint of generalized abdominal pain and constipation. The pain was dull, non-radiating, and severe in intensity. Physicial examination was remarkable for abdominal distention, tenderness to palpation, guarding, rebound tenderness, and mild global jaundice. Laboratory values demonstrated elevated bilirubin and C-reactive protein levels, transaminitis, thrombocytopenia, and hepatitis C virus antibodies. Laxatives were given due to her constipation, and within 24 hours, she passed a large bowel movement, which relieved her abdominal pain. A new-onset rash then developed the following morning. It was a pruritic, burning rash present primarily on her abdomen and lower extremities. Non-palpable, non-blanching petechiae and ecchymoses were appreciated. Punch biopsies confirmed the presence of a superficial leukocytoclastic vasculitis with intravascular microthrombi. Direct immunofluorescence confirmed the presence of colloid bodies positive for IgG, IgM, and IgA. Per pathology, these findings were pathognomonic for mixed cryoglobulinemia. Methyl-prednisolone was given every 8 hours for treatment, which abated the patient’s rash within 24 hours. This presentation of mixed cryoglobulinemia syndrome is not typical. The non-palpable, non-inflammatory petechiae and ecchymoses found on our patient are normally present in type I cryoglobulinemia on mucous membranes and not in mixed cryoglobulinemia. Despite this atypical presentation, the medical team was confident in the diagnosis due to biopsy results and the immunological analysis of cryoglobulins. Therefore, the common belief that mixed cryoglobulinemia is associated with palpable purpura may not always be true, and it is important to recognize that the clinical presentation of cryoglobulinemia can be a combination of the multiple types.

1333 A Rare Case of CMV Hepatitis With Guillain-Barré Syndrome in an Immunocompetent Young Female Omar Mousa, MD, Rushikesh Shah, MD, Vanessa Hoy, MD, Sekou Rawlins, MD. Medicine, SUNY Upstate Medical University, Syracuse, NY. Introduction: Cytomegalovirus (CMV) infections can cause substantial morbidity and mortality in immunocompromised patients. Multi-organ system involvement in the immunocompetent host with primary CMV infection is rare, but can lead to serious complications. The clinical presentation of hepatic and neurologic involvement in disseminated CMV and their management are not well described in the literature. Case Report: We present a case of a 19-year-old previously healthy woman who presented with malaise and tingling sensation in the hands and feet bilaterally for 4 days. This was associated with headaches, mild photophobia, and general weakness. She also reported nausea and vomiting 2 weeks prior. She denied other symptoms, including abdominal pain, fevers, or jaundice. Her physical exam showed decreased power in her upper and lower extremities, decreased sensation to vibration in her feet and hyporeflexia. Her past medical history, family, and social histories were insignificant. Her only medication was mirena. Blood work, lumbar puncture, and imaging were suspicious for a diagnosis of Guillain-Barré syndrome (GBS). Given her transaminitis on admission (liver panel ALT 177, AST 121, ALP 120, T bil 0.7), complete work-up for a hepatitis etiology was performed, including serologies for hepatitis A, B, C, and HIV, HSV, EBV, serum acetaminophen and alcohol levels, and abdominal imaging, which all came back negative. Meanwhile, she decompensated and had acute respiratory failure requiring intubation and monitoring in the ICU setting. Given her GBS diagnosis, CMV was suspected even though she is immunocompetent, and for the fact that CMV can cause both GBS and hepatitis. Her cytomegalovirus serology showed an IgM positive titre. After 1 week of monitoring, her liver panel showed persistence of transaminitis despite initiation of IVIG for GBS. Therefore, Ganciclovir was started. Her transaminitis resolved abruptly over a 2-day period of administration of Ganciclovir. She had no recurrence of transaminitis on further follow-up, despite a prolonged hospital stay for the management of GBS that exceeded 1 month. Discussion: Seroprevalence rates of CMV infection are low in the U.S., and the incidence is lower in young caucasians. Our unique case had both characteristics: being a teenager and caucasian. She did not improve on IVIG as reported in previous cases, but recovered from acute non-cholestatic CMV hepatitis with ganciclovir with no side effects or relapses on a 6-month follow up. We conclude that CMV hepatitis in immunocompetent hosts can be severe and persistent, requiring antiviral


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therapy to correct the transaminitis. This approach had a significant impact on the progress of CMV hepatitis.

1334 Painless Jaundice and an Ileocecal Mass: A Curious Presentation of an Autoimmune Phenomenon Amy Stratton, DO, Brian Park, MD, Dawn Torres, MD. Walter Reed National Military Medical Center, Bethesda, MD. Introduction: The clinical presentation for autoimmune hepatitis is highly variable, ranging from asymptomatic incidental lab findings to fulminant liver failure. Between these extremes live a broad spectrum of clinical features including nonspecific findings such as fatigue, anorexia, nausea, and vomiting, as well as more liver-specific signs such as pruritus and jaundice. Case Report: A 28-year-old active duty male presented to the emergency room with acute yellowing of his skin and eyes. He complained of a persistent cough not responsive to azithromycin or TMPSMX. On further inquiry, he reported subjective fevers and drenching night sweats, as well as severely diminished appetite and poor oral intake for 3 weeks prior. Physical examination was remarkable for scleral icterus and jaundice of the face and chest, mild hepatomegaly, and 5 palpable 10-mm mobile non-tender anterior cervical chain lymph nodes. Laboratory studies revealed elevated AST and ALT to 995 U/L, and 1323 U/L with elevated total and direct bilirubin to 13.5 mg/dL and 7.6 mg/dL, respectively. Right upper quadrant abdominal ultrasound and a CT scan of his abdomen and pelvis demonstrated substantial pre-caval and pre-esophageal lymphadenopathy with a 3.4-cm periportalprecaval soft tissue mass concerning for underlying malignant process. He was admitted to the inpatient medicine service, where TMP-SMX was stopped and further laboratory studies were remarkable for an elevated IgG and positive ANA. Alpha-1 antitrypsin, iron studies, haptoglobin, ceruloplasmin, herpes simplex virus PCR, cytomegalovirus PCR, Epstein barr virus PCR, HIV antibody (Ab), antismooth muscle Ab, and rapid plasma regain were negative. Liver biopsy was consistent with autoimmune hepatitis. PET CT scan to evaluate his lymphadenopathy and soft tissue mass showed a large ileocecal mass with increased metabolic activity. Colonoscopy with biopsy of aforementioned mass showed inflammatory mucosa without evidence of malignancy. Bone marrow biopsy was negative for lymphoma and leukemia. The patient was started on steroids and ultimately transitioned to azathioprine with good response. Discussion: For this patient with lymphadenopathy and constitutional symptoms, it was important to consider toxin-mediated hepatitis and underlying malignant process in addition to autoimmune hepatitis. This case demonstrates that autoimmune hepatitis can have a wide array of clinical presentations, rarely including inflammatory lymphadenopathy, and responds well to treatment.

1335 Cryoglobulinemic Vasculitis Occurring With Initiation of Interferon and Sofosbuvir for Treatment of Hepatitis C Tanima Jana, MD, Sanah Ali, MD, Shivang Mehta, MD, Sarah Sweeney, MD, Richard Jahan-Tigh, MD, Kevin Dasher, MD. University of Texas Health Science Center at Houston, Houston, TX. Introduction: A 58-year-old Hispanic woman presented with a 2-day history of a pruritic rash that had started on her hands before spreading to her abdomen, chest, upper extremities, and lower extremities. Her history was significant for chronic hepatitis C (HCV), genotype 1, but no prior history of vasculitis. She had been started on ribavirin, peginterferon alfa 2-a, and sofosbuvir 6 weeks prior to admission, with an undetectable HCV RNA PCR after 4 weeks. However, treatment had been stopped 2 weeks prior to admission due to neutropenia (ANC 400 cells/mL). Her temperature on admission was 101.7 °F. On physical exam, she had edematous pink plaques on the dorsal hands, elbows, and proximal bilateral lower extremities. There were purpuric papules and plaques on the bilateral midlower thighs, shins, ankles, and feet. White blood cell count was 2,4000 cells/μL with normal differential, hemoglobin 11.9 mg/dL, platelets 119000 cells/μL, and creatinine 0.7 mg/dL. Urinalysis did not show proteinuria. Liver function and iron studies were unremarkable. ANA, ANCA, CRP, ESR, HIV, anticardiolipin antibodies, beta-2-glycoprotein, and lupus anticoagulant were normal. Cryoglobulins were positive, with low complement levels, mildly elevated rheumatoid factor, and undetectable HCV viral load. Punch biopsy showed leukocytoclastic vasculitis. She was started on a steroid taper, and at 2-week follow-up, her rash had resolved completely. Here, we present a case of a patient with cryoglobulinemic vasculitis on co-therapy with interferon (IFN) and sofosbuvir. Cryoglobulins may be seen in 40-56% of patients with HCV infection, with vasculitis only seen in 1.1 with low total protein consistent with portal-hypertension secondary to underlying cirrhosis. Workup for other causes of chronic liver disease was negative. Transgular liver biopsy showed diffused canalicular and hepatocellular cholestasis, focal steatosis, and mild chronic portal inflammation with ductal reaction. Trichrome stain clearly revealed portal and periportal fibrosis with focal bridging fibrosis (Figure 1). Iron stain was negative, with findings consistent with liver toxicity secondary to TPN. The spectrum of liver disease in patients receiving TPN is broad. Steatosis can develop as early as 1-4 weeks after initiation of TPN and can progress to simple steatohepatitis or complicated with fibrosis. Therefore, it is important to recognize and treat TPN-associated liver disease by enteral stimulation when possible, and optimize TPN composition by limiting excess carbohydrates and lipids. Moreover, pharmacological therapy with ursodexocycholic acid and early referral for liver transplant is imperative.


[1340A]

Figure 1.

[1340B]

Figure 2.


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necrosis with minimal associated inflammation.” The patient continues to have anemia despite multiple PRBC transfusion. Then Serum parvovirus B19 DNA was ordered and came back +ve. The patient started on a 7-day-course of IVIG after consultation with hematology team. His HGB and liver enzymes start to improve. The patient was discharged in good condition from the hospital after recovery. His lab on discharge: HGB 7.9 g/dL, AST 277, and ALT 78 (Figure 1 and 2). Parvovirus B19 is a rare cause of sever hepatitis and anemia in HIV- infected persons. The early consideration of this condition will help in early diagnosis and prevent extensive work-up in those patents. The -ve parvovirus IgM can be misleading because of the immune status of those patients. Parvovirus PCR is important in diagnosis.

1341 A Rare Cause of Cholestatic Hepatitis in an Immunocompetent Male Roshan Patel, MD, Rahul Maheshwari, MD, Ram Subramanian, MD. Department of Medicine, Emory University, Atlanta, GA. Introduction: Histoplasmosis has been rarely reported in the literature in immunocompetent patients, much less in a disseminated fashion. A 69-year-old male with history of end-stage renal disease (ESRD), hypertension, and diabetes presented with 3 weeks of progressive abdominal swelling and jaundice with worsening colicky abdominal pain, nausea, and diarrhea. Review of symptoms revealed several months of non-productive cough and intermittent low-grade fevers and chills. He was found to be febrile with icteric sclera and a mildly distended abdomen. Initial laboratory evaluation revealed a total bilirubin of 8.6 mg/dL, a direct bilirubin of 5.4 mg/dL, elevated ALP of 424 units/L, and normal AST and ALT. A miliary pattern was seen on chest x-ray. Investigation of the cholestatic labs, including a right upper quadrant ultrasound and CT abdomen, showed no intra or extrahepatic biliary duct dilation. MRI was remarkable only for iron deposition in the liver. These findings raised suspicion for a process involving both the lungs and liver. A bronchoscopy was completed with unrevealing initial cultures and pathology. HIV ELISA, fungal blood cultures, a viral hepatitis panel, and urine histoplasma antigen were negative. His fevers, hyperbilirubinemia, and elevated ALP persisted, and ultimately, a liver biopsy was completed, which revealed mixed inflammatory infiltrate with severe granulomatous hepatitis. Numerous well-formed granulomas were present, lacking overt caseating features but having fibrinoid material identified within them as well as areas of hepatic necrosis. There were no organisms detected on GMS fungal stain or acid-fast bacillus (AFB) stain, and liver biopsy cultures were negative as well. Final bronchoscopy cultures grew mold consistent with histoplasmosis. The patient was promptly started on itraconazole, after which he quickly defervesced with marked improvement in bilirubin and ALP. The myriad causes of hepatic granulomas can be broadly categorized into immunologic disorders, infiltrative bacterial and fungal infections, neoplasia, and hypersensitivity to drugs or metals. This case highlights the challenges in identifying a fungal etiology of granulomatous hepatitis based on histopathology alone, and underscores the importance of tissue microbiology in making the diagnosis. The patient’s liver histopathology did not have classic features of caseating granulomas typical of histoplasmosis, and neither GMS fungal stain nor liver biopsy identified any organism. It was not until the bronchoscopy culture grew mold that the diagnosis was reached. Histoplasmosis as a cause of unexplained cholestatic jaundice and fever must be considered even in immunocompetent patients from nonendemic areas.

CLINICAL VIGNETTES/CASE REPORTS - COLON

1342 Recurrent Epiploic Appendagitis: Conservative Versus Surgical Approach Jagpal Klair, MD, Mohit Girotra, MD, Neelima Velchala, MD, Aneet Kaur, MD, Daniel Brown, MD. University of Arkansas for Medical Sciences, Little Rock, AR. Introduction: Epiploic appendagitis (EA) is a rare, benign inflammation of epiploic appendices (with unknown physiological function) that are small, fat-filled pouches of peritoneum present on the external surface of colon. Most common causes of EA are torsion, venous thrombosis, or spread of infection from adjacent diverticulitis. Usual presentation is acute abdominal pain mimicking acute appendicitis, diverticulitis, or cholecystitis, depending on the location of abdominal pain. CT scan findings are pathognomic for the diagnosis for EA. A 33-year-old male presented with acute left lower quadrant abdominal pain, nausea, and vomiting concerning for diverticulitis. He was recently discharged after a presumable attack of acute cholecystitis. He has a past medical history of diverticulitis. He was afebrile with no leukocytosis. CT scan revealed localized omental infarction and inflamed epiploic appendages in descending colon. He was discharged after conservative management, but since has been admitted 2 times in 6 months for acute abdominal pain in the right or left lower quadrants. Due to recurrence of acute EA, the patient was seen by general surgery, who will follow up with patient in their clinic for a possible elective laproscopic removal of inflamed epiploic appendages. EA is benign, self-limited diagnosis with a mainstay conservative management with anti-inflammatory and analgesics. With an increased awareness and suspicion among surgeons and internists, EA is preoperatively with CT imaging preventing unnecessary medical and surgical interventions like laparotomy/antibiotics. Most case reports have shown resolution of pain within 1-4 weeks with conservative, non-surgical mangement; however, we suspect that conservative management might not be the best treatment option due to a risk of recurrent epiploic appendagitis. Laparoscopic surgery to remove epiploic appendages might prevent the recurrence as recommended by Sand et al. with his study of 10 patients with EA in 2007. There is a risk (although small) of complications like formation of adhesions and development of abscess requiring surgical interventions. We need to weigh the risk of multiple follow-up CT scans with the risk of surgery done at the time of diagnosis of EA. We conclude by pointing out the need of a consensual treatment algorithm that EA is currently lacking, for all physicians and surgeons to follow.


1343 Acute Bowel Obstruction Due to Endometriosis Treated With Colonic Stent Muhammad Sohail, MD,1 Ikram Umaira, MD,3 Gordon Hunt, MD2. 1. Gastroenterology, UCSD, San Diego, CA; 2. Kaiser Medical center, San Diego, CA; 3. Ross University, Newark, NJ. Introduction: Endometriosis is defined as the presence of extrauterine endometrium. It affects up to 8% of premenopausal women. Intestinal involvement is the most common extrapelvic site, affecting 5.4% of women with endometriosis, and out of which rectosigmoid endometriosis comprises 90%. Endometriosis is an extremely rare cause of large bowel obstruction. Urgent surgical intervention carries high morbidity and mortality, and operative intervention can be more difficult in extensive pelvic endometriosis. Less invasive alternatives can be considered in this situation. Case Report: A 35-year-old female presented with 2 weeks of progressive abdominal pain, nausea, and constipation. She denied hematochezia and reported no other gastrointestinal problem. She was afebrile, hemodynamically stable, and in moderate distress due to abdominal pain. Abdomen was diffusely tender, distended, and bowel sounds were present. Rectal exam revealed no abnormality. WBC count was 15 K. CT abdomen showed distended large bowel and colonic obstruction due to distal sigmoid colon stricture. A discrete mass was not seen. Colonoscopy showed tight colonic stricture with sharp angle at 18 cm above dentate line, unable to pass endoscope. The edge of the stricture was biopsied. A guide wire was advanced into the dilated colon proximal to stricture. Contrast injection revealed a 2.5-cm-long stricture. A 2.5-cm x 8-cm uncovered stent was deployed after consulting with the surgical team. Pathology showed benign edematous colonic mucosa. She did well for 2 days with scant semi-formed stools, but her symptoms got worse, and she ultimately underwent surgery. Upon initial inspection of bowel during surgery, the cecum and sigmoid colon were very dilated. The cecum was ischemic in appearance with splitting of the serosa in several areas. There was a hard, obstructing lesion in the proximal rectum, just distal to the confluence of tenia. The proximal sigmoid was resected. The initial surgical impression was diverticular disease, but pathology revealed extensive sigmoid colon endometriosis. Discussion: It is very rare to have endometriosis leading to bowel obstruction without any prior symptoms or history of endometriosis. This is the second reported case of acute bowel obstruction treated initially with colonic stent. Colonic stenting is currently widely used in malignant obstruction. The use of self expanding metallic stents to treat benign conditions is controversial; however, due to associated long-term complications. This case demonstrates that stenting can provide a bridge to major surgery in the rare event of acute endometriotic colonic obstruction. The initial treatment with stent can provide time to prepare and medically optimize the patient for surgery.

1344 Mesenteric Thrombophlebitis: An Uncommon Complication of Diverticulitis Avin Aggarwal, MBBS. Hennepin County Medical Center, Minneapolis, MN. Introduction: Mesenteric vein thrombosis (MVT) is a rare condition accounting for 6-9% of all cases of mesenteric ischemia. Here is a case of incidentally discovered inferior mesenteric vein (IMV) thrombosis secondary to an underlying diverticular disease. A 59-year-old male presented with 2 weeks of back pain, vague abdominal discomfort (mainly left lower quadrant), poor appetite, non-specific symptoms of fatigue, profound night sweats, and chills. Exam was unremarkable except low-grade fever (100.7 F), mild peri-umblical tenderness, and a soft epigastric bruit. White count, liver function, lipase, and lactate were normal. Abdominal ultrasound (US) showed a non-occlusive thrombus in mid-splenic vein. Computed tomography (CT) confirmed IMV thrombus extending to the confluence with the splenic vein. CT also showed inflammatory changes about the sigmoid-descending colon junction with a hyperdense diverticulum. Review of old colonoscopy revealed focal diverticula in that area. Acute MVT is a rare but important cause of intestinal ischemia, and early diagnosis requires a high index of suspicion. Clinical presentation can be confusing, but with widespread availability of CT imaging and early use of anticoagulation, mortality has decreased (0-23%). Prothrombotic states (inherited or acquired), local factors causing vessel wall injury (pancreatitis, IBD, diverticulitis, peritonitis, and appendicitis), and venous stasis (splenomegaly, cirrhosis) contribute to MVT. It often involves the portal and splenic veins, but only rarely IMV (0-11%) for reasons that are poorly understood. Neoplastic and inflammatory conditions of the descending or sigmoid colon should be expected to spread along the IMV, yet inflammatory involvement of IMV is rare. Septic thrombophlebitis results from direct decompression of the pericolonic abscess into the vein. Most authorities recommend 3-6 months of anticoagulation when risk factors are temporary, while therapy is lifelong for idiopathic or persistent thrombophilic state. Our patient had partially occlusive thrombus likely related to focal diverticulitis. We decided to anticoagulate for 3 months followed by repeat imaging to decide further. Thrombophilia work-up was also deferred, given clear correlation and treatment focused on reversible cause such as diverticulitis.

1345 A Rare Case of an Isolated AL-Amyloid Polyp in the Colon Jennifer Phemister, MD,1 Aaysha Kapila, MD,1 Pranav Patel, MD,1 Thomas Borthwick, MD,2 Mark Young, MD1. 1. East Tennessee State University, Johnson City, TN; 2. VA Mountain Home, Mountain Home, TN. Introduction: Amyloidosis refers to a condition where amyloid is deposited in the extracellular space of various organs or tissues, disrupting normal function. A subtype of amyloidosis known as AL-amyloidosis, is the most common primary systemic form, where the abnormal protein fibers have components of light chain, which cause localized disease. A 62-year-old white male underwent a surveillance colonoscopy with findings of a polyp in the hepatic flexure of the colon (Figure 1). Pathology revealed the hepatic flexure polyp was hyperplastic with amyloid deposition in the vessels, lamina propria, and submucosa, confirmed with H and E and Congo red stain (Figures 2 and 3). Diagnosis of amyloidosis with subtype AL kappa was confirmed by mass spectrometry. Radio-


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[1344A]

Figure 1. USG and CT.

