Letters to the Editor
which after a while leads to formation of the biliary calculosis. Therefore, we believe that evaluation of 2 separate cohorts of patients with GB sludge and comparison of cohorts of patients who underwent cholecystectomy and those who retained their GBs would be more appropriate. Also, we believe that comparing cohorts of patients with GB sludge and patients with GB calculosis (without acute cholecystitis, acute cholangitis, and acute pancreatitis in any cohort at the begining of the study) would be more appropriate. Secondly, relationship between functional GB disorder and the development of biliary events, such as acute cholecystitis, acute cholangitis, and acute pancreatitis, in non-GB sludge cohort of patients is quite vague. The authors reported that, during the follow-up, biliary events occurred in 8 patients (11.4%) in the non-GB sludge cohort. Acute pancreatitis occurred in 6 of 8 (in 5 patients as solely a disease and in 1 patient as acute pancreatitis associated with acute cholecystitis) patients in the non-GB sludge cohort during the followup. It remains debatable whether, in this series, acute pancreatitis is a cause or a consequence of biliary disorders. Only 2 remaining biliary events of 70 patients (2.9%) in the non-GB sludge cohort make this even more questionable. Concluding, we believe that more open questions remain regarding the role of GB sludge and its relationship to subsequent biliary events. However, despite its limitations, this study represents a significant step toward gaining more clarity in this matter. Enver Zerem, MD, PhD*w Lidija Lincender-Cvijetic´, MD, PhD* Admir Kurtcˇehajic´, MDz Josip Samardzˇic´, MDy Omar Zerem, BSc8 *Department of Medical Sciences, The Academy of Sciences and Arts of Bosnia and Herzegovina, Sarajevo wDepartment of Gastroenterology University Clinical Center Tuzla zMedical Center “Plava Poliklinika” 8Medical Faculty, University of Tuzla Tuzla, Bosnia and Herzegovina yDepartment of Surgery, County Hospital “Dr Josip Bencˇevic´,” Slavonski Brod Croatia
REFERENCES 1. Lee YS, Kang BK, Hwang IK, et al. Long-term outcomes of symptomatic gallbladder sludge. J Clin Gastroenterol. 2015;49:594–598. 2. Zerem E, Omerovic´ S. Minimally invasive management of biliary complications
J Clin Gastroenterol
after laparoscopic cholecystectomy. Eur J Intern Med. 2009;20:686–689. 3. Zerem E, Omerovic´ S. Can percutaneous cholecystostomy be a definitive management for acute cholecystitis in high-risk patients? Surg Laparosc Endosc Percutan Tech. 2014;24:187–191. 4. Zerem E, Omerovic´ S, Omerovic´ M, et al. Is transpapillary gallbladder stenting better than percutaneous cholecystostomy for the treatment of symptomatic gallbladder disease in decompensated cirrhotic patients? J Clin Gastroenterol. 2015; 49:448–449. 5. Zerem E, Omerovic´ S, Latic´ F. Comments on the article about the evaluation of the results of percutaneous cholecystostomy versus cholecystectomy. Ann Surg. 2015;261:e114.
Me´ne´trier Disease and Ulcerative Colitis To the Editor: Me´ne´trier disease (MD) is a rare hyperplastic, protein-losing gastropathy of an unknown etiology which manifests with nausea, vomiting, abdominal pain, and lower extremity edema. A relationship between ulcerative colitis (UC) and MD has been suggested by reports of patients with both the diagnoses. Upon review of the literature, we identified 8 such cases.1–7 We sought to quantify and describe our experience of patients with concurrent MD and UC. Cases were identified in our electronic medical record using institutional software to search by International Classification of Diseases, 9th Revision codes between the dates of January 1, 1994 and May 15, 2014. Records eligible for the softwarebased search were limited to those patients between the ages of 18 and 99 at the time of both MD and UC diagnoses. From a database of over 7.4 million patients, we identified 2 patients with both MD and UC. These 2 patients were both men with a known history of mild UC (8- and 35-y durations) based on Montreal classification before MD diagnosis (established at ages 34 and 53, respectively). Neither patient had extraintestinal manifestations of UC. Both patients presented with symptoms of episodic nausea, vomiting, and B.A.: acquisition of data and drafting of manuscript; S.S.: drafting of manuscript and critical revision of the manuscript for important intellectual content. Data were presented in part at the American College of Gastroenterology Annual Scientific Meeting October 2014, in Philadelphia, PA. The authors declare that they have nothing to disclose.
Volume 49, Number 9, October 2015
abdominal discomfort. Only 1 had lower extremity edema, whereas both had hypoalbuminemia. Endoscopic evaluation, in both cases, (Fig. 1A) with endoscopic mucosal resection confirmed the diagnosis of MD with histopathology showing glandular cystic dilatation and foveolar hyperplasia (Fig. 1B). At MD diagnosis, each patient’s UC was in symptomatic remission while on differing UC maintenance regimens. In 1 case, 6mercaptopurine and adalimumab were used, whereas the second patient was maintained on mesalamine monotherapy. Following both MD diagnoses, cetuximab infusion treatments were initiated resulting in symptomatic resolution. Both patients remained on cetuximab therapy and underwent annual endoscopic surveillance for gastric neoplasia. The simultaneous occurrence of MD and UC seems rare and may be a coincidence. However, a pathophysiological explanation for their cooccurrence is based on transforming growth factor (TGF)-a overexpression. Both MD and UC exhibit TGF-a excess in gastric and colonic mucosa, respectively. In MD, TGF-a stimulates gastric mucosal hyperplasia through enhanced epidermal growth factor receptor activation.8 In UC, upregulation of TGF-a occurs during epithelial regeneration of inactive UC.9 Increased TGF-a expression with inactive UC may then induce MD which explains why UC was in remission in both our patients. The TGF-a mechanism is further supported by symptomatic improvement in cases of coexistent MD and UC after initiation of cetuximab, an epidermal growth factor receptor inhibitor.1 The rarity of concomitant MD and UC, despite the relative commonality of UC (estimated prevalence of 7.6 to 246 cases per 100,000 patient years10), suggests that these 2 diseases are likely independent pathologic processes. While certain biological pathways may overlap between MD and UC, one would expect more cases reported in the literature and at our institution if