[1345A]

Figure 1.

logic imaging revealed hepatosplenomegaly, with no evidence of systemic amyloidosis. Transthoracic echocardiogram determined an ejection fraction of 50-55% and no evidence of amyloid infiltration. Immunoelectrophoresis revealed Kappa light chains elevated at 28.46 mg/L, normal levels of lambda light chains, and no evidence of monoclonal bands. Bone marrow biopsy was consistent with myeloproliferative neoplasm with no overt morphologic evidence of plasma cell neoplasm and no evidence of amyloid deposition (Figure 4). Therefore, it was determined that the patient had AL-amyloidosis localized to the colon, which was rarely reported in the literature. Currently the patient continues to be asymptomatic with surveillance follow-up every 6 months. AL-amyloidosis is caused by deposition of protein derived from immunoglobulin light chain fragments with 15% of patients having plasma cell neoplasms. Amyloidosis, confirmed by tissue biopsy, should be considered in patients with cardiomyopathy, proteinuria, neuropathy, weight loss, hepatomegaly, or gastrointestinal symptoms. Amyloid deposition in the gastrointestinal tract is greatest in the small intestine with symptoms including diarrhea, steatorrhea, or constipation. It is important to distinguish between localized amyloidosis versus systemic disease because patients with localized amyloidosis require surveillance, whereas patients with systemic disease are treated with chemotherapy and autologous hematopoietic cell transplantation.


1346 Two Cases of Primary Malignant Melanoma of the Colorectal Area Rahman Nakshabendi, MD,1 Matthew Clark, MD,1 Juan Munoz, MD, FACG,1 Imad Nakshabendi, MD, PHD, FACG2. 1. University of Florida COM, Jacksonville, FL; 2. Tampa General Hospital, Tampa, FL. Case 1: A 74-year-old white female with history of breast cancer s/p lumpectomy, presented with painless hematochezia of 6 months’ duration attributed by the patient to hemorrhoids. She became symptomatically anemic and underwent a colonoscopy with biopsy. The first biopsy was a polyp in the ascending colon and the second was a large mass arising in the rectal area that was not reached by initial digital rectal examination. Histological examination of the rectal mass was consistent with malignant melanoma. Thorough clinical examination of the skin and eyes did not confirm presence of primary skin or orbital lesions. Further evaluation with CAT scan and whole body PET scan revealed wide skeletal, hepatic, pulmonary, and lymph node metastasis, both mesenteric and mediastinal. The patient had a previous colonoscopy in 2008 that only showed tubular adenoma. Case 2: A 53-year-old white female presented with complaints of abdominal pain, constipation, and


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[1346A]

Figure 1. Case 2: gross image on the left and histopathology from biopsy on the right.

occasional red blood in her stool for 6 months’ duration. The patient also noticed increased hair loss over the previous few weeks. Physical examination was unremarkable and did not show any pigmentation of the skin or the eyes. Colonoscopy revealed internal hemorrhoids as well as a rectal polyp measuring 1.5 cm, which was snared and retrieved. Histopathology confirmed the presence of malignant melanoma. Discussion: Primary melanoma of the colorectal area is a very rare clinical encounter and very few cases have been reported in literature. Secondary metastasis to the colon is much more common. Melanocytes are not usually found in the colon; however, neural crest cells are extensively found in the colon, and studies have shown that these cells have the potential to differentiate to melanocyte. The anorectum contains the most abundant melanocytes in the GI tract. The anorectum is also the third most common location of malignant melanoma after the skin and retina. The most common symptom is rectal bleeding, which is often mistaken for bleeding associated with hemorrhoids. Malignant melanoma has a very poor prognosis due to its aggressive nature. The reported 5-year survival rate is 6-15% after surgical resection. Prognosis depends on factors such as stage, size, duration of symptoms, and depth of node. The mainstay treatment for malignant melanoma is surgical resection, as chemotherapy and radiation have not shown to be as effective.

Discussion: Based on the medical literature, colorectal cancer rarely metastasizes to bone. Studies with chart review of medical or autopsy records have reported an incidence of 2-24% and even lower, 1-2%, for isolated bony metastasis. Further, the bone metastases were almost always discovered after initiation of treatment for the colorectal cancer. Herein, we present 2 patients without gastrointestinal symptoms who both presented with spinal cord compression from vertebral metastases of adenocarcinoma, later revealed to originate from a colonic source. While we acknowledge its rare occurrence, these 2 cases underscore the importance of having colon cancer on the differential diagnosis for adenocarcinoma of unknown primary in the bone.

1347

Introduction: Dieulafoy’s lesions are an uncommon cause of gastrointestinal hemorrhage, and colonic Dieulafoy’s lesions are even more rare. We present the case of a lower gastrointestinal bleed secondary to a transverse colonic Dieulafoy’s lesion, highlighting the importance of careful endoscopic evaluation in investigating GI bleeding and the consideration of rare entities in the differential diagnosis of a common clinical presentation. A 75-year-old female presented with 2 episodes of melena, 1 episode of bright red blood per rectum, and presyncope. Her comorbidities included coronary artery disease, congestive heart failure, and persistent atrial fibrillation requiring warfarin anticoagulation. Examination found a benign, non-tender abdomen, and rectal examination showed residual melena stool. Her initial hemoglobin was 69 g/L and her INR of 6.2 was supratherapeutic. The patient was supportively managed initially with intravenous crystalloid fluid and packed red blood cell transfusion. Her anticoagulation was reversed with vitamin K and transfusion of fresh frozen plasma. Esophagogastroduodenoscopy was normal with no evidence of active bleeding. On ileocolonoscopy, a large overlying fresh blood clot was visualized in the transverse colon. After disruption of the clot with irrigation, an actively oozing Dieulafoy’s lesion was visualized (Figure 1). Bipolar cautery with a 7 French probe was applied, and subsequently, 2 hemostatic endoclips were deployed at the bleeding site (Figure 2), achieving hemostasis. The patient did not experience any immediate or delayed post-endoscopy complications and she had no evidence of ongoing or recurrent bleeding.

Improvement of Chronic Diarrhea Associated With Radiation Enteritis With Cholestyramine Therapy Matthew Drew, MD,1 Louis Chaptini, MD2. 1. Internal Medicine, Yale New-Haven Hospital, New Haven, CT; 2. Department of Digestive Disease, Yale School of Medicine, New Haven, CT. Introduction: Radiation enteritis is a well-described complication of pelvic or abdominal radiation therapy. Its presentation can be acute, occurring within hours to weeks of therapy, or chronic, appearing within years to decades. Symptoms vary, and can include anorexia, nausea and vomiting, small bowel obstruction, and diarrhea. The most common mechanism to explain diarrhea in chronic radiation enteritis is bile acid malabsorption. Excess bile salts in the colon stimulate water secretion, leading to increased motility and diarrhea. We present a patient who received pelvic radiation for a testicular seminoma while in his thirties, developed symptoms of radiation enteritis in his fifties, and was successfully treated with cholestyramine at age 74. Cholestyramine irreversibly binds bile salts, thus acting as a surrogate ileum and preventing concomitant electrolyte and water secretion into the colon.

1349 Colonic Dieulafoy’s Lesion: A Rare Cause of Lower Gastrointestinal Hemorrhage Christopher Ma, MD,1 Edwin Cheng, MD2. 1. Medicine, University of Alberta, Edmonton, AB, Canada; 2. University of Calgary, Calgary, AB, Canada.

1348 Vertebral Metastasis as the Initial Manifestation of Colon Cancer Tushina Jain, N/A, Renee Williams, MD, Lea Ann Chen, MD. NYU School of Medicine, New York, NY. Introduction: Traditionally, colon cancer is not thought to metastasize to bone, unlike breast, prostate, or lung cancers. In fact, both United States and European cancer society guidelines recommend against endoscopy in the work-up of adenocarcinoma of unknown primary, unless otherwise suggested by clinical symptoms, laboratory, or imaging findings. We would like to present 2 cases of colorectal cancer that presented solely as bony metastases. Case 1: A 34-year-old female presented with bilateral lower extremity paralysis and numbness for 1 day. The patient had an 8-month history of back pain. An MRI 1 month prior at an outside hospital showed a T11 vertebral lesion causing spinal canal stenosis and cord compression. She received outpatient follow-up until this new onset of symptoms, when she was transferred to our hospital for further management. Upon presentation, she was taken emergently for T10-11 laminectomy with biopsy of the vertebral lesion, which revealed adenocarcinoma. Subsequent CT of the chest, abdomen, and pelvis showed a 4.5-cm ascending colon mass, but no other signs of metastases. Colonoscopy with biopsy confirmed primary colonic adenocarcinoma. Case 2: A 61-year-old female presented with worsening pain and numbness of her upper extremities. Two months prior in Russia, she experienced severe neck pain, leading to discovery of a C5-6 compression fracture. She underwent decompression with a vertebral biopsy, which revealed adenocarcinoma. CT scans then revealed several pulmonary nodules, enlarged mediastinal lymph nodes, and lytic skull foci. Upon presentation to our hospital, spine MRI revealed cervical lesions and a T3 lesion with cord compression. CT scans for staging of her adenocarcinoma of unknown primary again revealed pulmonary nodules, as well as 4 hepatic metastases up to 2 cm and a 15-cm sigmoid colonic thickening concerning for neoplasm. Colonoscopy with biopsy confirmed primary colonic adenocarcinoma.


[1349A] lesion.

Figure 1. Presence of active oozing blood from transverse colonic Dieulafoy’s


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Abstracts the left lower quadrant. Computed tomography ( CT ) scans showed diffuse wall thickness of the sigmoid and the rectum with blood clot inside the lumen. High protein C reactive was observed. She had uneventful recovery 5 days after a conservative treatment. Case 2: An 82-year-old white female with an adenocarcinoma of the sigmoid colon underwent colonoscopy to rule out a synchroid tumor. We performed an endoscopic mucosal resection of a benign lesion in the cecum. A tattoo close to a sigmoid tumor was done to facilitate surgery. The procedure was uneventful and she was discharged without complaints. Three hours later, she was distressed with abdominal distension and pain. The abdomen was soft and the bowel sounds were hyperactive. She underwent a routine chest and abdominal X-ray that disclosed only hyperdistension and no free air. Twenty hours later, she got worse with clinical sings of peritonitis. Right hemicolectomy was performed for ischemic colitis. Conclusion: We describe Ischemic colitis following uneventful colonoscopies. Both patients had reduced blood flow with damage to microvasculature, probably due to a high intra luminal pressure related to hyperinflation. On the first case, the cause was the long procedure time and in the second, a partial colonic obstruction due to a sigmoid tumor as a risk factor we found only a previous abdominal surgery on the first case. It is important to pay attention to colonoscopic procedure time, hyperinflation, and hyperextension. We should always leave the patient with the least possible amount of gas.

1351 EUS Findings of Rectal Splenosis

[1349B] Figure 2. Application of hemostatic endoclip to colonic Dieulafoy’s lesion after bipolar cautery, achieving hemostasis.

1350 Ischemic Colitis After a Routine Colonoscopy: Report of Two Cases Edson da Silva, MD, FACG. Hospital Federal dos Servidores do Estado do Rio de Janeiro, Rio de Janeiro, Brazil. Introduction: Ischemic colitis following colonoscopy is rare. We report 2 cases after uneventful colonoscopies. Case 1: A 67-year-old white female with COPD underwent screening colonoscopy. She had a previous pelvic surgery. The bowel was well prepared. The blood pressure was kept normal during the difficult procedure that was time consuming with hyperinflation. The patient was discharged without any complaints. Six hours later, she started to pass bright red blood from the rectum and to complain about abdominal pain that got worse 20 hours later. At this time, the abdomen was soft to palpation with tenderness on

Bakht Cheema, MD, Mohammed Zaidan, MD, Inder Singh, MD. UT Southwestern Austin Programs, Austin, TX. Introduction: Splenosis is a benign asymptomatic condition acquired after mechanical or iatrogenic injury to the spleen. It is incidentally found most commonly during work-up of other diseases. We report a case of splenosis presenting as a rectal mass with extensive peritoneal lymphadenopathy and massive ascites seen on CT imaging. The patient had a history of hepatitis C cirrhosis and had not had good medical care. A work-up for malignancy and lymphoma was started and the patient underwent flexible sigmoidoscopy and an endoscopic ultrasound (EUS) evaluation. Fine-needle aspiration (FNA) of the mass was done. Results showed mature lymphocytes with no atypical cells. Results were later on confirmed with a core biopsy which showed splenic tissue. However, non-invasive tests like nuclear medicine scintigraphy can also point towards the diagnosis of splenosis accurately. If scintigraphy is negative, and the presentation is equivocal, an EUS evaluation and FNA should be considered before core biopsies and surgical interventions are done.

[1351A]

Figure 1. Axial view CT of the pelvis with the rectal mass.

[1351C]

Figure 3. EUS images of the mass. Note the irregular but well demarcated borders. EUS guided FNA biopsy on the right.


[1351B]

Figure 2. Flexible sigmoidoscopy of the extrinsic rectal mass.


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1352 Widely Metastatic Colon Cancer After Previous Prostate Irradiation Adeeti Chiplunker, MD, MMS,1 A. Aziz Aadam, MD,2 William Berger, MD1. 1. Medical College of Wisconsin, Milwaukee, WI; 2. Rush Medical College, Chicago, IL. Introduction: The risk of colorectal cancer is known to exist in patients with prior history of prostate cancer, especially if diagnosed before age 50. Prior radiation therapy increases the risk of both colorectal and bladder cancers. No formal recommendations exist for colorectal screening in patients with prior history of external beam radiation therapy for prostate cancer. Here, we present a case of a patient with widely metastatic colorectal cancer after prior history of prostate irradiation and unremarkable colonoscopy 4 years prior to diagnosis. Case Report: An 85-year-old man with prior history of prostate cancer treated with external beam radiation reported diarrhea, intermittent hematochezia, and abdominal pain for the past 4 months. He also noted a 20-lb weight loss in the past month. A colonoscopy done about 4 years prior to presentation showed small external hemorrhoids and some neovascularization of the anterior wall of the rectum consistent with prior history of radiation therapy for his prostate cancer. The patient was admitted for further management of these symptoms. On exam, the abdomen was soft, mildly distended, and diffusely tender to palpation. A rectal exam noted a circumferential hard lesion 2 cm from the anal verge. A colonoscopy was then performed. The colonoscopy showed a circumferential stricture in the proximal rectum extending into the recto-sigmoid junction, where a large ulcerated mass with areas of necrosis was identified. The remainder of the colon showed some mild diverticulosis and otherwise normal mucosa. Multiple biopsies taken of the mass showed moderately differentiated invasive adenocarcinoma consistent with colorectal origin. A CEA level was elevated at 16 ng/mL (range: 0-3 ng/mL). CT scans of the chest, abdomen, and pelvis showed the mass invading the urinary bladder, extensive intra-abdominal metastases, and possible lung metastases. The patient opted to pursue comfort care and died approximately 20 days after diagnosis. Discussion: Given the higher risk of the development of colorectal cancer after previous external beam radiation therapy for prostate cancer, a high index of suspicion must be maintained in the setting of new GI symptoms. Patients with a history of prostate cancer and irradiation should undergo appropriate endoscopic evaluation, especially with warning signs of weight loss and hematochezia. Metastatic colorectal cancer can develop rapidly in this subset of patients as evidenced by our case. Prompt diagnosis is critical in further management of these patients.

importance of multiple biopsies throughout the colon. Clinical recovery after drug therapy suggests that intestinal spirochetosis may play a pathogenic role in causing symptoms.

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Colonic Spirochetes in a Patient With HIV

CMV Proctitis in an Immunocompetent Young Adult

Belen Tesfaye, MD, Michael Windham, MD, Rehana Begum, MD. Howard University Hospital, Washington, DC.

Nikhil Kapila, MD, Justin Goralnik, MD, Andrew Hamarich, DO. Internal Medicine, University of Connecticut Health Center, Farmington, CT.

Introduction: Spirochetosis of the colon was first reported in 1967 in a patient with chronic diarrhea. Since this first description, however, the clinical significance of spirochetosis has been controversial, as its relationship with human disease has remained unclear. Spirochetosis has been associated with abdominal pain, appendicitis, chronic diarrhea, and rectal bleeding in some cases, but in the majority of cases, spirochetosis is an incidental finding with no clear clinical correlates.The anaerobic intestinal spirochetes Brachyspira aalborgi and Brachyspira pilosicoli seem to be responsible for most cases of colonic spirochetosis. Treatment with metronidazole is advisable in patients with persistent symptoms. Case Report: We report a case of a 38-year-old African American male with HIV on HAART who presented with intermittent rectal pain, blood in the stool, and anal itching for 2 years. He underwent colonoscopy with multiple biopsies which revealed spirochetes in the colon. He was treated with a 10-day course of oral metronidazole with symptom resolution. Conclusion: A high degree of suspicion is required in cases presenting with abdominal pain, chronic diarrhoea, and/or hematochezia associated with a normal endoscopic examination, thus emphasizing the

Introduction: Cytomegalovirus (CMV) proctitis may present in otherwise young, healthy, and immunocompetent individuals. CMV proctitis/colitis may mimic ischemic colitis and Clostridium difficile infection. A high index of suspicion must be maintained when evaluating such patients Case Report: An 18-year-old male presented to the emergency room with a 3-day history of abdominal pain and bright red blood per rectum. The patient reported multiple episodes of bright red blood per rectum and had never experienced similar symptoms in the past. His past medical history is significant for post-traumatic stress disorder and intermittent migraines. Patient attests to regular alcohol consumption, frequent marijuana use, and intermittent tobacco use. He is a heterosexual and is sexually active. There is no significant family history of inflammatory bowel disease, polyps, or colon cancer. Patient’s vital signs were stable at the time of admission. His abdomen was soft and diffusely tender to palpation with no guarding or rigidity and his rectal exam was positive for bright red blood. His complete blood count showed a hemoglobin of 15.8, hematocrit of 44.4, WBC of 4, and platelets of 105. His chemistries, coagulation profile, and liver function tests were all within normal limits. He was HIV negative. The computed tomography (CT) scan of the abdomen demonstrated wall thickening and inflammatory changes of the rectum and distal sigmoid colon. Sigmoidoscopy revealed congested ulcerative mucosa in the rectum. Esophagogastroduodenoscopy (EGD) showed erythematous mucosa in the gastric antrum. Pathology from the rectum demonstrated CMV proctitis that was confirmed by immunohistochemical stains. The patient was subsequently started on a 14-day course of valganciclovir. Discussion: Our patient, who was an otherwise healthy, immunocompetent male, presented with bright red blood per rectum secondary to CMV proctitis. In the era of HIV and immunosuppression, CMV has emerged as a well-known pathogen in those patients who are immunocompromised. The widespread use of highly active antiretroviral therapy (HAART) has seen a recent decline in the incidence of opportunistic CMV infection. CMV proctitis is an infrequently reported disease entity in patients with an intact immune system. Various risk factors for development in the immunocompetent host include mucosal injury by a disease process such as inflammatory bowel disease or aging. Thus, our patient, with no significant past medical history and an intact immune system, had a unique presentation of an uncommon disease process.

[1353B]

Figure 2. Warthin-Starry stain showing the surface coating by spirochetes.

1355 Gastrointestinal Bleeding in the Setting of Invasive Aspergillus Infection in an Immunocompromised Patient Chad Cooper, MD, MHA, Jorge Bizet, MD, Marc Zuckerman, MD, FACG, Alireza Torabi, MD, Antonio Mendoza Ladd, MD. Internal Medicine, Texas Tech University Health Sciences Center, El Paso, TX.

[1353A]

Figure 1. Normal-appearing colonic mucosa.


Introduction: Invasive Aspergillus (IA) commonly involves the lungs, but can also affect other organs such as the skin, adrenal glands, central nervous system, liver, spleen, and the gastrointestinal tract. Case Report: A 36-year-old female presented with septic shock secondary to extensive Fournier gangrene and required multiple surgical debridement of the perineal and retroperitoneal area. Vital signs on admission were a temperature of 39.4 C and blood pressure of 85/56 mm Hg, pulse rate of 108/min, and respiratory rate of 25. Physical examination revealed bilateral rhonchi and abdominal


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Abstracts tenderness. Examination of the perineum/genital area revealed bilateral gluteal and perilabial edema, erythema, and focal areas of necrotic tissue with purulent discharge. Other surgeries included small and large bowel resections with colostomy and diverting ileostomy. Eleven weeks after admission, the patient developed hematochezia from the colostomy associated with a decrease in hemoglobin and hematocrit to 6.4 g/dL and 20.2%, respectively. Colonoscopy through the ostomy revealed blood throughout the colon and a 3-cm necrotic ulcer with an adherent clot in the transverse colon. Biopsies were taken from the edge of the ulcer. Histopathological analysis of the specimen with Grocott’s methenamine silver (GMS) stain revealed septated hyphae with the 45 degree angle branching that is morphologically consistent with Aspergillus species. The patient was treated with intravenous voriconazole for 30 days with a prolonged hospitalization but no recurrent bleeding. Discussion: Gastrointestinal aspergillosis is an unusual presentation of IA associated with a high mortality rate. Characteristic features of gastrointestinal aspergillosis include invasion of the mesenteric arteries, intravascular thrombosis, and subsequent tissue ischemia. Clinical manifestations of IA of the gastrointestinal tract can include fever, abdominal pain, ileus, peritonitis, bloody diarrhea, or hematochezia. In an autopsy series of patients with IA, 37 of 107 patients had Aspergillus involvement of the gastrointestinal system; the most common pathological findings included ulcers and abscesses. Although rare, invasive aspergillosis may present with gastrointestinal bleeding associated with necrotic ulcers on endoscopic examination.

1356 A Case Of Amyloid Colitis in a 23-Year-Old Patient Kawtar Alkhalloufi, MD, Suneel Tammana, MD, Rehana Begum, MD, Taddesse Heath, MD, Andrew Sanderson, MD. Howard University Hospital, Washington, DC. Introduction: We are presenting a case of 23-year-old Ethiopian female with a history of hypertension and end-stage kidney disease dialysis dependent diagnosed at age 8 years, as well as rheumatoid arthritis since age 6 years, who presented with the complaint of bloody diarrhea of 4 months’ duration. The diarrhea was associated to a crampy abdominal pain and nausea. She also reported a lowgrade fever and a weight loss. On admission, the patient was found to have a microcytic anemia, with positive fecal occult blood. Colonoscopy was performed and revealed evidence of moderate to severe pancolitis involving mainly the rectum and the left colon, multiple biopsies were taken. A Congo red stain performed on the biopsy specimens showed a positive staining with apple green birefringence consistent with amyloid colitis. Amyloidosis is a rare disease caused by an extracellular deposits of insoluble fibrillar proteins in various organs and tissues.The gastrointestinal (GI) tract involvement with both symptoms and biopsy proof of involvement of the intestinal tissue itself is uncommon 3-7% in some series. Commonly reported symptoms of GI amyloidosis are esophageal reflux, constipation, nausea, and abdominal pain. Other symptoms, such as diarrhea, weight loss, and early satiety, which are commonly attributed to GI amyloidosis, may be caused by autonomic neuropathy and small bowel bacterial overgrowth. Diagnosis of amyloidosis, relies on clinical, laboratory and histological findings. Serum and urine immunoelectrophoresis are the initial laboratory tests, but confirmation requires histological evaluation.Treatment should be directed at the underlying cause and the gastrointestinal complications are managed with symptomatic control.

[1356B]

Figure 2. Positive Congo red stain with birefringence.

1357 Early Diagnosis and Treatment of Stercoral Colitis With an Aggressive Bowel Regimen Aly Mohamed, MD, Minh Nguyen, MD, Rebecca Tsang, MD, Andelka LoSavio, MD, Omar Khan, MD. Loyola University Medical Center, Maywood, IL. Introduction: Stercoral colitis is a rare inflammatory colitis which results from fecal impaction causing increased colonic intraluminal pressure, which may progress to ischemic necrosis, ulcer formation, and colonic perforation. The majority of cases continue to be reported in the surgical literature with late complications of bowel perforation requiring surgical intervention, which is associated with a 35% mortality rate. We present a patient with acute symptoms of increased bowel urgency and frequency who was diagnosed with stercoral colitis and successfully treated with an aggressive bowel regimen, thus avoiding surgery. Case Report: A 92-year-old female with a history of chronic constipation presented with frequent diarrhea associated with pain, pressure, and small blood streaks for a period of 1 week. She had previously discontinued her anticonstipation bowel regimen and was taking Norco after sustaining a fall 3 weeks prior to admission. Abdominal radiograph revealed a large fecal ball in the rectosigmoid colon and CT abdomen showed stercoral colitis with impaction, dilation of the proximal sigmoid colon, and marked rectal wall thickening. Manual disimpaction was unsuccessful and an aggressive bowel regimen consisting of fleet’s enemas, magnesium citrate, mineral oil enema, and oral mineral oil was initiated. After 4 days of treatment there was clinical and radiographic evidence of resolution. Discussion: Stercoral colitis can be fatal and requires prompt treatment. The importance of early recognition is underscored by the high mortality rate associated with late complications reported in the surgical literature. Early diagnosis with CT imaging demonstrates a fecaloma, focal wall thickening of a dilated sigmoid colon and rectum representing edema from ischemia or ulceration, and peri-colonic or peri-rectal fat stranding. The most common site of impaction occurs in the sigmoid and rectosigmoid colon, which, in addition to having a relatively poor blood supply, have the narrowest colonic diameter allowing for higher intraluminal pressure. Ischemic pressure necrosis results when luminal distention increases pressure above bowel wall capillary perfusion pressure. Ulcerations are seen in up to 27% of cases, with 77% occurring in the sigmoid and rectosigmoid colon. The best way to prevent stercoral colitis is to prevent constipation, which is present in approximately 60% of patients with fecal impaction. Early diagnosis of fecal impaction should prompt aggressive bowel cleansing and manual disimpaction, which may reduce pressure and decrease the risk of ulceration.

1358 Ileocaecal Tuberculosis Mimicking Crohn’s Disease in a Nigerian

[1356A]

Figure 1. Diffuse erythematous mucosa.

Adegboyega Akere, MD, MACG,1 Temitope Oke, MBBS,1 Oludolapo Afuwape, MBBS,2 Abideen Oluwasola, MBBS3. 1. Dept. of Medicine, College of Medicine, University of Ibadan/University College Hospital, Ibadan, Nigeria; 2. Dept. of Surgery, College of Medicine, University of Ibadan/University College Hospital, Ibadan, Nigeria; 3. Dept. of Pathology, College of Medicine, University of Ibadan/University College Hospital, Ibadan, Nigeria. Introduction: Both tuberculosis and Crohn’s disease affect the terminal ileum and ileocaecal region, and this may pose a challenge. A typical case is presented here. Case Report: A 23-year-old man with recurrent abdominal pain and weight loss of 7 months’ duration. Pain was at epigastric area and radiated to the right iliac fossa, dull in nature, and disturbed his daily activities. Had watery nonmucoid and nonbloody stool. Also had non-productive cough. He was chronically ill looking, febrile, and pale. He had tenderness in the right iliac fossa. Vital signs: respiratory rate 26 breaths/min, pulse 120 beats/min, blood pressure 80/60 mm Hg. Colonoscopy revealed polypoid lesions in the caecum, deformed and nodular ileocaecal valve, and cobblestone appearance in the ileum. The patient had right hemicolectomy done.



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Discussion: Increasing incidence of abdominal tuberculosis has been reported worldwide, about 23% of these patients have isolated colonic involvement.[1] Misra et al reported abdominal pain, fever, anorexia, weight loss, and diarrhoea as the presenting symptoms in patients with colonic tuberculosis, as it was the case in our patient.[2] These symptoms also occur in Crohn’s disease. In tuberculosis colitis, typical features on colonoscopy are transverse ulcers, deformed ileocaecal valve and caecum, nodules, fibrous bands, inflammatory polyps.[3] In contrast,features of Crohn’s disease are longitudinal ulcers with a cobblestone appearance, stricture, perianal lesions, and pseudopolyps.[4] In our patient, transverse ulcers were not seen during colonoscopy because these ulcers were located beyond the reach of colonoscope in the ileum, but cobblestone appearance of the ileum was very prominent and this is typical of Crohn’s disease. Colonic biopsy did not reveal tuberculosis. Lee et al found cobblestone appearance to be significantly more common in Crohn’s disease, whereas a patulous ileocaecal valve, transverse ulcers were seen more in tuberculosis.[5] In our patient, transverse ulcers were seen only in the resected portions of the ileum and tuberculosis was confirmed at histology. References: [1] Marshall JB. Tuberculosis of the gastrointestinal tract and peritoneum. Am J Gastroenterol 1993;88:989-999. [2] Misra SP, Misra V, Dwivedi M, Gupta SC. Colonic tuberculosis: Clinical features, endoscopic appearance and management. J Gastroenterol Hepatol. 1999;14(7):723-9. [3] Aoki G, Nagasako K, Nakae Y, et al. The fiber colonoscopy diagnosis of tuberculous colitis. Endoscopy 1975;7:113121. [4] D’Haens G, Rutgeerts P. Endoscopic Evaluation. In: Prantera C, Korelitz B, eds. Crohn’s Disease. 1st ed. New York: Marcel Dekker, Inc. 1996:113-123. [5] Lee YJ, Yang SK, Byeon JS, et al. Analysis of colonoscopic findings in the differential diagnosis between intestinal tuberculosis and Crohn’s disease. Endoscopy 2006;38(6):592-597.

1359 Laxatives Can Paint Your Colon Black! Aaysha Kapila, MD,1 Pranav Patel, MD,1 Ravindra Murthy, MD,2 Mark Young, MD1. 1. East Tennessee State University, Johnson City, TN; 2. James H. Quillen VA Medical Centre, Johnson City, TN. Introduction: Melanosis coli refers to diffuse brown or black pigment deposition in the mucosa of the gastrointestinal tract that is associated with long-term usage of anthraquinone-containing laxatives. It takes an average of 3-13 months to develop color changes. Melanosis coli was first described in the colonic mucosa by Cruveilhier, but the term “melanosis coli” was first used by Virchow. We report a case of a 50-year-old male with a family history of colon cancer who underwent surveil-

lance colonoscopy. Past medical history was significant for chronic degenerative disc disease which was managed by opioid pain medications. He was using cascara sagrada, an anthraquinone laxative for pain medication-induced constipation. Endoscopic examination demonstrated classic, diffuse, extensively dark colored pigmentation of the entire colon consistent with a diagnosis of melanosis coli. Tubular adenomas were seen in the ascending colon and the cecum, which were spared from the pigmentation. Pathologic examination of the colonic mucosa was significant for pigmented macrophages in the lamina propria. The patient was advised to start a high-fiber diet and avoid anthraquinone laxatives. Repeat colonoscopy was scheduled in 1 year. Anthraquinone laxatives have been associated with colonic epithelial cell apoptosis with subsequent phagocytosis by the macrophages. These apoptotic bodies are transformed into lipofuscin pigment in macrophage heterolysosomes, causing brownish and black pigmentation of the colonic mucosa. Melanosis coli is a reversible condition that infrequently involves the esophagus, duodenum, ileum, and jejunum. It is mostly an incidental finding. The association of melanosis coli with colorectal adenomas has been observed, but its association with colorectal cancer is controversial. Thus it is wise and prudent to discourage the usage of these laxatives and inform patient of other safer alternatives.

1360 An Incidental Discovery of Low-Grade Appendiceal Mucinous Neoplasm Aaysha Kapila, MD,1 Jennifer Phemister, MD,1 Pranav Patel, MD,1 Ravindra Murthy, MD,2 Chakradhar Reddy, MD,1 Mark Young, MD1. 1. East Tennessee State University, Johnson City, TN; 2. James H. Quillen VA Medical Centre, Johnson City, TN. Introduction: Low-grade appendiceal mucinous neoplasm (LAMN) is a rare entity with an incidence ranging from 0.2% to 0.7% of all excised appendixes. Approximately 50% are incidental findings with initial discovery during radiologic and endoscopic examinations or during surgery. Initial presentation can range from being asymptomatic, right lower quadrant abdominal pain, or a palpable abdominal mass. Diagnosis is established using ultrasound, computed tomography, and a colonoscopy. We present a case of a 65-year-old male who underwent a surveillance colonoscopy, which revealed a large smooth cystic bulge at the appendicular orifice (Figure 1A). Subsequent computed tomography of abdomen with contrast revealed an appendiceal mucocele, measuring 13.3 x 4.5 cm (Figure 1B). Given the abnormal imaging findings, an elective appendectomy was performed. The gross specimen was 9 cm in length and 3 cm in diameter with the appendiceal lumen filled with mucoid yellow material.

[1359A] Figure 1. (A) Endoscopic image demonstrates a dark brown and black appearing colon, a finding that is consistent with the diagnosis of melanosis coli. (B) A biopsy specimen from the colon revealed sheets and clusters of macrophages laden with brownish pigment in the lamina propria.

[1360A] Figure 1. (A) Colonoscopy image showing a large cystic lesion at the appendicular orifice. (B) Computed tomography with contrast demonstrating a large appendix with diffuse wall thickening indicative of appendiceal mucocele neoplasm. (C) Histopathologic image (10 x) shows villiform mucinous epithelium, glandular epithelium with tall columnar mucinous cells and pseudostratified nuclei at the base.



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Abstracts Histopathological evaluation revealed low-grade appendiceal mucinous neoplasm (Figure 1C). The patient had an uneventful recovery and is currently doing well. Repeat colonoscopy was scheduled in 1 year. Surgical removal of the mucinous neoplasm is the definitive treatment. There has been a lack of consensus regarding surgical management of LAMN, with appendectomy being professed by some and others suggest right hemicolectomy via laparoscopic or surgical means. In patient with peritoneal implants surgical debulking needs to be performed with rare reports of intraperitoneal chemotherapy. Poor prognosis is associated with perforation and spillage of the mucocele into the peritoneal cavity, thus developing pseudomyxoma peritoni, which is a rare condition with mucinous peritoneal implants and mucinous ascites.

1361 An Acute Abdomen Leading to an Unexpected Price Ali Alsayed Hussain, MD, Michelle Hadley, DO. Department of Medicine, Saint Vincent Hospital, Worcester, MA. Introduction: Acute abdominal pain grants immediate surgical evaluation and possible emergent intervention. The differential diagnoses of an acute abdomen are broad. Some diseases may mimic acute abdominal presentations and hence result in unnecessary hospitalizations, surgical interventions, and the overuse of hospital resources. Case Report: A 39-year-old white male presented with 1 day history of abdominal pain and nausea. He described his pain as severe, sharp, non-radiating, and located in the left lower quadrant. There was no association with food intake, no history of fever, or vomiting. Past medical history was significant for hypertension and gastroesophageal reflux disease. The physical examination revealed moderate tenderness with deep palpation to the left lower abdominal quadrant, lacking rebound tenderness or guarding. Laboratory data did not reveal a leukocytosis. Basic metabolic panel was within normal limits except for a low potassium. A computed tomography (CT) scan of the abdomen illustrated an ovoid fat density structure with mild associated inflammatory changes that extended from the anterior left colonic wall and lacked any evidence for diverticulitis. A diagnosis of primary epiploic appendagitis (PEA) was therefore established. Conservative management with non-steroidal anti-inflammatory agent was recommended and fulfilled. A 2-week follow-up evaluation revealed complete resolution of the patient’s symptoms. Discussion: PEA is a rare identity with an estimated frequency at 1.3% and incidence at 8.8 cases per million per year 1. PEA mimics an acute abdominal presentation, and therefore can be easily misdiagnosed. In one case study, 7 out of 660 abdominal CT scans were misdiagnosed initially as diverticulitis or appendicitis. These misdiagnoses resulted in all 7 of the patients being admitted and an average hospital stay of 4.33 days. Six out of the 7 patients received unnecessary antibiotic therapy, with an average cost per patient of $4,1172. An awareness of PEA’s clinical and radiological features, as well as the proper evaluation, may decrease unnecessary hospitalizations, consultations, antibiotic therapy, and the overuse of hospital resources.

[1362A]

Figure 1.

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Figure 2.

1362 Colon Neuroganglionoma: A Rare Cause of Hematochezia Azfar Niazi, MBBS, Omar Khokhar, MD, FACG. Department of Medicine, Division of Gastroenterology, University of Illinois-Peoria, Bloomington, IL. Introduction: Ganglioneuromas (GN) are rare and benign tumors of autonomic nerve fibers. These tumors can grow wherever sympathetic nervous tissue is found, but are most frequently found in the abdomen. Other locations are adrenal gland, paraspinal retroperitoneum (sympathetic ganglia), posterior mediastinum, head, and neck. Uncommon locations include urinary bladder, bowel wall, abdominal wall, and gallbladder. We report a case of a 50-year-old white male who presented with blood in stool. There was no family history of gastrointestinal malignancy. Physical exam and lab investigations were unremarkable. CT scan with contrast enhancement of abdomen and pelvis did not show any anomaly. Colonoscopy revealed polypoid erythematous mucosa in the proximal ascending colon. Biopsy confirmed neuroganglionoma. The tissue was excised. Ganglioneuromas are rare tumors of the colon. GN can mimic colon adenocarcinoma in initial signs and symptoms. Most GN are benign, and treatment may not be necessary in asymptomatic individuals. In this case, however, removal of the lesion was necessary because of bleeding.

[1361A]

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1363 Metastatic Melanoma to the Colon Azfar Niazi, MBBS, Omar Khokhar, MD, FACG. Department of Medicine, Division of Gastroenterology, University of Illinois-Peoria, Bloomington, IL. Introduction: Melanoma is the most ominous type of skin cancer.[1] It is highly malignant and frequency metastasizes to lymph nodes, liver, lungs, bones, and brain. Colonic tumors secondary to metastasis are uncommon.[2] Case Report: A 65-year-old female was referred to GI clinic for abnormal CT scan. She reported constipation. CT scan was performed as part of follow-up for cutaneous malignant melanoma and bladder cancer 2 years ago. Colonoscopy revealed a large firm mass in the splenic flexure. Histopathology confirmed metastatic malignant melanoma. She received an enteric stent with improvement in symptoms. Conclusion: Malignant melanoma metastasis to the colon is a rare occurence. Treatment includes surgical removal of the affected area of the colon. In this case, advanced metastases led to palliative stent placement.

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Figure 1. Multiple small ulcers and a single polyp.

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Figure 2. Strongyloides stercoralis larvae.

Figure 1.

1364 Strongyloides Colitis: A Lethal Mimic of Ulcerative Colitis Belen Tesfaye, MD, Dilhana Badurdeen, MD, Justice Arhinful, MD, Getachew Mekasha, MD, PhD. Howard University Hospital, Washington, DC. Introduction: Strongyloides colitis is a severe but easily curable form of strongyloidiasis that carries a high mortality rate if untreated. Autoinfection characteristic of Strongyloides frequently makes the infection a life-long disease unless it is effectively treated. We present a 35-year-old Ethiopian male with HIV on HAART who presented with 3 years history of abdominal pain and weight loss. On physical examination he had diffuse abdominal tenderness and laboratory evaluation showed mild eosinophilia. Colonoscopy revealed pancolitis characterized by aphthoid ulceration and a single polyp. Biopsy showed intense tissue eosinophilic infiltrates and larvae of Strongyloides stercoralis, thus confirming this parasite as the causative agent for the colitis. Patient was treated with ivermectin with resolution of symptoms. Strongyloides stercoralis is a nematode infection that predominantly involves the small bowel. Spillover infection to the colon does occur, but is uncommon and is usually associated with an immunocompromised host. The diagnosis is usually made by detecting rhabditiform larvae in concentrated stool (25/hpf, negative C. difficile stool antigen and toxin, and negative stool cultures. Severe colitis was seen on colonoscopy with histological confirmation of autoimmune colitis, and patient was initiated on prednisone (50 mg tapered over 10 days), with no improvement rising concern about steroid-resistant colitis. At this point Infliximab therapy (5 mg/kg) was started with resolution of diarrhea. Second case of 88-year-man also had similar presentation, but responded well to steroids with resolution of diarrhea due to early recognition and constituted steroid-responsive autoimmune colitis. Third case of 51-year-old man with malignant melanoma, currently on ipilimumab (3 mg/kg, 2 cycles), presented with nausea/vomiting, diarrhea, and severe abdominal pain for 1 week. Infectious work-up was all negative. Sigmoidoscopic evaluation revealed severe colitis; prednisone (50 mg tapered over 10 days). Bowel perforation was suspected and confirmed on acute abdominal series. Patient underwent emergent laparotomy with right hemicolectomy and ileostomy. Patient recovered after an extended hospital stay. Discussion: Ipilimumab-induced autoimmune colitis is becoming a more frequent entity among patients treated for metastatic melanoma. Currently, first line approach is a 4-6 weeks steroid taper (starting oral prednisone 1-2 mg/kg daily or dexamethasone 4 mg every 4 hours), which leads to a significant improvement of symptoms within 1-2 weeks. Infliximab is a second line salvage therapy and used for steroid-resistant cases. Given the limited number of cases reported there are no formal guidelines on when to start infliximab and more information is needed in order to prevent complications as perforation and hemorrhage. Our case series intends to make practicing gastroenterologists cognizant regarding this emerging entity, and also urge them to maintain a high suspicion for possible complications (perforation) in patients started on steroids for this autoimmune colitis.

1377 A Rare Case of Entamoeba histolytica and Colonic Strictures Orel Benshar, MD, Evan Grossman, MD, Veronika Dubrovskaya, MD. SUNY Downstate Medical Center, Brooklyn, NY.

[1374A]

Figure 1. Proctocolitis.

Introduction: Colonic strictures may have several etiologies: infectious, inflammatory, and malignancyrelated. Amebiasis should be considered in the differential diagnosis of colonic stricture especially in patients with known past exposure or infection. Case Report: A 55-year-old male from Trinidad with a past medical history of recent pyogenic liver abscess secondary to Entamoeba histolytica infection presented with intermittent episodes abdominal pain about 2 months later. Physical exam and basic labs were normal. Colonoscopy demonstrated benign stricture of the sigmoid colon. Multiple sigmoid biopsies demonstrated acute and chronic moderate inflammation of the lamina propria with limited glandular distortion and multiple acute cryptitis with increased eosinophilic infiltration with no dysplasia. Stool culture,

[1375A] Figure 1. CMV inclusion body with characteristic ‘owl's eye’ appearance in the patient's biopsy.

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Clostridium difficile, and ova and parasites were negative. Based on the histopathology the patient was empirically treated for inflammatory bowel disease (IBD) with mesalamine (Lialda® and Rowasa®); however, his symptoms persisted. Repeat CT scan of the abdomen/pelvis revealed an unchanged stricture in sigmoid with mild diverticulosis, minimal fat stranding, and multiple circumscribed lesions in the liver consistent with cysts. Serology was positive for Entamoeba histolytica antibody. Given that our patient recently had an extraintestinal amebiasis infection, followed by a clinically symptomatic stricture, the diagnosis of stricture secondary to amebiasis was strongly entertained. Since the patient was partially treated with metronidazole in the past for extraintestinal coverage, paromomycin was added for intestinal amebiasis eradication. The patient’s symptoms improved after therapy. Discussion: Amebiasis should be considered with patients presenting with colonic strictures. Our patient’s mild diverticulosis status, lack of response to IBD treatment, nonspecific biopsy results, combined with nearly concurrent development of hepatic and colonic findings increased our suspicion of colonic stricture secondary to amebiasis. To confirm the diagnosis in future cases, Entamoeba histolytica stool antigen should be sent and stool microscopy should be performed.

1378 A Patient With Colon Perforation Due to Amebiasis: A Rare and Fatal Complication Iswan Nusi, MD, SpPD, K-GEH, Amie Vidyani, MD, SpPD, Putu Niken Ayu Amrita, MD, SpPD, Herry Purbayu, MD, SpPD, K-GEH, Ulfa Kholili, MD, SpPD. Gastroenterology and Hepatology Division, Department of Internal Medicine, Dr. Soetomo Teaching Hospital, Airlangga University, Surabaya, Indonesia. Introduction: Amebiasis is an infection due to Entamoeba histolytica. The clinical picture of amebic colitis is vague and could wrongly diagnosed as inflammatory bowel disease (IBD) due to similar clinical findings. Acute colitis with intestinal perforation is rare, occurs in less than 0.5% of cases and associated with mortality rate more than 405 .We report a case of a 60-year-old female patient with colon perforation due to amebiasis. She came with clinical presentation abdominal tenderness, missing bowel sound, abdominal wall rigidity, and missing liver dullness. The patient had history assessed as IBD due to diarrhea with bloody stool, abdominal cramps, and fever, and has been given steroid and immunosuppresant in previous rural hospital. Diagnosis of generalized peritonitis due to intestinal perforation was made. Exploratory laparotomy was performed immediately and the findings were perforation of caecum, colon ascenden, colon transversum, and colon descenden. Subtotal colectomy, ileostomy, and Hartmann procedure was performed. The correct diagnosis was established after histopatology examination of the surgical specimen showed amebic colitis with necrosis, ulceration, and perforation. Because the erroneous diagnosis of IBD can lead to disastrous complications, it is important to exclude amebic colitis prior to undertaking immunosupressant and steroid therapy. Treatment of amebic colitis with metronidazole 500 mg 3 times a day for 10 days were given.

1380 A Rare Case of Primary Colonic Non-Hodgkin’s Diffuse Large B-Cell Lymphoma Charles Rives, MD, John Anong, MD, John Litchfield, DO, Atif Saleem, MD, Atul Khanna, MD, Pranav Patel, MD, Eric Carter, DO, Mark Young, MD, Ravindra Murthy, MD. East Tennessee State University, Johnson City, TN. Introduction: Primary colonic lymphoma is a rare manifestation of colonic malignancy. We report a rare case of primary colonic non-Hodgkin’s diffuse large B-cell lymphoma (PCNHDLBL) presenting as a symptomatic rectal stricture in a patient with ulcerative colitis (UC), who was being treated with azathioprine and adalimumab. Case Report: A 66-year-old male with a 7-year history of UC treated with azathioprine for 5 years and adalimumab for 3 years presented with complaints of 4 weeks of frequent loose stools, bloody bowel movements, and lower abdominal pain while defecating. On labs, hemoglobin was 10.6 g/dL, and WBC and the metabolic panel were within normal limits. The stool was negative for Clostridium difficile. Flexible sigmoidoscopy revealed rectal polyps and a partially obstructing stricture 10 cm from the anal verge. Biopsies were taken for pathology. The colonoscope could not be advanced beyond the stricture. A CT of the abdomen and pelvis showed distal sigmoid and rectal wall thickening, as well as pericolonic fat stranding consistent with active inflammation. Pathology of the stricture was positive for PCNHDLBL. The patient declined colectomy and elected to undergo chemotherapy with rituximab, cyclophosphamide, hydroxydaunorubicin, oncovin, and prednisone (R-CHOP). Discussion: PCNHDLBL is a rare extranodal type of lymphoma of the gastrointestinal (GI) tract and makes up approximately 72 hours at time of hospital discharge. Unfortunately, due to insurance and drug formulary issues, oral mesalamine was restarted as an outpatient. Once restarting the mesalamine, the patient’s fevers returned, confirming the diagnosis of mesalamine-induced drug fever. Although not a common reaction, mesalamine-induced fever should be considered in a patient with fevers of unknown etiology after a thorough work-up. Once the diagnosis is confirmed, a desensitization to mesalamine can also be considered.

1485  Please see page S665 for OUTCOMES RESEARCH  PANCREATIC/BILIARY.

1486 A Rare Disease Mimicking Crohn’s Disease Huafeng Shen, MD,1 David Cave, MD,2 Seymour Katz, MD3. 1. NUMC, East Meadow, NY; 2. UMass Memorial Medical Center, Worcester, MA; 3. New York University School of Medicine, New York, NY.



Case Report: A 30-year-old man with a history of anemia since age 15 presented with intermittent abdominal pain and a decrease appetite for the preceding 4 months. The pain was sharp and


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wave-like, associated with melena, which spontaneously resolved. He was otherwise asymptomatic between episodes. He denied diarrhea, blood in the stool, or NSAID use, but lost 20 pounds over the last year. Esophagogastroduodenoscopy (EGD) and colonoscopy 3 years ago were unremarkable. On physical exam, his body mass index (BMI) was 19.9, but was otherwise normal. Work-up with colonoscopy was normal to the terminal ileum. Video capsule endoscopy showed mid-jejunal ulcerations and stenosis. The capsule did not pass into the cecum and required surgery for small bowel obstruction due to the retained capsule. A laparotomy with intraoperative enteroscopy revealed 6 tight ulcerated stenoses within a 45-cm segment of small bowel approximately 120-140 cm from the ileocecal valve. The 45 cm of small bowel was resected. Pathology revealed cryptogenic multifocal ulcerous stenosing enteritis. Post-operatively, the patient was started on infliximab. However, at 9 month post-operative follow up, the patient developed iron deficiency anemia and intermittent abdominal pain. Discussion: Since the disease was first described by Debray et al in 1964, there have been about 60 cases of CMUSE published. Other entities causing multifocal small bowel ulcerations include Crohn’s disease (CD), chronic ulcerative jejunoileitis (CUJI), nonsteroidal anti-inflammatory drug (NSAID)-induced enteropathy, lymphoma, Behçet’s disease, infections (e.g. Campylobacter, Shigella, Yersinia, Salmonella, tuberculosis, and cytomegalovirus), trauma, and ischemia. The clinicopathological features of CMUSE include: 1.) unexplained small intestinal strictures found in adolescent and middle-aged subjects, 2.) multiple superficial ulceration of the mucosa and submucosa, 3.) a chronic or relapsing clinical course even after surgery, 4.) no biological signs of systemic inflammatory reaction, and 5.) beneficial effect of systemic glucocorticosteroids. The treatment of CMUSE is symptomatic. Systemic glucocorticosteroid therapy is still the mainstay of treatment, but results in steroid dependence. Anti-tumor necrosis factor (TNF)-alpha therapy (infliximab) has been reported to induce remission. However, our patient failed to respond to anti-TNF therapy. To date, the optimal treatment strategy for CMUSE is still open to discussion.

1487 An Unusual Case of Inflammatory Bowel Disease (IBD) Presenting as Phlegmasia Cerulea Dolens (PCD) Sumeet Munjal, MD, Akriti Dewanwala, MD, Thomas Mahl, MD. Department of Gastroenterology, Hepatology and Nutrition, University at Buffalo, New York, Buffalo, NY. Introduction: Patients with IBD are at increased risk for thromboembolism, especially during exacerbations. PCD is a rare form of massive proximal venous thrombosis of a limb presenting as sudden severe pain with swelling, cyanosis, edema, venous gangrene, arterial compromise, often followed by circulatory collapse, and shock. PCD is associated with underlying malignancy in 50% of cases. We report a rare occurrence of undiagnosed Crohn’s disease manifesting as PCD. Case Report: A 64-year-old white male with history of hypertension, alcoholism, COPD, recurrent DVTs, and non-compliance with warfarin presented with extreme weakness and bluish discoloration of legs along with nausea, vomiting, and lower abdominal pain. On examination, he was hemodynamically unstable and bilateral lower extremities were mottled, cyanosed, and edematous without palpable femoral or pedal pulses. Laboratory values revealed leukocytosis 24,500 cells/ mcl, thrombocytosis, and elevated creatinine/BUN of 5.3/100mg/dL. Venous Doppler showed occlusive filling defects in bilateral common femoral and popliteal veins with absent flow, but patent arteries consistent with massive Iliocaval thrombosis. The patient underwent emergent bilateral iliocaval thrombectomy and was anticoagulated with heparin. His course was complicated by AKI, septic shock, and multiorgan failure. Thrombophilia work-up was negative with no identifiable explanation for recurrent thrombosis. A colonoscopy, prompted by abdominal pain and CT findings of thickened small bowel, noted a terminal ileal stricture with inflammation of cecum and ascending colon. Histopathology was consistent with Crohn’s ileocolitis. On detailed review, the patient had several prior thrombotic events that were associated with abdominal distress, elevated ESR, and CRP. The patient was discharged on glucocorticoids, adalimumab, and a recommendation for life-long anticoagulation. No repeat episode of thrombosis was reported in 6-month follow up. The patient was poorly compliant and died of a bowel perforation 9 months after the initial diagnosis. Discussion: To our knowledge, this is the first reported case of IBD presenting as PCD. IBD imparts a 3fold relative risk of thrombosis, which rises to 15-fold during exacerbations. Most are unprovoked events, and suggested mechanisms include endothelial dysfunction, abnormal fibrinolysis, platelet aggregation, and increased elaboration of cytokines. Awareness of this risk led to the diagnosis of IBD in our patient. Prompt recognition of extensive thrombosis prevented life-threatening limb ischemia and mortality. Evidence suggests that thrombo-prophylactic regimens be considered during flares of active IBD, especially in subjects with history of thromboembolism.

1488  Please see page S665 for OUTCOMES RESEARCH  PANCREATIC/BILIARY. 1489  Please see page S665 for OUTCOMES RESEARCH  PANCREATIC/BILIARY. 1490  Please see page S666 for OUTCOMES RESEARCH  PANCREATIC/BILIARY.


1491 Crohn’s Flare Causes a Catastrophe Anam Khan, MD,1 Yamini Natarajan, MD,2 Joseph Sellin, MD, FACG3. 1. Internal Medicine, Baylor College of Medicine, Houston; 2. Baylor College of Medicine, Houston, TX; 3. Baylor College of Medicine, Houston, TX. Introduction: Crohn’s disease (CD) has been associated with other autoimmune conditions, and a higher prevalence of antiphospholipid antibody syndrome (APS) has been demonstrated. We describe the first case of a flare of CD precipitating catastrophic antiphospholipid antibody syndrome (CAPS). Case Report: A 17-year-old male presented to the ER with abdominal pain, bloody diarrhea, and a Crohn’s flare. He developed worsening shortness of breath and hemoptysis. A rigorous cardiopulmonary work-up was done. Laboratory data revealed profound troponin elevation (17 ng/mL) with EKG consistent with pericarditis. Echocardiogram was suggestive of myopericarditis. Imaging demonstrated ground glass opacities in the lungs, which worsened, and a bronchoscopy was performed, which showed alveolar hemorrhage. Two days later, the patient had an acute hemorrhagic stroke involving the left frontoparietal region with symptoms of right-sided neglect and homonymous hemianopia. Imaging revealed hemorrhagic transformation and a cerebral venous thrombosis. The patient developed marked thrombocytopenia with coagulopathy (elevated PT 19.1, PTT 48.5, LDH 446 U/L and D-dimer >20 ug/mL, and low fibrinogen 129 mg/dL). This prompted a work-up for causes of arterial and venous thrombosis, and co-existing coagulopathy. Work-up revealed positive lupus anticoagulant and elevated antibeta 2 glycoprotein antibodies (AB2G) in high titers (105 GPI). On hospital day 6, the patient had worsening shortness of breath with hypoxia, and CT revealed pulmonary embolism. At this point, a diagnosis of probable CAPS was made, and treatment with systemic anticoagulation and high-dose pulse steroids was initiated. However, he continued to deteriorate and plasma exchange was initiated. Once stabilized, the patient continued to have gastrointestinal bleeding intermittently and colonoscopy revealed extensive active inflammation and ulceration consistent with Crohn’s flare. Calprotectin level was highly elevated (>2100). Azathioprine was initiated for its dual role in treating both CD and CAPS, and the patient was recommended to be on lifetime anticoagulation. Discussion: The diagnostic criteria of CAPS consists of 4 clinical features including evidence of 3 organ system involvement, development of manifestations within a week, histopathology of small vessel occlusion, and presence of AB2G in high titers. Since a biopsy was not obtained in our patient, a diagnosis of probable CAPS was made. Approximately 60% of catastrophic episodes are preceded by a precipitating event, and a flare of CD has not been described previously. It is important to recognize and ameliorate this precipitant with medication, as it may alter the course of CAPS.


1493 Use of Serum-Derived Bovine Immunoglobulin/Protein Isolate (SBI) to Manage Refractory Ulcerative Colitis Symptoms and Avoid Surgery Gerald Dryden, MD. School of Medicine - University of Louisville, Louisville, KY. Introduction: This case reports a patient with refractory ulcerative colitis (UC) who avoided surgery by initiating a nutritional therapy, serum-derived bovine immunoglobulin/protein isolate (SBI) and continues to be maintained on this prescription medical food product. A 60-year old female presented to clinic reporting 7-8 watery, bloody bowel movements per day. The patient had a 10-year history of ulcerative colitis (pan-colitis), which had been treated successfully with anti-TNF therapy (adalimumab) over the last 2 years. However, she developed septic arthritis in the left knee and adalimumab was discontinued. She underwent multiple wash-out surgeries and was treated with a long-term antibiotic regimen. The patient then experienced 2 episodes of C. difficile and was treated with oral vancomycin both times. After the second course, the patient reported improvement in her symptoms. Three months later, the patient returned with the aforementioned 7-8 watery, bloody stools per day, yet C. difficile testing was negative. A flexible sigmoidoscopy demonstrated grade 2 colitis. Patient co-morbidities included deep vein thrombosis complicated by a pulmonary embolism. She was initially treated with oral prednisone, 30 mg daily, and rectal mesalamine, 1 g QHS, at bedtime. No improvement was noted, prednisone was increased to 40 mg daily. Despite escalating therapy, stool frequency increased to 10-15 watery stools per day with frequent bleeding. The patient refused to re-initiate therapy with a biologic agent due to her history of septic arthritis. If her condition continued to decline, surgery would be strongly considered. At this point, she was initiated on a nutritional therapeutic, SBI, 5 g 4 times a day for 1 week, after which time SBI was decreased to 5 g daily. At the one-month follow-up visit, the patient reported 1-2 formed bowel movements per day, no rectal bleeding, and no abdominal cramps. Over the next 6 weeks, her prednisone dose was tapered down to 5 mg daily. An erythrocyte sedimentation rate decreased from 90 mm/h to 11 mm/h over 4 months. During this time, an elevated white blood cell count normalized, her serum albumin increased from 4.1 mg/dL to 4.5 mg/dL, and C. difficile toxin B remained negative by PCR. A repeat flexible sigmoidoscopy demonstrated completely normal colonic mucosa approximately 2 months after beginning SBI therapy (grade 0 colitis). The patient has been on SBI for a total of 4 months, and remains on 5 g SBI daily. Disclosure - Dr. Victoria S Jasion - Employee of Entera Health, Inc.


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Abstracts 1494 Development of Collagenous Colitis in Inflammatory Bowel Disease After Initiation of TNF Inhibitors Rahoma Elharari, MD, Rima Shobar, MD, Ece Mutlu, MD, MBA, MS, FACG. Rush University Medical Center, Chicago, IL. Introduction: Collagenous colitis (CC) is believed to be a separate entity from classical IBD (Crohn disease [CD] and ulcerative colitis [UC]), and the co-existence of CC and IBD is very uncommon. In most reported cases of CC and IBD in the literature, CC preceded CD or UC. Herein, we report two IBD cases that developed CC after successful treatment of their IBD with 2 different TNF inhibitors. Both cases did not have any clear inciting causes such as NSAIDs or infections. Case 1: A 49-year-old female with a 10-year history of ulcerative colitis (pancolitis), diabetes, Hashimoto’s thyroiditis, anxiety, gastroesophageal reflux disease, and multiple drug allergies was successfully being treated for years with maintenance doses of adalimumab with complete mucosal healing. The patient had undergone multiple colonoscopies with surveillance biopsies in 2007, 2009, 2010, and 2011 with minimal to no active disease, presence of multiple pseudopolyps, and no evidence of CC. In 2013, the patient developed diarrhea and reported that this was very different from what she usually experiences with UC flares. A repeat colonoscopy showed a few 1-4-mm ulcerations around the IC valve and in the sigmoid, and large pseudopolyps in the left colon. The rest of the colonic mucosa appeared normal, but was scarred and stiff. Histopathology of the surveillance colonic biopsies revealed new onset CC in the transverse and left colon biopsies with a thickened subepithelial collagen band. She was started on cholestyramine and budesonide with resolution of her symptoms of CC. Case 2: A 60-year-old female with a 2-year history of CD (affecting her esophagus, stomach, ileum, and colon) was maintained on infliximab with great improvement in her disease. She additionally had a history of diabetes, hypothyroidism, diverticulosis, and gastroesophageal reflux disease. A year after the start of infliximab, she presented with an unintentional weight loss of 5 lbs, fatigue, abdominal pain, and diarrhea with some rectal bleeding. A colonoscopy revealed few scattered aphthous ulcerations in the distal terminal ileum and complete mucosal healing of the colon. Histopathology of the colonic biopsies revealed inactive CD and a diffuse mild chronic colitis with thickened collagen band throughout the colon, consistent with CC. She was started on cholestyramine with resolution of her symptoms of CC. Conclusion: CC can occur after successful treatment of patients with classical IBD. Our cases illustrate the need for random biopsies of the colon in IBD patients with new onset diarrhea, and especially those with complete mucosal healing, before symptoms are attributed IBS, and highlight that CC may develop despite immunosuppressives such as TNF inhibitors.

1497 Oral Lichen Planus: An Emerging Paradoxical Adverse Effect Of Anti-TNF-α Therapy Patrícia Andrade, MD,1 Susana Lopes, MD,1 Andreia Albuquerque, MD,1 Joana Pardal, MD,2 Filipa Osório, MD,3 Guilherme Macedo, MD, PhD, FACG1. 1. gastroenterology, Centro Hospitalar São João, Porto, Portugal; 2. Department of Anatomic Pathology, Centro Hospitalar São João, Porto, Portugal; 3. Department of Dermatology, Centro Hospitalar de São João, Porto, Portugal. Introduction: The efficacy of anti-tumor necrosis factor alpha (TNF-α) inhibitors in the treatment of inflammatory bowel disease (IBD) is well established. The increasing use of these agents in clinical practice has led to the recognition of several adverse events, some of them being considered as paradoxical. Many skin and mucosal lesions have been described under anti-TNF-α therapy, including lichenoid reactions. Case Report: The authors present 3 cases of oral lichen planus (OLP) in 3 female patients with IBD (2 with Crohn’s disease and 1 with ulcerative colitis) treated with infliximab (2 patients) and adalimumab (1 patient). A few weeks after starting anti-TNF- α therapy, the patients complained about oral burning pain and significant limitation of food intake and speech. On examination, they had white, reticular lesions in the buccal mucosa and soft palate (Figure 1). The lichenoid origin of the lesions was confirmed histologically (Figure 2). Other etiologies were excluded. Despite the treatment, it was necessary to discontinue anti-TNF-α therapy in 2 patients due to persistent lesions and symptoms. Discussion: To our knowledge, there are 11 reported cases of OLP due to anti-TNF-α therapy. The development of these lesions appears to result from immunological mechanisms that disrupt the delicate balance between TNF-α and interferon-α in susceptible patients. The treatment and malignant potential of these lesions remains controversial. In light of the increasing use of TNF-α inhibitors, the occurrence of OLP is a potentially emerging side effect; thus, we recommend a thorough oral examination as a routine component of gastroenterologists’ evaluation.


1496 Use of Golimumab in Pregnancy in Ulcerative Colitis Nisha Patel, MD,1 Julie Weatherly, NP,1 Bincy Abraham, MD2. 1. Gastroenterology, Baylor College of Medicine, Houston, TX; 2. Houston Methodist, Houston, TX. Introduction: We present a case of a 26-year-old white woman who was diagnosed with ulcerative colitis in 2007 after presenting with bloody diarrhea and left-sided colitis. She was treated with mesalamine. Despite poor adherence, she had only mild flares until December 2009. At this time, she had a flare, which required a steroid taper and initiation of azathioprine. She did well until a hospitalization in May 2010 for worsening of bloody diarrhea, severe nausea, vomiting, respiratory failure, and an esophageal tear from presumed severe side effect from azathioprine (after which it was discontinued). She underwent colonoscopy at that time, showing pancolitis, and was started on infliximab, which led to clinical remission. However, over time she developed additional symptoms, and in 2011, she underwent a colonoscopy showing pancolitis. Her infliximab was escalated to 10 mg/kg every 6 weeks. She returned to clinical remission and became pregnant March 2013. She required a hospitalization in her first trimester for a flare requiring transfusion of 4 units of packed red blood cells for severe iron deficiency anemia (hemoglobin of 5 g/dL). Infectious etiologies were ruled out and the patient was started on intravenous steroids, which improved her diarrhea from 15-10 bowel movements per day. She was then switched to adalimumab and oral prednisone. She continued to have hematochezia, diarrhea, and urgency, including nocturnal symptoms. She required a second hospitalization during her second trimester with 2 more units of packed red blood cell transfusions, repeat intravenous steroid infusion, and eventual discharge on oral prednisone 40 mg per day. She was followed by a high-risk obstetrician and her baby was found to have intrauterine growth restriction on ultrasound. Due to lack of efficacy on adalimumab, even with dose escalation to 40 mg weekly, she was then started on golimumab during her 26th week of gestation. After induction therapy, she was able to taper off prednisone completely and had resolution of her gastrointestinal symptoms with no diarrhea, no hematochezia, and no further hospitalizations during clinic follow-up. She later delivered a healthy baby weighing 6.6 pounds at term. This report shows that despite its use as a third anti-tumor necrosis factor agent in ulcerative colitis, golimumab provided steroid-free clinical remission to a patient who was undergoing a severe flare during her pregnancy. It is one of the early case reports showing the use of golimumab (FDA pregnancy category B) in a pregnant patient with ulcerative colitis. It also shows that despite an ultrasound showing intrauterine growth restriction prior to starting this medication, the patient was able to deliver a full term, healthy baby. Disclosure - Nisha Patel, MD – none. Julie Weatherly, NP – none. Bincy Abraham, MD - consultant & Speakers Bureau: Janssen, UCB, Abbvie, Prometheus, Takeda; Speakers Bureau: Salix; Consultant: Shire.


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[1498A] Figure 1. (A) Abdominal MRI revealing 10 x 6 x 12 cm mass in the mid abdomen encasing the aorta and great vessels and displacing the IVC and ureters laterally. (B) H&E stain of the retroperitoneal mass revealing a diffuse atypical lymphoid infiltrate.

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Conclusion: In conclusion, anti-TNF therapies can safely and effectively treat de novo IBD post-solid organ transplantation even in the setting of previous CMV colitis.

Burkitt Lymphoma Complicating Azathioprine Therapy in Ulcerative Colitis Patient With Autoimmune Hepatitis Syndrome/Primary Sclerosing Cholangitis Overlap Syndrome Jennifer Lewis, MD, Maisa Abdalla, MBBS, Bing Ren, MD, Christine Granato, MD, Andrew Evans, MD, PhD, Gopal Ramaraju, MD, Ashok Shah, MD, MACG, FACG. University of Rochester Medical Center, Rochester, NY.

1500 C. Difficile Enteritis After Total Proctocolectomy Successfully Treated With Fecal Transplant

Introduction: Immunosuppressive therapy (IST) is widely used by gastroenterologists to treat inflammatory bowel disease (IBD) and autoimmune hepatitis (AIH). Such therapies have been linked to increased risk of intestinal and extra-intestinal lymphomas. Case Report: A 25-year-old male evaluated for epigastric pain, nausea, and bilious emesis. He has ulcerative colitis diagnosed at the age of 14 and AIH/primary sclerosing cholangitis (AIH/PSC) overlap syndrome diagnosed based on liver biopsy 10 months prior to his presentation. He was maintained on mesalamine therapy for the past 11 years, but 8 months prior to his presentation, prednisone taper and azathioprine 75 mg daily were added. Work-up revealed mild elevation of liver enzymes, anemia, and normal WBC. MRI/MRCP of the abdomen revealed a large retroperitoneal mass encasing the aorta and great vessels and displacing adjacent structures. This was confirmed to be Burkitt lymphoma (BL) on biopsy. Azathioprine was discontinued and chemotherapy was initiated. He received 2 cycles of chemotherapy with good response. Unfortunately, 2 months later, he was diagnosed with cholangicarcinoma. He is now status post radiation therapy and awaiting his first post-treatment abdominal imaging. Discussion: Several studies have shown a small increase in the risk of lymphoma among IBD patients receiving IST. It has also been suggested that IBD can predispose patients for lymphoma even without IST. Studies showed a median time of 3.5 years for the development of lymphoma after initiating IST. Our patient was diagnosed with lymphoma after only 8 months of azathioprine therapy. His lymphoma could be related to the underlying IBD and was accelerated with the addition of azathioprine. Additionally, AIH has been also linked to increased risk of lymphoma. Finally, our patient tested positive for Epstein Barr virus (EBV), a known predisposing factor for BL. In conclusion, the association of lymphoma and IBD is not well-understood, but in part related to the IST. In our patient, a combination of IBD, AIH/PSC overlap syndrome, EBV infection, and IST likely contributed to his lymphoma.

Chuan Long Miao, MD, MPH, Andrew Mowery, DO, Harshit Khara, MD, Matthew Shellenberger, DO, Michael Komar, MD. Geisinger Medical Center, Danville, PA. Introduction: There have been small numbers of reported C. difficile small bowel enteritis. Mortality rate is high (60-83%) and treatment can be difficult. We report a case of C. difficile enteritis after total proctocolectomy that was successfully treated with fecal transplant. Case Report: A 29-year-old man with history of relapsing, chronic ulcerative colitis refractory to medical therapy, underwent proctocolectomy with ileal pouch-anal anastomosis in 2008. Four years later, he developed C. difficile infection and was treated with 2 courses of Metronidazole. Endoscopy at the time revealed pouchitis, for which he took probiotics with good results. In March 2013, he was admitted for nausea, dehydration, and leukocytosis. No infectious source was identified. EGD was unremarkable, but colonoscopy again revealed pouchitis, for which he was discharged on ciprofloxacin. He was readmitted for persistent nausea and vomiting, weight loss, worsening diarrhea, and significant leukocytosis (28K), with bandemia (16%) and eosinophilia (33%). Push enteroscopy showed jejunitis with ulceration (see picture). Multiple C. difficile PCR tests were negative. He was started on vancomycin empirically with gradual improvement of clinical symptoms and leukocytosis. Repeat push enteroscopy 1 month later demonstrated endoscopic improvement. However, once vancomycin dosing was decreased, his symptoms and leukocytosis recurred. He was therefore started on high-dose vancomycin with prolonged taper (7 weeks). Unfortunately, after this course of treatment, his symptoms again recurred. In October 2013, he had a positive C. difficile toxin A and B EIA with stool culture. He underwent fecal transplant in November 2013, after which his symptoms resolved. Discussion: Clinicians should have a high suspicion of C. difficile enteritis in patients with inflammatory bowel disease s/p total proctocolectomy. After failed medical treatment, fecal transplant is a viable option for these difficult cases.

1499 Anti-TNF Therapy for De Novo IBD Following CMV Colitis After Renal Transplantation Priyam Tripathi, MD, MPH, Jeffry Katz, MD, FACG. Case Western Reserve University/University Hospitals Case Medical Center, Cleveland, OH. Introduction: De novo inflammatory bowel disease (IBD) after organ transplantation is a rare clinical entity. Although anti-tumor necrosis factor (anti-TNF) therapy is a well-established treatment for patients with IBD, limited data is available regarding its use in patients with IBD after organ transplantation. Case Report: A 51-year-old man with a history of renal transplant secondary to end stage renal disease from hypertensive glomerulosclerosis presented with persistent abdominal pain, nausea, and vomiting. Post-renal transplant in 2004, he was maintained on tacrolimus, prednisone, and azathioprine. Beginning in 2006, he complained of episodic abdominal pain, nausea, vomiting, and nonbloody diarrhea requiring multiple hospitalizations. In 2007, serum CMV DNA hybrid capture assay was positive; colonoscopy revealed a patchy colitis with ulceration, and biopsies confirmed CMV colitis. Despite initial clinical improvement with ganciclovir, he suffered intermittent episodes of recurrent abdominal pain, vomiting, and diarrhea, with repeat serum and and histology both negative for CMV. Repeat colonoscopy in 2011 showed persistent transverse and ascending colon inflammation. A diagnosis of Crohn’s disease was made and the patient had significant clinical response to high-dose steroids, but was unable to taper prednisone without recurrent symptoms. He was begun on infliximab and had dramatic improvement in his symptoms without recurrence on maintenance infusions. Follow-up colonoscopy revealed substantial improvement in colitis and nearly complete healing of ulcerations. Discussion: Though rare, this case shows that de novo IBD can develop in the immunosuppressed patient after solid organ transplant. The incidence of de novo IBD after transplant has been reported to be 0.21%. The diagnosis and management of IBD in these uncommon cases can be challenging. Our patient initially had CMV colitis, which was likely the stimulus for the subsequent development of Crohn’s disease. Although there was a concern for an increased infection risk with infliximab, including potential reactivation of CMV colitis, the patient had an excellent clinical, endoscopic, and histologic response without complication. Nonetheless, the complex interplay between anti-rejection immunosuppressive agents and biologic therapies for IBD creates a challenging clinical scenario, which needs to be further investigated.


[1500A]

Figure 1. C. difficile jejunitis. VOLUME 109 | SUPPLEMENT 2

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Abstracts 1501

1504

Abdominal Actinomycosis Complicating Active Crohn’s Disease: A Case Report

Clostridium difficile in Ulcerative Colitis Complicated by Underlying Aplastic Anemia

Ahmad Malli, MD,1 Guru Trikudanathan, MD,1 Courtney Ferch, MD,1 Ashish Malhotra, MD2. 1. University of Minnesota Medical Center, Minneapolis, MN; 2. Minneapolis VA Medical Center, Minneapolis, MN.

Bret Stysly, MD, MPH, Tarun Kukkadapu, MD, Erick Singh, MD. Bret Stysly, Georgia Regents University, Augusta, GA.

Introduction: Abdominal actinomycosis complicating an underlying Crohn’s disease (CD) is an exceedingly rare entity that imposes diagnostic and therapeutic dilemmas to physicians regarding the timely intervention and treatment of this combined entity. Herein, we report a case of secondary infection of active CD by abdominal Actinomyces. Case Report: A 31-year-old female with active ileo-colonic CD was admitted for further evaluation and management of recent onset pelvic abscesses and peri-anal fistulas while on prednisone after a recent percutaneous drainage of an intra-abdominal pelvic abscess at a different hospital that yielded Actinomyces odontolyticus. She underwent further percutaneous abscess drainage on admission, along with broad-spectrum antibiotics and prednisone tapering in the context of her active infection. She was found to have a levonorgestrol-releasing intrauterine device (IUD), which was thought to be related to her Actinomyces secondary infection. She was stabilized and discharged on long-term oral antibiotic treatment after the IUD removal, with plans to re-initiate immunomodulation therapy in the nearest safe timing. Discussion: Abdominal actinomycosis is a rare chronic granulomatous disease that can be caused by invasion of this commensal GI tract organism into the breached intestinal tissue secondary to an active CD. Abdominal actinomycosis is known to mimic diverticulitis, cancer, or inflammatory bowel disease on clinical grounds. It is also an emerging entity secondary to the prolonged current use of IUDs, being an established risk factor for abdominal actnomycosis. The presence of IUD in our patient heightened our suspicion for this entity that might require a different approach to treating a regular CD flare. The diagnosis of abdominal actinomycosis could have been easily missed on clinical grounds due to the low sensitivity of Actinomyces cultures (35%) based on literature review (mainly related to handling and culture techniques with low pretest probability of Actinomyces). Clinicians should be aware of this entity, especially in patients with existing IUDs, where a different type of contraception might be pursued. Abdominal actinomycosis needs long-term antibiotic treatment, which can also complicate the timely administration of immunomodulator therapy in this patient population.

Introduction: The co-infection of Clostridium difficile (C. difficile) in patients with ulcerative colitis has long complicated management and limited effective therapies. When severe recurrent C. difficile affects those with underlying inflammatory bowel disease, management often turns to surgical interventions once medical options are exhausted. Only making things worse, aplastic anemia severely limits available pharmacologic agents along with surgical interventions due to severe thrombocytopenia and immunosuppression. A 54-yea-old woman is admitted to the hospital for a worsening 3-month history of bloody diarrhea. She was diagnosed with UC 4 years prior from a colonoscopy. She had been treated in the past 4 times for C. difficile infection. She had been managed as an outpatient with mesalamine, sulfasalazine, steroid enemas, and oral steroids. Her management was further complicated due to a history of severe, transfusion-dependent aplastic anemia, which prevented her from using many immunomodulators. She was recently started on rifaximin due to several episodes of recurrent C. difficile during the past year, along with cyclosporine by her hematologist for aplastic anemia. During hospitalization, she was found to be PCR-positive for C. difficile. Her cyclosporine was held and she was given a total of 5 units of platelets, as her initial CBC showed a platelet count of 6,000. Her colonoscopy revealed severe ulcerative colitis throughout the colon with severely erythematous, friable mucosa, and multiple areas of ulceration. Also found were several areas of punched-out deep cratered ulcers in the sigmoid colon and numerous pseudo polyps. Pathology was consistent with ulcerative colitis, with no evidence of granulomas or dysplasia. Following the results, she began a prednisone taper and 6-week vancomycin taper with improvement in her symptoms. Our patient presents an important case in managing patients with UC and concomitant C. difficile infections complicated by another treatment limiting co-morbidity. Aplastic anemia had resulted in severe transfusion-dependent thrombocytopenia. This in turn had left our patient as a very poor surgical candidate. The use of cyclosporine as well, to control her aplastic anemia, had compounded her immunosuppression. This precluded her from being a candidate for fecal microbiota transplant at our institution, per the FDA guidelines, and limited our treatment options. The decision was made, in spite of an active C. difficile infection, to also treat her UC flair with prednisone, which led to her improvement.

1502 Infliximab and Colchicine Therapy in the Treatment of Systemic Secondary Amyloidosis in Crohn’s Disease Geoffrey You, MD,1 William Ferges, MD,2 Kiron Das, MD, PhD2. 1. Department of Medicine, Rutgers Robert Wood Johnson Medical School, New Brunswick, NJ; 2. Division of Gastroenterology and Hepatology, Department of Medicine, Rutgers Robert Wood Johnson Medical School, New Brunswick, NJ. Introduction: Systemic secondary (AA) amyloidosis is a rare complication of long-standing Crohn’s disease (CD) with an incidence of 0.9-3%. At present, no established standard of treatment exists for AA amyloidosis in CD. We present a case of AA amyloidosis with renal and colonic involvement in a patient with CD who experienced both improvement in renal function and complete histologic resolution of colonic amyloidosis after infliximab (IFX) and colchicine therapy. Case Report: A 50-year-old male with refractory CD on 5-aminosalicylic acid, 6-mercaptopurine, and chronic steroid therapy was noted to have acute onset anasarca in the fall of 2007. Laboratory studies revealed serum creatinine of 1.2 mg/dL, albumin of 1.3 gm/dL, and proteinuria of 8,258 mg over 24 hours, consistent with nephrotic syndrome. Renal biopsy was performed, and immunohistochemical staining was positive for serum amyloid A, confirming the diagnosis of AA amyloidosis. The patient was subsequently started on IFX and colchicine therapy. In 3 months, he noted significant clinical improvement in gastrointestinal symptoms and was able to wean off of steroids; however, he continued to have nephrotic-range proteinuria. IFX and colchicine therapy was continued with routine follow-up. Gradually, the patient’s anasarca resolved and his renal function was stable, with only trace protein on urinalysis. A colonoscopy with biopsy in July 2009 revealed chronic active colitis with amyloidosis of the rectum, despite a long period of clinical remission. At this time, the patient was continued on IFX and colchicine. He underwent repeat colonoscopy with biopsy in November 2011, which revealed colonic inflammation, but no evidence of rectal amyloidosis. Another colonoscopy in 2012 again showed colonic inflammation with complete resolution of amyloidosis in the rectum. Given the patient’s overall state of clinical remission and stable renal function, colchicine was subsequently discontinued and he was maintained on IFX therapy alone. Discussion: Few case reports have documented clinical improvement of AA amyloidosis in CD patients receiving IFX; however, complete histologic resolution of gastrointestinal amyloidosis after IFX and colchicine therapy has not been previously reported in the literature. It is unclear if this finding occurs in other affected organ systems. Further research is necessary to identify this phenomenon, which has important implications in the future medical management of AA amyloidosis in CD patients. Additionally, AA amyloidosis is a serious complication; routine histopathologic evaluation of bowel biopsy specimen may aid in early diagnoses and treatment of gastrointestinal amyloidosis, as well as assess response to therapy.

1505 Extensive Cerebral Sinus Venous Thrombosis in a Crohn’s Patient on Adalimumab Therapy Presenting as Severe Headache and Vision Change Margaret Adamcewicz, DO, Katherine Chen, BS, Jennifer Lewis, MD, Danielle Marino, MD, Ashok Shah, MD, FACG. Gastroenterology, University of Rochester Medical Center, Rochester, NY. Introduction: Thromboembolic phenomena are rare in patients receiving tumor necrosis factor alpha (TNF-α) blocking agents. In vivo, TNF-α, a pro-inflammatory cytokine, exhibits pro-thrombotic effects. Crohn’s disease, given its inflammatory state, can by itself lead to endothelial dysfunction and activation of coagulation. We present a case of a patient with Crohn’s disease who developed venous thrombosis after administration of adalimumab. Case Report: A 22-year-old male with a past medical history of Crohn’s ileo-colitis presented with a headache, vision change, and a new onset seizure. His prior therapy included azathioprine, pentasa, and intermittent steroids. Due to poor compliance, he required frequent hospitalizations for flares. Given the findings of severe inflammation of the descending colon and terminal ileum on recent colonoscopy, he was started on adalimumab and received 1 160-mg SQ injection. Several days after administration of the biologic, patient reported frontal headaches associated with blurry vision. Brain imaging revealed an extensive venous sinus thrombosis of the superior sagittal, straight and bilateral transverse sinuses, and evidence of increased intracranial pressure. An ophthalmologic exam showed bilateral papilledema as a consequence of elevated intracranial pressure. Adalimumab was discontinued. An extensive hypercoagulable work-up was negative. He continued steroids and was started on anticoagulation with enoxaparin. His papilledema was managed with acetazolamide and bilateral optic nerve sheath fenestration. Overall, the patient did well. He was tapered off of steroids, and his Crohn’s disease is currently being managed with azathioprine, ciprofloxacin, and metronidazole. His vision returned to normal and he has not experienced any headaches or seizures thus far. Discussion: It has been hypothesized that the induction of autoantibodies such as anti-phospholipid, anti-cardiolipin, anti-B2-glycoprotein, or lupus anticoagulant after long-term TNF-α blockade may lead to an increased thrombosis risk related to anti-TNF-α agents. One year after treatment, studies have found newly induced autoantibodies that resolved after resolution of treatment. Occurrence of thromboembolic events while on adalimumab was reported to be higher in patients with anti-adalimumab antibodies. Our patient had no autoantibodies, yet developed an extensive venous clot burden after only 1 dose of TNF-α blockade. The pathophysiology between this therapy and thrombosis remains unclear, but is likely related to multiple factors. Our case suggests there is a link independent of the induction of autoantibodies that cannot be overlooked, and requires further investigation.

1506 1503  Please see page S666 for OUTCOMES RESEARCH  PANCREATIC/BILIARY.

Carcinoid Tumor Development in Crohn’s Disease Benjamin Levy, MD, Milin Patel, MD, Elizabeth McCord, BS, Brett Hymel, MD, John Hutchings, MD, Daniel Raines, MD, FACG. Louisiana State University, New Orleans, LA. Introduction: A 2007 study at Vanderbilt University indicated that carcinoid tumors are 15 times more common in patients with Crohn’s disease (CD). There has previously been debate in the literature about the exact pathophysiological link. It takes approximately 10 years for enterochromaffin-like cell (ECL) hyperplasia to develop into a carcinoid. A 1998 study by Szabo showed that carcinoid tumors are found more frequently in an inflamed appendix (0.24%) compared to an appendix from autopsy (0.03%). Several inflammatory cytokines involved with CD, such as interleukin 12, tumor necrosis factor alpha, and



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interferon gamma contribute to carcinoid tumor formation. This case report adds to the growing body of literature illustrating a possible link between the inflammatory environment of CD and the development of a gastrointestinal carcinoid tumor. A 37-year-old female first diagnosed with CD via colonoscopy in 2001 was initially treated with azathioprine and mesalamine. Her symptoms were never completely controlled on this regimen. In 2008, the patient stopped all medications and follow-up. In 2013, she was admitted for a Crohn’s flare, and a high-grade small bowel obstruction was noted on CT and MR enterography. She was loaded with certolizumab and she restarted azathioprine. One month later, her symptoms persisted, and she underwent an 18-cm jejunal resection. An esophagogastroduodenoscopy and a colonoscopy were scheduled 2 months later to evaluate the extent of her disease and to work up severe weight loss. EGD was normal, but a 4-mm rectal polyploid-appearing lesion with yellow hue was found during colonoscopy and biopsied in a bite-on-bite fashion. Pathology revealed a carcinoid tumor strongly positive for synaptophysin (SP11) and negative for chromogranin (LK2H10). Researchers have hypothesized that the inflammation and hyperplasia caused by CD predisposes patients to develop carcinoid tumors. The incidence of carcinoid among CD patients appears to be higher than would be expected, possibly as a consequence of distant inflammatory cytokine effects. Radiographically, carcinoid tumors may appear like Crohn’s disease. Histologically, carcinoid tumors also appear similar to CD with fibrosis and wall thickening. Due to these similarities, the incidence of carcinoid among CD patients may actually be higher than the less than 50 case reports that exist in the literature. This case adds to the growing body of evidence illustrating the development of carcinoid tumor among CD patients.


terminating biologics in the second trimester so as to minimize placental transfer in the third. An important issue that has not been addressed adequately is how to manage the recurrence of IBD activity in the third trimester. We present such a scenario. Case Report: A 33-year-old woman with a history of ulcerative colitis (UC) was admitted to our hospital 30 weeks into her second pregnancy, passing 10-15 bloody bowel movements per day with crampy, LLQ abdominal pain, and tenesmus. She was diagnosed 3 years prior with mild left-sided UC that responded well to mesalamine enemas. An exacerbation during her first pregnancy also responded to topical therapy. She was otherwise healthy, without any other significant past medical or family history, and stopped smoking over a decade ago. Her disease was in clinical remission until 6 weeks prior to presentation. She was initially treated with oral mesalamine and steroids without response, so she was admitted to a hospital and given IV and PR steroids. But she continued to pass bloody stools, required 4 units of pRBCs, and was transferred to our hospital. Her examination was significant for a gravid abdomen with LLQ tenderness. The hemoglobin was 10.2, CRP was elevated at 4.6, and work-ups for C. difficile and latent infections were negative. A flexible sigmoidoscopy demonstrated severely friable, ulcerated mucosa from rectum to hepatic flexure. Infliximab was then initiated at 5mg/kg, leading to an improvement in her symptoms the very next day. After 5 days of observation, she was discharged passing semi-formed stool without any gross blood. Eight weeks later, she delivered a healthy 7-lb 13-oz (3.54 kg) baby girl via Csection at full term without any complications. The infant did not receive any live vaccines for the first 6 months, and did not develop any infections. The mother’s UC continues to be in remission on infliximab every 8 weeks. Discussion: Biologics have proven to be relatively safe in the treatment of IBD during pregnancy. In patients whose disease is in remission, the timing of the last dose of a biologic should be determined after weighing the proven risks of disease activity against the theoretical risks of the drug on the newborn. Conversely, uncontrolled disease during the third trimester is clearly an imminent threat to the mother and fetus. Our experience favors continuing or even initiating biologics in the third trimester when clinically warranted.

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Immunocompromised Transplant Patient Shows Promising Findings to Serum-Derived Bovine Immunoglobulin/Protein Isolate (SBI) Carl Crawford, MD. New York Presbyterian-Weill Cornell Medical Center, New York, NY.

Management Challenges in Crohn’s Disease With History of Acute Myeloid Leukemia Leonid Shamban, DO, Lyle Goldman, MD. Providence Hospital Medical Center, Southfield, MI. Introduction: In recent years, biologic and immunomodulator therapy has become a vital therapeutic option for managing inflammatory bowel disease. However, the therapy can become problematic when used for a prolonged period. Immune-suppression places patients at high risk for hematologic malignancies and can develop years after maintenance therapy. The challenge then becomes managing concomitant diseases. The literature to date does not offer recommendations on optimum management therapy modalities. Here, we present a case of a patient with recent history of acute myeloid leukemia (AML) and active Crohn’s disease. Case Report: A 62-year-old male presented to the oncology clinic for routine follow-up and Crohn’s therapy recommendations, particularly with infliximab use. The patient has a history of FLT-3 AML with normal cytogenetics and positive NPM1 mutation diagnosed in 2011, currently in remission. The patient has active moderate Crohn’s disease with perirectal fistulas, and recent fistulotomy with seton placement and on corticosteroid taper. The patient was diagnosed with Crohn’s in 2005, and required colonic resection with his last flare prior to his present presentation at the ileocolonic anastomosis. He was on oral 5-aminosalicylates, but due to the severity of his disease, was started on infliximab maintenance therapy prior to his diagnosis of AML. His AML was treated with high-dose daunorubicin and cytarabine with complete remission, and then received 4 cycles of high-dose cytarabine consolidation. Bone marrow done in December 2012 showed complete remission. The patient was started on 6-mercaptopurine for maintenance, but was discontinued after a repeat bone marrow done on July 2013 showed mild dysplastic changes with 3% ringed sideroblasts and no evidence of AML relapse. The patient’s gastroenterologist was advised to continue steroid therapy and not be started on immunomodulator or biologic therapy for maintenance and consider reintroducing oral 5-aminosalicylates. Discussion: The theoretical concern of infliximab therapy, which uses T-cell immunosuppression modality, may increase the risk of relapse of his acute leukemia. The American College of Gastroenterology does not advise the use of systemic steroid therapy or budesonide for maintenance Crohn’s therapy. However, given the incomplete literature with AML and concomitant Crohn’s disease, it was decided prolonged steroid therapy was the most beneficial treatment option. The recurrence of his AML posed a greater concern than corticosteroid induced side effects. Treating clinicians need to weigh the risks and benefits with each treatment modality when guidelines are limited to the course of management.

Introduction: Transplant patients can often develop various infections and gastrointestinal disorders as a result of their immunocompromised state. A 60-year-old male white patient with mantle cell lymphoma status post (s/p) auto stem cell transplantation and a medical history that included ulcerative colitis status post (s/p) colectomy, impressive malabsorptive/secretory diarrhea secondary to a norovirus infection, pancreatic insufficiency, mild proctitis, and rituximab immune deficiency. Together, this complex medical history has resulted in protracted diarrhea. His treatment has had minimal effect to address his diarrhea symptoms. Treatment post rituximab therapy includes unsuccessful treatment of norovirus with nitazoxanide. The reduction of steroid has resulted in only mild improvement in diarrheal symptoms given the persistent norovirus infection. Other treatment efforts have included rifaximin, pancrelipase, loperamide, diphenoxylate/atropine, and tincture of opium. The diarrhea has resulted in a significant impact to the patient’s quality of life, resulting in a need to work from home due to frequent bowel movements and a need to wear a diaper at home for incontinence. He was treated with octreotide, which has eliminated the need for a diaper, but diarrhea episodes continue up to 6 watery stools a day. Florescu and McCartan (2008) have previously shown that 2 patients who developed Norwalk virus enteritis after small bowel transplantation received oral human serum immunoglobulin and had resolution of diarrhea within 48 hours. A prescription medical food composed of serum-derived bovine immunoglobulin/protein isolate (SBI) indicated for the management of chronic and frequent loose stools has been shown to address diarrhea related symptoms in patients with diarrhea-predominant irritable bowel syndrome (Wilson et al, 2013) and HIV-associated enteropathy (Asmuth et al, 2013). In March 2014, SBI 5 g twice a day was started and increased to 3 times a day at the end of May 2014. Since starting SBI, the patient reports having better-formed stools for the first time in several years and a reduction to 4 bowel movement per day with moderately formed stools. This case suggests that SBI can help provide additional benefit in patients with complex gastrointestinal etiology and may sure as an additional arsenal in the management of diarrhea symptoms in these complex patients. Disclosure - Contact person (Bryon Petschow) - employee of Entera Health, Inc.

1512 Use of Serum-Derived Bovine Immunoglobulin/Protein Isolate (SBI) in a Patient With Refractory Ulcerative Colitis Carl Crawford, MD. New York Presbyterian-Weill Cornell Medical Center, New York, NY.


1510 The Management of IBD With Biologics in the Third Trimester of Pregnancy Anish Mammen, MD, Burton Korelitz, MD, FACG. Lenox Hill Hospital, New York, NY. Introduction: The management of inflammatory bowel disease (IBD) during pregnancy can provoke a great deal of anxiety in patients and physicians alike. Fortunately, biologics - the most effective therapeutic option, have proven relatively safe during pregnancy. Many IBD gastroenterologists consider


Introduction: Patients with refractory ulcerative colitis can create a challenge to manage, especially when steroid therapy is also less than effective than normal. However, serum-derived bovine immunoglobulin/protein isolate (SBI) was considered as a possible option for this difficult case, and helped to address the gastrointestinal symptoms. The patient was a 28-year-old white male with ulcerative colitis since 2001. There were no comorbidities, but the family history included an uncle and sister with ulcerative colitis. The patient has been treated with different medications, including steroids and suppositories including sulfasalazine 1,500 mg three times a day, azathioprine 150 QHS, 10% hydrocortisone steroid enemas, 2.5% hydrocortisone suppositories, and mesalamine suppositories. None of these were fully effective. Pancolitis resolved on medications, but switched to adalimumab 40 mg weekly for refractory anorectal inflammation confined to the distal 1 cm of bowel/anal verge. This was also refractory to topical treatments from below. He was started on budesonide 9 mg, but later changed to prednisone 20 mg and tapered to 5 mg but remained refractory to therapy. Symptoms manifested as tenesmus and frequent bowel movements (5-8 per day with formed to semi-formed stool). He was started on SBI 5 g for times a day in March 2014. All symptoms of tenesmus resolved within 4 weeks, and he now has 3 wellformed bowel movements per day. He has been weaned off prednisone all together. SBI was decreased to 5 g three times a day in May 2014, and continues on sulfasalazine and adalimumab. Ongoing course of action includes spacing adalimumab back to every other week and continued reductions in SBI every 2-3


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Abstracts weeks to an ongoing maintenance dose. This case indicates the potential use of SBI, a prescription medical food, as part of a therapy program in patients who present with difficult to manage gastrointestinal symptoms. This is the first demonstration of mucosal healing with this agent, suggesting greater utility beyond nutritional support. Disclosure - Contact person (Bryon Petschow) - employee of Entera Health, Inc.

of ischemia. There are likely multiple contributing factors that cause the symptoms of MALS, and once more is learned about its pathophysiology, treatment can be optimized. Conclusion: MALS is a real entity that is well-described, and needs high clinical suspicion based on history and physical in order to pursue the right diagnostic testing, which includes ultrasound with dopplers or CT scan specifically to evaluate for MALS. Our cases demonstrate 3 patients with varying demographics and presentations who had different treatment approaches with 2 out of 3 patients having complete resolution of symptoms.


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[1515A] Figure 1. Peak flow velocity at end inspiration.

Gastric Outlet Obstruction Caused by Crohn’s Disease Victor Velocci, MD,1 Mohammad Nasser, MD,1 Peter McCullough, MD2. 1. Internal Medicine, Providence Hospital, Southfield, MI; 2. Baylor Heart and Vascular Institute, Dallas, TX. Introduction: Crohn’s disease is characterized by chronic inflammation involving any part of the gastrointestinal tract. Gastroduodenal disease is extremely rare. We present a case of a young male presenting with gastric outlet syndrome as an initial manifestation of Crohn’s disease. Case Report: A 31-year-old male with no past medical history presented to the emergency department with nausea, vomiting, and epigastric discomfort of 1 month’s duration. Eating resulted in non-bloody emesis, usually half an hour after intake. The patient denied abnormal bowel habits, hematochezia, or melena, but reported a 20-pound weight loss in 2 months. On physical examination, his abdomen was distended and mildly tender in epigastric region with no rebound or guarding. Initial CT scan demonstrated marked distention of the stomach and proximal duodenum with abrupt duodenal narrowing representing obstruction. There was diffuse wall thickening of the duodenum and proximal jejunum. Subsequently, the patient underwent an EGD, which revealed a large, ulcerated, circumferential small bowel mass in the second portion of the duodenum with gastric distention. Biopsies of the mass revealed acute and chronic enteritis. No metaplasia or H. pylori were seen. The patient underwent surgical resection of the proximal small bowel with duodenojejunostomy to relieve the obstruction. Pathology from the specimen revealed transmural active enteritis consistent with Crohn’s disease. The patient’s recovery was uneventful and he was discharged on steroid therapy. Discussion: Gastroduodenal Crohn’s disease is a rare entity occurring in less than 4% of patients with this disease. One third of patients do not have disease elsewhere in the GI tract. Therefore, patients presenting with a mass causing gastric outlet obstruction as the initial manifestation of Crohn’s disease are extremely rare. Gastroduodenal involvement usually presents with symptoms of epigastric non-radiating pain relieved by food or antacids simulating peptic ulcer disease. Profound pain with nausea and vomiting suggest outlet obstruction. Diagnosis requires a high level of suspicion, especially if patients have never been diagnosed with Crohn’s disease. Endoscopy with biopsy remains the gold standard for diagnosis. Endoscopic findings include patchy erythema, mucosal friability, thickened folds, and ulcerations, both aphthous and linear, unlike peptic ulcer disease, which are circular. Approximately 1/3 of patients with duodenal involvement of Crohn’s disease require surgical intervention. Persistent hemorrhage, gastric outlet obstruction, fistula, or abscess formation are all indications for surgery. Gastrojejunostomy with or without vagotomy is the procedure of choice.

[1515B] Figure 2. Peak flow velocity at end expiration.

1516 A Clinical Vignette Demonstrating the Efficacy of Treating CIPO in a Patient With ALS Joshua Anderson, MD,2 Felix Leung, MD, FACG,1 Jonathan Kaunitz, MD, FACG1. 1. West Los Angeles Veteran’s Affairs Medical Center, Los Angeles, CA; 2. Internal Medicine, Cedars Sinai Medical Ceneter, Los Angeles, CA. Introduction: Amyotrophic lateral sclerosis (ALS) is a progressive incurable neurodegenerative disorder leading to worsening dysphagia, respiratory failure, and ultimately death. Chronic intestinal pseudoobstruction (CIPO) is a pan-enteric functional bowel disorder characterized by chronic obstructive symptoms and multiple air fluid levels on radiographic imaging without any evidence of mechanical obstruction. To date, there is only one case published demonstrating efficacy of neostigmine in treating constipation in an ALS patient (Fu A. Dynamics. 2005:16(1):13). Here we report a case of an ALS patient suffering from CIPO who showed response to treatment with neostigmine infusion.

CLINICAL VIGNETTES/CASE REPORTS - FUNCTIONAL BOWEL DISORDERS

1515 Three Cases of Median Arcuate Ligament Syndrome in a Tertiary Care Setting Samuel Kallus, MD, Pooja Singhal, MD, Caren Palese, MD, Nadim Haddad, MD. Georgetown University Hospital, Washington DC, DC. Introduction: To increase awareness of median arcuate ligament syndrome as a cause of abdominal pain, weight loss, nausea, and vomiting. Methods: This is a case series of 3 patients. Results: There is no established gold standard to diagnose MALS. It is a diagnosis of exclusion, and therefore a thorough evaluation must be done prior to its selection as the etiology of abdominal pain and weight loss. The flow velocity and the angle of the celiac artery are influenced by diaphragmatic excursion during respiration, and therefore, were used in the proposed diagnostic criteria of MALS. Due to the low prevalence of the disease, the epidemiology remains poorly known and at-risk populations are not defined. Optimal treatment of median arcuate ligament syndrome (MALS) is difficult because the exact cause of the abdominal pain is unknown. One theory is that the median arcuate ligament, a tendinous and muscular tissue, may have a compressive effect on the celiac artery, causing ischemia and pain. Another proposed mechanism of the pain in MALS is related to the celiac plexus, which is in close proximity to the celiac artery. Direct stimulation of the plexus may irritate pain fibers, causing abdominal pain as well as fibrotic changes, or celiac plexus neuromas can mechanically constrict the celiac trunk. It remains unclear to what extent ischemia plays a role in the symptomatology of MALS. Some patients undergo re-vascularization of the celiac artery to treat MALS, which proves a component

[1516A] Figure 1. © 2014 by the American College of Gastroenterology


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Case Report: Our patient is a 48-year-old African American male who was diagnosed with ALS 2 years prior to presentation after initially presenting with bilateral lower and upper extremity weakness. One and a half months prior to presentation he developed chronic dysphagia and PEG tube was placed. He presented to ER in respiratory distress and progressive weakness. His ICU stay was protracted secondary to unresolving respiratory failure. Despite treatment for pneumonia, he required intubation and ultimately tracheostomy tube placement. One month later he developed nausea, vomiting, and obstipation. He was found to have ileus on KUB (Fig A). Despite aggressive interventions his symptoms persisted for 1 month. The patient was then given a trial of 1.5 mg neostigmine IV push with atropine and glycopyrrolate, which he tolerated well without any significant change in his vital signs. His symptoms resolved immediately, passing 5 bowel movements in the first 24 hours. Discussion: The etiology of the patient’s CIPO is likely multifactorial and due to a combination of electrolyte abnormalities, immobility, medication side effects, and being in the post operative period. His symptoms did not respond to correction of these issues. Neostigmine has long been shown to be a useful adjunct in the treatment of acute colonic pseudo-obstruction but its efficacy in an ALS patient with CIPO has not previously been demonstrated. Conclusion: Neostigmine was effective at treating this ALS patient with CIPO.

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10 years. A double contrast upper GI series was unremarkable and negative for gastroesophageal reflux. Due to concern for potential gastroparesis in the setting of diabetes and dyspepsia, the patient underwent a gastric emptying scintigraphy which revealed rapid gastric emptying, with T1/2 of 41 minutes, 26% activity in the stomach at 1 hour and 2% activity in the stomach at 2 hours. Discussion: Functional dyspepsia, as seen in this patient, is defined by Rome III criteria as one or more of the following symptoms: bothersome postprandial fullness, early satiation, epigastric pain or burning without any evidence of structural disease. Functional dyspepsia is a complaint in approximately 15-20% of the population within a given year and is contributing to an increasing health burden. It has been noted that the symptoms associated with functional bowel disorders are endorsed by 40% of patients seeking medical care. There are many considerations for causes of functional dyspepsia in the general population. Among diabetics, functional dyspepsia is often presumed to be gastroparesis, but as seen in this case, rapid gastric emptying can also be an explanation. Rapid gastric emptying is likely indicative of poor accommodation of the stomach and impaired postprandial receptive relaxation. Consequently, there is an accelerated exposure of the duodenum to nutrients, particularly lipids. Typically, once there is inflow of fatty chyme into the duodenum there is a negative feedback mechanism resulting in the inhibition of antral contraction and an increase in pyloric resistance. In patients with rapid gastric emptying, the duodenum is overwhelmed and therefore cannot appropriately initiate the feedback loop, causing similar symptoms as seen in dumping syndrome. In this patient, treatment with an antispasmodic agent (dicyclomine) prior to meals, resulted in significant improvement in symptoms.

Does She Have a Double Stomach? Rotimi Ayoola, MD, Humberto Sifuentes, MD, Neal Patel, MD, Satish Rao, MD, PhD, FRCP, FACG. Georgia Regents University, Augusta, GA. Introduction: A 33-year-old female with history of GERD, Nissen fundoplication with truncal bilateral vagotomy, pyloroplasty, and gastrojejunostomy presented to our clinic with a history of gastroparesis, constipation, severe post-prandial abdominal pain, bloating, nausea, and vomiting that started after her gastrojejunostomy. Physical examination was significant for an abdominal succussion splash and mild epigastric tenderness. Labs were unremarkable. We recommended an EGD with duodenal aspirates, smart pill study, and antroduodenal manometry. EGD demonstrated severe bile gastritis, a large dilated stomach with absent motility, partially intact Nissen fundoplication, widely patent pyloroplasty, patent gastro-jejunostomy, and a 15-20 cm jejunal loop connecting back to the distal duodenum in a Roux-en-Y anastomosis. The smart pill demonstrated delayed gastric emptying and delayed whole gut/small bowel transit time. An increase in pH was noted upon entry of the smart pill into the small bowel, with a transient decrease in pH to gastric levels approximately 8 hours after entering the small bowel. The patient’s altered anatomy likely accounted for the smart pill entry into the jejunostomy, followed by entry into the duodenum approximately 20 cm distal to the pylorus as seen on EGD. The pill may have encountered an increased acidic environment at this point due to known pyloroplasty or secondary to transient retrograde movement back into the gastric antrum. The smart pill is an orally ingested, non-digestible data recording device that enables measurement of gastric emptying, and small bowel, colonic, and whole gut transit times, as well as pH, pressure, and temperature. The test was selected for this patient to evaluate gastroparesis refractory to medical therapy. The smart pill provided a single transit study to assess transit times and determine the presence of delayed gastric emptying throughout her GI tract. Furthermore, the pill demonstrated tracings consistent with altered anatomy status-post gastrojejunostomy, a possible cause for this patient’s gastroparesis with retrograde movement of food demonstrated by two distinct pH drops. This information was significant as it allowed us to appropriately direct therapy and provided improved causal understanding of her symptoms, as well as preventing the pursuit of therapeutic interventions that might worsen her symptoms, such as repeat surgery.

1519 Prostate Cancer: A Novel Cause of Paraneoplastic Ileus Simranjit Singh, MD, Sahibzada Latif, MD, FACG, Fnu Sanna, MD, Dhananjay Kulkarni, MD. Carle Foundation Hospital, University of Illinois at Urbana-Champaign, Urbana, IL. Introduction: Paraneoplastic neurological syndromes (PNS) affect less than 1/10,000 cancer patients. Intestinal pseudo-obstruction (IPO), a type of autonomic dysfunction, is one of the manifestations of PNS. IPO is characterized by dysmotility of the bowel without mechanical obstruction. PNS are rare in prostate cancer, published literature mostly describes cerebellar degeneration, brainstem syndrome and peripheral neuropathies. However, prostate cancer manifesting as IPO has not been reported. Case Report: An 80-year-old male with history of non-metastatic, non-recurrent colon cancer 8 years ago s/p chemotherapy and partial colectomy, presented with 2 weeks of worsening nausea, vomiting, obstipation and abdominal distention. He had chronically elevated PSA, with no evidence of cancer on multiple prostate biopsies. He was conservatively managed with Leuprolide alone. CT scan showed dilated loops of small intestine. Extensive workup including unremarkable EGD, pill cam study, colonoscopy with normal anastomosis site, showed no signs of mechanical intestinal obstruction. Small bowel follow through showed prolonged transit time, consistent with diffuse ileus. Trial of rifaximin for possible small intestinal bacterial overgrowth and prokinetics did not help either. Further studies including celiac panel, congo-red staining of biopsy samples were unremarkable too. After 4 weeks of extensive workup, his elevated PSA was investigated further. Bone scan followed with MRI thoraco-lumbar spine showed multiple bony metastatic lesions. Octreotide therapy for paraneoplastic ileus resulted in complete resolution of symptoms within 1 week. Patient was discharged on monthly long acting octreotide. At 2 months follow up, he was asymptomatic from GI standpoint. Discussion: PNS are rare, heterogeneous group of neurologic disorders which are remote effects of a cancer. These syndromes can affect any part of the nervous system, either in isolation or association. IPO is well established manifestation of PNS, mostly in association with SCLCs or carcinoid tumors. Pathogenesis is immune mediated and patients usually have anti-Hu or anti-Yo antibodies. PNS are rare in prostate cancer, with very few citations mentioning Lambert-Eaton myasthenic syndrome, cerebellar degeneration, brainstem syndrome, limbic encephalitis or peripheral neuropathies. For the first time, present case establishes IPO as a PNS manifestation of prostate cancer. Octreotide improves IPO by reducing secretions, increasing phase 3 of intestinal migratory motor complexes and by hormone-like mechanisms. To our knowledge, only 2 cases have been reported showing paraneoplastic IPO treatment with octreotide.

1520 Fecal Incontinence With Chronic Mesenteric Ischemia: Case Report in Response to Serum-Derived Bovine Immunoglobulin/Protein Isolate Larry Good, MD. South Nassau Communities Hospital, Oceanside, NY.

[1517A] Figure 1.

1518 Rapid Gastric Emptying: An Alternative Cause of Functional Dyspepsia Anna Platovsky, MD, Aaron Tokayer, MD, FACG. Internal Medicine, Montefiore Medical Center, Bronx, NY. Case Report: M.S. is a 65-year-old woman with a history of type 2 diabetes mellitus, diastolic heart failure and irritable bowel syndrome (IBS). IBS was diagnosed approximately 4 years ago with predominance of constipation but also occasional loose stool. She presented with a new complaint of abdominal fullness after meals with early satiety and an inability to complete a full meal for numerous months. She complained of epigastric discomfort following meals but denied nausea, vomiting, heartburn, dysphagia, or weight loss. On examination, her vital signs were within normal limits; she appeared comfortable and had no abdominal tenderness, succussion splash or hepatosplenomegaly. Laboratory studies including white count, hemoglobin and liver tests were normal. Hemoglobin A1C ranged from 6.2-7.3 over the past


Introduction: Chronic diarrhea with fecal incontinence (FI) is a severe, underreported, and intractable problem in many patients with gastrointestinal (GI) disorders. In mild to severe FI patients, diminished quality of life dramatically affects daily activities and psychosocial behavior causing embarrassment, depression, and self-isolation. There are currently no effective pharmaceutical treatments for this condition. A case history of administration of a FDA-regulated, prescription medical food composed of serum-derived bovine immunoglobulin/protein isolate (SBI) is described for FI in a patient with chronic mesenteric ischemia (CMI), a high grade obstruction of the celiac axis and superior mesenteric artery (SMA) not amenable to stenting. Comorbid conditions in this patient included: atherosclerotic cardiovascular disease (ASCVD), coronary artery bypass grafting (CABG), coronary stents, right carotid stent, chronic atrial fibrillation, gastroesophageal reflux disease (GERD), benign prostrate hyperplasia (BPH), and diarrhea with FI. The patient was an 84-year-old white male with a 20-year history of chronic diarrhea with 6-8 watery stools per day, urgency, nocturnal diarrhea, and fecal incontinence with a lack of response to conventional drug therapy. After 4 weeks of oral SBI at 5 g once daily, the patient had 2-3 soft, semi-formed stools per day with no nocturnal diarrhea, urgency, or incontinence. The patient also exhibited dramatically improved quality of life. This case underscores how a safe, nutritional therapy with a medical food may offer a new modality for physicians to address chronic FI in patients with chronic mesenteric ischemia in this difficult to manage GI population. SBI should be considered in patients with FI as an option for therapy. Disclosure - Dr. Gerald L. Klein - employee of Entera Health, Inc. Dr. Bruce P. Burnett - employee of Entera Health, Inc.


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Abstracts 1521 A Case of Short Bowel Syndrome Managed With a Prescription Medical Food Product, SerumDerived Bovine Immunoglobulin/Protein Isolate (SBI) Raouf Hilal, MD. University of Central Florida Medical School, Orlando, FL. Introduction: Short bowel syndrome (SBS) results in poor absorption and metabolism of nutrients in patients who have had resection of the small intestine. The primary symptom of SBS is diarrhea which can cause nutrient malabsorption. Treatment consists primarily of nutritional support with oral hydration solutions to restore electrolytes, vitamin, minerals, amino acids and lipids as well as medications to control diarrhea. Nutritional interventions consist of medical foods and dietary supplements. Medical foods are a class of therapies which are FDA-regulated products with strict requirements for safety, manufacturing, clinical proof of efficacy, and physician oversight whereas dietary supplements are loosely regulated with no safety or clinical testing required and no physician supervision. A medical food consisting of serum-derived bovine immunoglobulin/protein isolate (SBI) was utilized in a 37-year-old Caucasian female to manage SBS. Small bowel resection was performed after complications of infarction that ensued from gastric bypass surgery more than 5-years-ago. Symptoms of SBS have existed ever since. The patient experiences generalized abdominal pain, bloating/distention and chronic diarrhea as well as expressed poor QoL, a chronic rash on her face, malar and uses skin moisturizer to maintain skin tone. Comorbidities consist of GERD, Barrett’s esophagus, hemorrhoids, hypothyroidism, anorexia, pancytopenia, cachexia, abnormal weight loss, anemia-iron and vitamin B12 deficiency and thrombocytopenia. Nutritional support consisted of Mg-oxide (400 mg), vitamin B12 (500 mcg), topical vitamin A and D3, oral vitamin D3 (2,000 IU), L-carnitine (500 mg), folic acid (1 mg), multivitamin, vitamin B complex, vitamin C (500 mg), oral iron (125 mg elemental iron) and vitamin E. The patient is also treated with calcitriol (0.25 mcg), omeprazole (20 mg), loratadine (10 mg), alprazolam (0.5 mg BID prn), zolpidem (10 mg), promethazine oral (25 mg QID prn), and simethicone (125 mg). Albumin levels was 2.6 g/dL (3.4-5.4 g/dL), prealbumin 15 mg/L (19.5-35.8 mg/L), hemoglobin 10.4 (female 12.0-15.5 grams/dL) and platelets 113 billion/L (150-450 billion/L) indicative of significant malnutrition. Initial dosing of 5 g SBI QD decreased diarrhea over 3 months. When the dose was increased to 5 g SBI BID, the patient’s weight stabilized and albumin, prealbumin, hemoglobin and platelets significantly improved. Based on these results, SBI, which has been shown in malnourished infants and HIV-enteropathy patients to improve nutritional status, may help improve nutritional status in SBS as well as manage chronic diarrhea and global symptoms of abdominal pain, bloating, and distention. Disclosure - Contact Bryon Petschow, PhD - employee of Entera Health Inc.

1522 Post-Infectious Irritable Bowel Syndrome Following Recurrent C. difficile Infections: Case Report of Response to Serum-Derived Bovine Immunoglobulin/Protein Isolate Carl Crawford, MD. New York Presbyterian-Weill Cornell Medical Center, New York, NY. Introduction: Recurrent C. difficile infections can be difficult to manage but can also lead to the patient experiencing post-infectious irritable bowel syndrome (IBS). This case history reviews a patient who was managed with an FDA-regulated, prescription medical food composed of serum-derived bovine immunoglobulin/protein isolate (SBI), to address serious diarrhea symptoms associated with post-infectious IBS. This medical food is indicated for the management of chronic loose and frequent stools with supportive evidence in IBS-D (Wilson et al., 2013) and HIV-associated enteropathy (Asmuth et al., 2013). The patient was a 39-year-old white female presented in January 10, 2014 with a C. difficile infection which was treated using vancomycin standard dose 125 mg QID for 10 days, but then relapsed 2 weeks later. She was again treated with vancomycin 125 mg QID for 10 days and relapse again 2 weeks later. She was then treated with fidaxomicin for 10 days but her diarrhea never resolved. Follow up C. difficile cultures were negative every two weeks. Cholestyramine 1 packet BID - QID was administered, but was complicated by bloating. Medical history included antiphospholipid antibody syndrome, methylenetetrahydrofolate reductase (MTHFR) homozygous, HSV-1, and cholecystectomy. The patient had filed for disability due to the severity of her condition. In May 14, 2014, she was provided SBI 5 g QID and within 2 weeks, her diarrhea had resolved. She stopped taking SBI and her diarrhea returned 1 week later and was C. difficile negative. SBI was restarted again with resolution of her diarrhea. She is currently on SBI 5 g QID and has returned back to work. This case underscores the potential disability that post-infectious IBS may have on a patient but also the potential benefit that SBI can have when considered as an option for therapy. Further study is warranted of this agent in this post-infectious IBS populations. Disclosure - Contact person (Bryon Petschow, PhD) - employee of Entera Health, Inc.

was performed showing a disorganized motility pattern in the interdigestive (fasting) state consistent with a visceral neuropathy. Despite treatment with several prokinetics and antibiotics for overgrowth and pseudoobstruction, the patient continued to deteriorate and required TPN for nutritional support. She later developed neurologic symoptoms including tremors and was referred to neurology team for further evaluation. After evaluations for familial mediterranean fever and other neurologic causes of her dysmotility were ruled out, she was worked up for hereditary fever syndrome which prompted genomic studies revealing the patient had a R121Q variant in the TNFRSF1A gene. This variant is also referred to R92Q which is the accurate location in the mature, processed protein. She was then started on immunosupressives. To our knowledge this is the first case that describes a motility disorder in a patient with TRAPS. Our patient’s complicated medical course sheds light into some of the GI symptoms associated with TRAPS and the importance of early diagnosis in these patients before the onset of profound malnutrition.

CLINICAL VIGNETTES/CASE REPORTS - ENDOSCOPY

1524 Role of Preoperative EUS-Guided Fine-Needle Tattooing of a Pancreatic Head Insulinoma: A Case Report Pornchai Leelasinjaroen, MD, Wuttiporn Manatsathit, MD, Richard Berri, MD, Barawi Mohammed, MD, FACG. St. John Hospital and Medical Center, Detroit, MI. Introduction: Up to 67% of pancreatic head insulinomas are non-palpable, thus surgical resection of the non-palpable insulinoma in this area could become problematic resulting in prolonged surgical time, increased risk of pancreatic duct injury and need for pancreaticoduodenectomy. Although endoscopic ultrasound guided fine-needle tattooing (EUS-FNT) has been widely used for localizing pancreatic lesions in the body and tail, the role of EUS-FNT for pancreatic head lesions has never been established or reported. We report a case of preoperative EUS-FNT for localization of a non-palpable pancreatic head insulinoma. Case Report: A 70-year-old female, had persistent episodes of hypoglycemia which required aggressive intravenous dextrose replacement. Laboratory showed high levels of C-peptide and proinsulin. Urine sulfonylurea was negative. Computer tomographic revealed a 1.6 cm lesion in the pancreatic head. EUS revealed a 15.5 mm hypoechoic in the head of pancreas. The tumor was adjacent to GDA and close to the pancreatic duct. EUS-guided fine-needle aspiration biopsy and EUS-FNT were performed. Intraoperatively, the insulinoma was non-palpable and located deep in the pancreatic parenchyma between GDA and SMV. The preoperative tattooing was easily identified. The insulinoma was meticulously dissected with the guidance of the tattoo marker to preserve the pancreatic duct located posteriorly without complication. The patient had uneventful postoperative hospitalization and remained euglycemic during outpatient follow-up at 6 months. Discussion: Our report is the first to describe safe EUS-FNT for preoperative localization for non-palpable pancreatic head insulinoma by using sterile purified carbon particles (GI Spot) technique. This case, the insulinoma, that we localized, was intraoperatively non-palpable and located in the head of pancreas. The insulinoma was located very close to a major vessel and the pancreatic duct. EUS-FNT can play a role in precisely localizing the tumor margin, in the pancreatic head area, which can help facilitate surgery in non-palpable insulinoma intraoperatively and helps avoid pancreatic duct and local vascular injury, preserves normal pancreatic tissue, reduces operative time and most importantly decreases the chance to proceed to pancreaticoduodenectomy. Conclusions: EUS-FNT represents a safe and useful role for the preoperative localization and surgical planning of the pancreatic head lesion. Further studies will need to be performed to confirm the efficacy and safety of EUS-FNT in the pancreatic head and confirm whether EUS-FNT of pancreatic head lesion will be able to decrease rate of pancreaticoduodenectomy and facilitate successful resection.

1525 Gastric Adenocarcinoma in an Excluded Stomach Diagnosed by Double Balloon Enteroscopy Deena Midani, MD,1 Adam Ehrlich, MD, MPH,1 Truptesh Kothari, MD,2 Stephen Heller, MD2. 1. Medicine/Gastroenterology, Temple University School of Medicine, Philadelphia, PA; 2. Fox Chase Cancer Center, Philadelphia, PA.

1523 Abnormal Motility Associated With Tumor Necrosis Factor Receptor-Associated Periodic Fever Syndrome Adam Godsey, MD,1 Baharak Moshiree, MD2. 1. University of Miami, Miami, FL; 2. University of Virginia, Charlottesville, VA. Introduction: Tumor necrosis factor receptor-associated periodic fever syndrome (TRAPS) is a rare autosomal dominant condition with mutations in the TNFRSF1A gene encoding for the tumor necrosis factor receptor 1 (TNFR1) and is commonly associated with gastroenterological related symptoms. An NIH cohort of 53 patients with TRAPS reported that 92% of patients with TRAPS present with abdominal pain. The pathophysiology of TRAPS may be a defective shedding of the mutant TNFR1 receptor. Lack of shedding of this receptor leads to decreased neutralization of serum TNF and to increased proinflammatory signaling. The motility profile of patients with this syndrome has not been delineated. We present a 62-year-old female with a history of acute gastroenteritis 5 years prior to presentation, marking the beginning of persistent GI symptoms including postprandial abdominal pain, constipation, myalgias, nausea, progressive weight loss and fever of unknown origin diagnosed with TRAPS. GI evaluation including colonoscopy showed microscopic colitis and EGD was otherwise negative. Other motility evaluation done such as breath testing showed small bowel overgrowth. Gastric emptying study supported a diagnosis of gastroparesis. As her GI symptoms progressed, a 6-hour antroduodenal manometry


Introduction: Gastric bypass with Roux-en-Y reconstruction is an increasingly common procedure for morbid obesity. Access to the Roux limb and excluded stomach is difficult endoscopically. This case highlights the use of double balloon enteroscopy to evaluate this anatomy. A 43-year-old female with a past medical history of morbid obesity and a strong family history of endometrial and ovarian cancer presented with complaints of severe right lower quadrant abdominal pain, nausea, and anorexia. She had a history of gastric bypass surgery with Roux-en-Y reconstruction performed 14 years prior to presentation. Initial evaluation by an outside gastroenterologist included a normal upper endoscopy of the esophagus and gastric pouch and a normal colonoscopy. Pelvic ultrasound and CT scan of the abdomen and pelvis revealed a right ovarian mass, abdominal and pelvic ascites, multiple liver nodules consistent with metastatic disease, and omental nodularity concerning for carcinomatosis. The patient was evaluated by a gynecologic oncologist at our institution. Ultrasound-guided core needle biopsy of one of the liver lesions revealed moderately differentiated adenocarcinoma with tumor cells positive for CK7, pCEA, CDX2, CK19, and CK20, suggesting a primary upper gastrointestinal or pancreaticobiliary neoplasm. Careful review of the patient’s CT scan suggested a mass in the portion of the stomach excluded as a result of her gastric bypass surgery. She was therefore referred to gastroenterology for upper double balloon enteroscopy (DBE) with the objective of examining the excluded stomach via a retrograde endoscopic approach and assessing for the presence of a primary gastric neoplasm. Upper DBE was performed under fluoroscopic guidance. The afferent Roux limb was intubated and the excluded stomach was reached via the retrograde approach. A large, fungating mass involving much of the gastric antrum and body was


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identified. Biopsies of the mass confirmed poorly-differentiated adenocarcinoma identical to the histology obtained by liver biopsy. The patient was diagnosed with metastatic gastric adenocarcinoma and palliative chemotherapy was instituted. Gastric cancer arising in a surgically excluded stomach is a rare entity. To our knowledge, this is the first reported case of the identification and diagnosis of gastric cancer in a surgically excluded stomach by DBE. This case underscores the importance of considering a neoplasm arising in a surgically excluded stomach in the differential diagnosis of upper gastrointestinal tumors, and the feasibility of the identification of such tumors by upper DBE.

1526 Endoscopic Closure of a Multifocal Leak From a Gastric Sleeve Janaki Patel, MD, Reza Akhtar, MD. Jersey Shore University Medical Center, Neptune Township, NJ. Case Report: A 41-year-old male with gastric sleeve procedure 6 months prior presented with abdominal abscesses. Upper endoscopy showed fistulous tracts: site 2 and site 3. Site 2 fistula took a 180° turn traveling retrograde to gastroesophageal junction (GEJ). Argon plasma coagulation was applied to both tracts, followed by 10 cc of Tisseel, a fibrin sealant. Repeat endoscopic fistulogram revealed a persistent leak. Cautery was applied to site 2 with 5 cc Tisseel. Glue was seen extruding from site 3 confirming communication. Repeat EGD showed a new fistula, site 1, at GEJ and closed site 3 fistula. Two cc Tisseel was injected and it extruded from site 2. Follow-up EGD showed a smaller site 1 tract and repeat cautery, and Tisseel injection was applied. The patient continues to undergo endoscopic surveillance and management of the fistulae. Discussion: This is a case of common, but one of the most challenging, complications of sleeve gastrectomy, responsible for approximately 50% of deaths. Gastric leaks are affected by high intragastric pressure. Minimally invasive endoscopic techniques, use of glue or stent placement, are effective. This case was interesting due to its multifocal nature of communication between the fistulae. Through continued effective endoscopic maneuvers, we demonstrated adequate closure of a multifocal leak from a gastric sleeve.

[1526C] Figure 3. APC ablation.

1527 Primary Gastric Anaplastic Lymphoma Kinase (ALK) Negative, Large-Cell Lymphoma Causing Gastrointestinal Bleeding in a Patient With Roux-en-Y Gastric Bypass Sara Ancello, DO, Badal Shah, DO, Robert Shmuts, DO, Alan Shienbaum, DO, Hong-Guang Gao, MD, John Chiesa, DO. Rowan University School of Osteopathic Medicine, Stratford, NJ. Introduction: Anaplastic large cell lymphoma (ALCL) is a rare, CD30 positive T-cell neoplasm accounting for 3% of all non-Hodgkin’s lymphomas. Primary lesions are rarely found in the gastrointestinal (GI) tract. Patients may present with dyspepsia, bleeding, etc. Treatment usually requires resection with adjuvant chemotherapy. Even with treatment, the anaplastic lymphoma kinase negative (ALK-negative) variant has a 30-49% 5-year survival rate. This is the case of a 54-year-old female with a history of Rouxen-Y gastric bypass presenting with severe GI bleeding due to reoccurrence of a primary ALK-negative ALCL tumor in the gastric remnant. This lead to hemorrhagic ischemic necrosis, perforation, and splenic invasion, requiring surgical intervention. Remnant perforation is rare, reported mainly in case reports. Endoscopy should be performed to rule out anastomotic ulcerations, and deep enteroscopy if remnant bleeding is suspected. Increased understanding of a bariatric patient’s altered anatomy and adequate cancer surveillance may improve outcomes if complications are recognized early on in these patients.

[1526A] Figure 1. Fistula tract.

[1527A] Figure 1. Anastomotic ulcer actively bleeding.

[1526B] Figure 2. Fluoro picture demonstrates communicating Fistula 2 and Fistula 3. The American Journal of GASTROENTEROLOGY


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Abstracts With continued hematochezia necessitating transfusions, the decision was made to proceed with IOE. Following laparotomy and abdominal exploration without abnormality, an endoscope was first advanced through the oropharynx to the distal jejunum/proximal ileum without signs of bleeding. The endoscope was then passed through an enterotomy to complete examination of the small bowel. An ulcer detected at the ileocecal valve was the presumed source of blood loss based on correlation with SPECT findings. Ileocecectomy was performed with subsequent resolution of bleeding. Pathology demonstrated 2 areas of ulceration in the resected specimen. She was re-admitted 5 days after discharge with abdominal pain and nausea secondary to constipation, but did not show signs of further bleeding. Discussion: By allowing for complete examination of the small intestine and immediate surgical treatment of detected pathology, IOE remains useful in cases of OGIB when bleeding lesions cannot be localized or managed with deep enteroscopy or angiography. Careful patient selection is essential to avoid subjecting patients to a procedure with potential for high morbidity. In this case, the addition of SPECT to RBC scintigraphy allowed localization of bleeding lesion to the terminal ileum/cecum, and in conjunction with IOE findings, allowed for definitive therapy of the bleeding source.

1529 Retroperitoneal Abscess Following EUS-Guided Celiac Plexus Block Benjamin Stein, MD, TImothy Gardner, MD, FACG, John Levenick, MD, Stuart Gordon, MD, Edward Merrens, MD, Richard Zuckerman, MD. Dartmouth Hitchcock Medical Center, Lebanon, NH.

[1527B] Figure 2. Anastomotic ulcer after hemostasis.

Introduction: A 75-year-old diabetic man underwent EUS-guided celiac plexus block for refractory abdominal pain secondary to sclerosing mesenteritis. A total of 20 mL of 0.25% bupivacaine and 20 mg of triamcinolone (40 mg/mL) were injected into the celiac plexus. He was treated with ciprofloxacin 250 mg twice a day for 3 days after the procedure. He reported symptomatic improvement for several weeks. A follow-up CT scan at 6 weeks showed multiple new heterogeneous peripherally-enhancing solid soft tissue nodules in the supra celiac region (Figure 1). He denied fevers and abdominal pain was under good control at the time. These findings were suspected to be reactive changes to the injected medications. Four weeks later, he developed malaise, recurrent abdominal pain, and a leukocytosis of 13.9. A CT scan demonstrated interval development of a large air and fluid collection along the right diaphragmatic crus, suspicious for abscess (Figure 2). He underwent IR-guided drainage of the fluid collection and culture of the aspirate grew multidrug-resistant E. coli. He had rapid clinic improvement following antibiotics and drainage and was discharged to complete a course of ertepenam. Retroperitoneal abscess has been described as a rare complication of both EUS-guided celiac plexus block (CPB) and neurolysis (CPN). Reported abscesses occurred within a week and up to 4 weeks following the procedure. This report adds to literature demonstrating the rare but serious complication of abscess formation following CPB/CPN, and demonstrates that there may be significant delay between the procedure and presentation of abscess.

[1527C] Figure 3. Immunohistochemical stain for CD30 showing infiltrative cells in the splenic tumor section.

1528 Intraoperative Enteroscopy Remains a Useful Modality in Obscure Gastrointestinal Bleeding Feng Li, MD,1 Jeffrey Kuo, MD,1 Samer El-Dika, MD,2 Marty Meyer, MD,2 Peter Stanich, MD2. 1. Department of Internal Medicine, Ohio State University Wexner Medical Center, Columbus, OH; 2. Division of Gastroenterology, Hepatology and Nutrition, Department of Internal Medicine, Ohio State University Wexner Medical Center, Columbus, OH. Introduction: Obscure gastrointestinal bleeding (OGIB) remains a diagnostic challenge despite advances in technology. Although video capsule endoscopy (VCE) and deep enteroscopy have reduced the need for intraoperative enteroscopy (IOE), this modality remains useful in certain cases. We present a case of OGIB with identification and guidance for definitive therapy of bleeding source by IOE. Case Report: A 48-year-old female presented with multiple episodes of hematochezia. Past medical history was significant for coronary artery disease, a recent NSTEMI with drug eluting stent placement, and stage 4 chronic kidney disease. Upper endoscopy was unremarkable. Colonoscopy demonstrated blood throughout the colon without a source of bleeding. VCE was non-diagnostic due to gastric retention. Tagged RBC scan with single photon emission computed tomography (SPECT) showed focus of abnormal radiotracer localizing to the terminal ileum and extending into the cecum. Due to chronic kidney disease, the patient was not a candidate for angiography. Retrograde single balloon enteroscopy was limited by the inability to pass the overtube through the ileocecal valve. Immediate repeat colonoscopy examined the distal 30 cm of ileum, which showed both fresh and old blood without an identified source of bleeding.


[1529A] Figure 1.


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sphincterotomy was performed. The 2 stones migrated to the right intrahepatic duct and stone removal was unsuccessful. The patient awoke with a new onset of left hemiparesis. Stroke alert was announced and Neurology consultation was requested. Head CT revealed infarctions in both right cerebral and cerebellar hemispheres. Although there was a delay in diagnosis, the patient was eventually believed to have suffered from an ischemic event from an air embolism following the ERCP. The patient was transferred to a neighboring institution where hyperbaric oxygen therapy was performed. The patient showed gradual improvement after the hyperbaric therapy, but suffered neurological sequela including development of status epilepticus, depression and persistent left sided hemiplegia. Eventually, patient did have repeat ERCP with removal of CBD obstruction. The pathophysiology of air embolism during ERCP involves disruption of the gastrointestinal mucosa from the sphincterotomy, creating a communication between the veins in the duodenal walls and the intestinal cavity filled with insufflated air. The air can travel to the heart causing a cardiovascular collapse or pulmonary embolism, or enter the systemic circulation via a patent foramen ovale and occlude coronary or cerebral arteries. Although air embolism following ERCP has been reported in literature, the rarity of this phenomenon led to a delay in diagnosis for this patient. Hence, we emphasize that progression of an air embolism should be strongly considered as the most likely etiologic factor in a patient presenting with acute cardiopulmonary symptoms or neurological deficits following ERCP. This should prompt immediate hyperbaric oxygen therapy.

1532 Endoscopic Removal of Accidentally Ingested Adult Toothbrush Sarfaraz Jasdanwala, MD,1 William Ferges, MD,2 Abhinav Agrawal, MD,1 Avik Sarkar, MD,2 Sita Chokhavatia, MD, FACG2. 1. Monmouth Medical Center, Long Branch, NJ; 2. Robert Wood Johnson University Hospital, New Brunswick, NJ.

[1529B] Figure 2.

1530 Successful Endoscopic Pancreatic Necrosectomy in 5-Year-Old Child Joan Kheder, MD, Swapnil Munsaf, MD, Wahid Wassef, MD, MPH, FACG. University of Massachusetts Medical School, Worcester, MA. Introduction: Endoscopic necrosectomy (EN) for treatment of Walled off Pancreatic Necrosis (WOPN) has been performed as an alternative to operative or percutaneous therapy. All available reports now in adult population, we report here the role of this approach in the pediatric population. Patient is a 5-year-old boy with a history of pre-B cell acute lymphoblastic leukemia diagnosed 11/2013 treated with protocol COG -AALL0932 consisting of cytarabine, methotrexate, vincristine, peg-asparaginase, and dexamethasone. He was admitted on 12/12/2013 with acute pancreatitis thought to be secondary to PEG asparaginase, his case was complicated by large peripancreatic fluid collection. On 12/20, CT abdomen was done due to high fever and worsening abdominal pain and showed organized collection in the left upper quadrant between the pancreas and the stomach measured 7.5X9 cm. Patient underwent US guided drainage with 8F pigtail catheter placement, and was treated with antibiotics, antibiotics regimen changed based on the bacteria sensitivity; After 3 weeks, the drain was removed after ultrasound showed improvement of the collection. Ten days later, CT of the abdomen revealed reaccumulation of large walled fluid collection adjacent to pancreas measured 5x5 cm. US aspiration of the collection showed thick green fluid positive for Enterococcus faecium. Patient was referred to the GI service for endoscopic drainage of the collection; patient underwent endoscopy ultrasound which revealed peripancreatic collection measured 45 X 50 mm. There was internal debris within the cavity. Cystgastrostomy was performed by passing a 19-gauge needle using a transgastric approach. A wire was inserted into the collection under fluoroscopic guidance. The cystotomy was dilated with a 10-12mm then 12-15 balloons and 5-7-10 Fr catheter dilators. One 7Fr x 4 cm and three 10Fr x 1cm plastic double pigtail stents were placed over the wire. Four weeks post cystgastrostomy, patient underwent EN via EUS approach; the cystotomy was dilated with a 12-13.5-15 mm balloon dilator, then entered. The cyst was partially filled with fluid and necrotic tissue. EN was performed with a forceps. Follow-up images showed resolution of the collection and 3 weeks post necrosectomy, the cystgastrostomy stents were removed. EN offers the advantage of minimally invasive endoscopic treatment without transabdominal surgery. In the last several years, endoscopic management of WOPN has come to serve as an important primary interventional technique in adult population. Recently, Trikudanathan et al. reported 3 cases with children between 11 and 17 years of age. To our knowledge, this is the youngest patient who underwent successful endoscopic necrosectomy.

1531 Unusual Complications Related to Endoscopic Retrograde Cholangiopancreatography With a Focus on Air Embolism Mohsen Khan, DO, Omat Hassan, BA, Marc Fine, MD. Advocate LGH, Park Ridge, IL. Introduction: Since its introduction, ERCP has become a standard method for exploring the hepatobiliary system. Although it largely remains a safe procedure, complications do occur with acute pancreatitis being the most common serious complication. Other well-known complications include biliary hemorrhage, cholangitis and duodenal perforation. Some of the unusual complications of ERCP include splenic injury, hepatic hematoma, and pneumothorax. Here, we focus on another unusual complication - air embolism presenting in a patient who developed neurological deficits following an ERCP. An icteric appearing 72-year-old female presented with a 10 day history of colicky epigastric pain, dark urine, pale stools, and anorexia due to nausea. Liver chemistries indicated elevated levels of AST, ALT, alkaline phosphatase, and total bilirubin. CT scan showed common bile dilation (CBD) up to 12 mm suggestive of choledocholithiasis. ERCP revealed 2 large stones in the CBD and a 9mm biliary


Case Report: A 23-year-old woman presented to the emergency department after accidentally swallowing an adult sized 7.5 inch toothbrush (TB). The physical exam and labs were normal. X-ray of the abdomen showed the TB head with bristles and handle within the gastric fundus (Figure 1). Emergent endoscopy was performed. The bristled end was facing the pylorus, and a polypectomy snare was used to rotate the TB so that the bristled end was now proximal. Retrieval was attempted using polypectomy snare and rat tooth forceps. The snare was firmly holding the bristles; however, the TB could not traverse through the gastro-esophageal (GE) junction. After 2 hours of repeated attempts, the procedure was abandoned. The following morning, using a 2-channel (T2) endoscope with a polypectomy snare and rat tooth forceps, the endoscopist was able to grab the bristled end of the TB and drag it into the overtube. Once in the overtube, the bristles of the TB were grabbed with a rat tooth forceps and it was successfully removed from the patients stomach. There were no complications after the procedure and the patient was discharged after 10 hours of observation. Discussion: The technically challenging part is maneuvering the tip of the TB through the GE junction, which is greatly facilitated by the use of a long overtube 1. The American Society of Gastrointestinal Endoscopy (ASGE) guidelines recommend use of a long flexible overtube >45 cm and either a polypectomy snare or basket as a retrieval tool 2. In our experience, the use of snare along with rat tooth forceps was helpful. Once successful grasping has been accomplished, the upper endoscope with the toothbrush should be pulled into the overtube and the overtube, along with the TB and the endoscope, should be withdrawn together 2. Conclusion: Ingested adult TB should be removed endoscopically on an emergent basis, and the use of a long flexible overtube greatly facilitates maneuvering it through the GE junction. References: [1] Chintniz MA. Gastrointest Endosc 1990;36:527-30. [2] Ikenberry SO, et al. Gastrointest Endosc 2011;73;6:1085-91.

1533 Catch 22: Management Dillema of Gastrointestinal AVM Ajayi Tokunbo, MD, Arooj Hyat, MD, Albert Namias, MD. Salem Hospital, Salem, MA. Introduction: Recognize the challenges in managing AVM-related UGIB in patients requiring life-long anticoagulation for mechanical valves. Appreciate non-endoscopic management options for UGIB, including tamoxifen. Case Report: An 80-year-old male presented to the emergency department with melena and fatigue. He denied abdominal pain, nausea, or vomiting. The patient denied any recent NSAID use. His past medical history is notable for mechanical mitral valve (on coumadin), SBO, and prior GI bleeds. His vitals were stable except for a temp of 101.3 F. His physical exam revealed dry mucous membranes, RRR with mechanical heart sounds, soft, non-tender abdomen with bowel sounds present, and rectal exam revealed black, tarry stool that was guaic positive. His initial labs were notable for hematocrit 28 and INR 2; LFTs were within normal limits at presentation. However, he became altered, dizzy, and hypotensive, needing 2U PRBC transfusion and admitted to MICU. The patient had an EGD that revealed Schatzki’s ring at the GE junction and non-bleeding AVMs in the duodenum and stomach. The AVMs were treated with argon coagulation. However, his hematocrit continued to trend down from 28% to 20%, and he subsequently underwent colonoscopy that did not reveal a source for the bleeding. The patient continued to require transfusions over the next 48 hours. He was also on a heparin gtt for anticoagulation for mechanical valve. Capsule endoscopy was discussed as the next diagnostic intervention to determine the source of bleeding. There was concern for capsule retention due to history of Schazki’s ring and SBO, and therefore, AVM treatment with tamoxifen was initiated. Pt received 10 mg po bid of tamoxifen and his hematocrit stabilized over a course of 10 days. During this time, he remained hemodynamically stable and only required 1 additional unit of PRBCs. His anticoagulation remained uninterrupted through his hospital stay. Discussion: Five percent of upper GI bleeding may be related to obscure source and about 30% may be related to AVMs, especially in elderly patients. Managements of AVMs can be challenging, especially in a case with multiple numbers of AVMs in the small bowel. Endoscopic intervention might be impossible in a patient with SBO and on life-long anticoagulation for mechanical valve because of inability to achieve hemostasis. Medical therapy is another option in these cases with the use of tamoxifen, somatostatin analogue, combined estrogen/progesterone therapy, and lenidelomide having been reported. This therapy


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Abstracts

[1532A] Figures. has been used in an anecdotal fashion without a know randomized control trial. Further research in this field would be of significant benefit in this challenging situation.

1534 An Uncommon Cause of Lower GI Bleeding in the Elderly: Blue Rubber Bleb Nevus Syndrome Zahra Iqbal, MD, Benjamin Robey, BS, Sabeen Abid, MD, Eslam Ali, MD, FACG. East Carolina University, Greenville, NC. Introduction: Blue rubber bleb nevus syndrome is a rare disorder consisting of gastrointestinal (GI) bleeding, cutaneous vascular nevi, and intestinal lesions. Venous malformations are located on the trunk


and arms. A common presentation is a lower GI bleed and iron deficiency anemia in a younger patient. We report this syndrome discovered in an older male after an acute GI bleed. A 76-year-old white man was admitted with 4 episodes of painless bright red blood per rectum in 1 day. His past medical history included stroke and atrial fibrillation. He was taking warfarin without a history of prior GI bleeding. He did not have a family history of GI bleeding or cancer. On physical examination, his pulse was irregular and his blood pressure was within normal limits. There were small, scattered blue papules present on his legs and trunk which were raised and compressible. He did not have external hemorrhoids. The remainder of his examination was unremarkable. On admission, his hemoglobin was 13.7 g/dl and his INR was 2.9. Leukocyte and platelet counts were also within normal limits. His warfarin was discontinued and 2 units of fresh frozen plasma and vitamin K were administered. His rectal bleeding improved within the next 24 hours. A colonoscopy performed the next day showed non-bleeding diverticulosis in the descending and sigmoid colon. There were several bluish vascular malformations of different sizes in the


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[1534A] Figure 1.

left colon which were not actively bleeding. His cutaneous and intestinal lesions were consistent with the diagnosis of Blue Rubber Bleb Nevus Syndrome. No further investigation or treatment was planned as per the patient’s decision. Blue rubber bleb nevus syndrome is clinically diagnosed by its characteristic lesions. The GI tract is most frequently involved but extra intestinal sites can be involved as well. It is thought to be inherited sporadically but autosomal dominant inheritance has been reported as well. Our patient did not have a family history of cutaneous lesions or GI bleeds making a sporadic mutation more likely. Our patient remained asymptomatic and undiagnosed til an older age and did not have iron deficiency anemia at presentation.

1535 Colonic Linear Hyperpigmentation in a Patient With Ulcerative Colitis Taking the Natural Supplement Indigo Naturalis Sasan Mosadeghi, MD, MS,1 Benny Liu, MD,1 Neil Stollman, MD, FACG2. 1. Alameda Health System/ Highland Hospital, Oakland, CA; 2. Alta Bates Summit Medical Center, Oakland, CA.

patient on treatment for EGPA who presented with recurrent small bowel obstruction and choledocholithiasis. A 64-year-old gentleman with a 12-year history of EGPA presented to our gastroenterology clinic with recurrent choledocholithiasis and 3 episodes of partial small bowel obstruction in a period of 6 weeks. The vasculitis was stable on methotrexate and prednisone, with serial stable inflammatory markers and absolute eosinophils prompting a reduction in immune suppression 3 months prior to presentation. On presentation, new lower extremity purpuric lesions were detected. Elevated inflammatory markers and eosinophilia were detected. MR enterography showed mechanical obstruction proximal to the ileocecal valve (Figure 1). ERCP and extended upper enteroscopy showed a dilated biliary tree, nodular mucosa in the gastric antrum, and duodenal polyps. A retrograde balloon-assisted enteroscopy showed thickened mucosal folds in the distal ileum corresponding to the abnormal MRI. Biopsies showed inflammatory expansion of the lamina propria, including the presence of increased eosinophils. Medical management with increased dose of MTX/prednisone was elected. After 2 months of being totally asymptomatic on higher dose immune suppression, the patient passed away. This was attributed to known pre-existing heart disease likely due to EGPA involvement. Although GI involvement of EGPA is relatively common, not many cases have reported the specific anatomical involvement through histopathological evaluation. The literature has reported cases of colitis, and gastric and colonic ulcers. We report a case of small bowel obstruction with histopathologic findings that also had widespread GI involvement. Awareness of the clinical presentation of GI involvement may allow more timely and effective management.

Introduction: Indigo naturalis is an herbal supplement used for centuries in Chinese medicine to treat inflammatory diseases. It has a dark blue color and is prepared in topical and oral forms. Its major components are indirubin, indigo, and tryptanthrin. Therapeutic effects against myelocytic leukemia have been demonstrated, and its long-term systemic use has been associated with adverse gastrointestinal effects and hepatotoxicity. Here, we present a novel endoscopic finding in a patient with ulcerative colitis (UC) who was taking indigo naturals. Case Report: A 35-year-old white male was diagnosed with UC at the age of 24. He started using indigo naturalis, consuming one-half teaspoon twice a day, and reported that his bowel movements decreased with a noticeable blue and greenish stool-color. After taking the supplement continuously for 2 years, he presented to us for colonoscopy, reporting 3 bowel movements daily. Colonoscopy revealed a normal ileum and normal mucosa visually in the ascending, transverse, and descending colon. In the sigmoid, hyperpigmented areas were noted, which were visually similar to melanosis coli; however, atypical in that these lesions were linear and in a striped pattern rather than the confluent pattern more commonly seen in melanosis. Additionally, the mucosa in the distal sigmoid and rectum appeared edematous with loss of vascularity and friability. No frank ulcers or erosions were seen. The impression at the time of endoscopy was mild proctosigmoiditis, as well as this unusual linear pigmentation. Subsequent histological analysis demonstrated benign colonic mucosa without any microscopic staining or pigmentation. Discussion: We are aware of 1 other report of endoscopic finding in patients taking indigo naturalis. In that manuscript, Sou et al reported a case series of 13 patients taking indigo for psoriasis or ITP, with associated ischemic lesion of colonic mucosa. Endoscopic and pathological characteristics were consistent with ischemia and chronicity. Our patient, in contrast, was minimally symptomatic without ischemic changes. We believe that the endoscopic findings are likely pigmentation caused by indigo naturalis’s deep blue pigment. Also of note is our patient’s symptomatic improvement, presumptively due to talking indigo naturalis. Indirubin has been shown to inhibit cyclin-dependent kinases such as CDK1/Cyclin B and CDK5/p25. Indirubin also inhibits EGFR activation and EGF-induced CDC25B gene expression in epidermal keratinocytes. Given the evidence of its potential anti-inflammatory and anti-proliferative properties, indigo naturalis may have a therapeutic role in UC, although further studies are needed to evaluate its pharmacological and safety profile.

1536 Eosinophilic Granulomatosis With Polyangiitis With Diffuse Gastrointestinal Involvement Diana Franco, MD,1 Kevin Ruff, MD,2 Lester Mertz, MD,3 Dora Lam-Himlin, MD,4 Russell Heigh, MD, FACG2. 1. Mayo Clinic, Internal Medicine, Scottsdale, AZ; 2. Mayo Clinic, Gastroenterology, Scottsdale, AZ; 3. Mayo Clinic, Rheumatology, Scottsdale, AZ; 4. Mayo Clinic, Pathology, Scottsdale, AZ.

[1536A] Figure 1.

Introduction: Eosinophilic granulomatosis with polyangiitis (EGPA) is a rare systemic, small, and medium-sized-vessel vasculitis. Gastrointestinal (GI) symptoms like diarrhea and abdominal pain are common; however, there are few reports of histological evidence of GI involvement. We report a case of a



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Abstracts 1537 A Rare Case of Ampullary Carcinoid Tumor: Emphasizing the Need for EUS for Diagnosis Jagpal Klair, MD, Mohit Girotra, MD, Johnny Jones III, MD, Harjot Kaur, MD, Rayburn Rego, MD, FACG. University of Arkansas for Medical Sciences, Little Rock, AR. Introduction: Ampullary carcinoids are extremely rare neuroendocrine tumors, comprising

Sudden death due to traumatic ascending aortic pseudoaneurysms ruptured into the esophagus: 2 case reports.

Case reports.

Why publish case reports in Physiological Reports.

The case for case reports.

Clinical case reports.

Evidence-based case reports.

Why medical case reports?

Writing case reports.

Drug Safety - Case Reports.

Neuroleukemiosis: Two Case Reports.

'Case reports: Giant sialolith.

Applause for case reports.

Why case reports matter.

Case Reports and Case Series: Expanding the scope of Journal of Orthopaedic Case reports.

The Value of Case Reports.

Two cheers for case reports.

Fainting (vasovagal syncope): case reports.

Sadfly fever: two case reports.

Erythrokeratodermia variabilis: Two case reports.

Poncet's disease: two case reports.

Coryneform endophthalmitis. Two case reports.

Congenital urethral fistula. Case reports.

Writing case reports for ecancer.

Disulfiram neuropathy: two case reports.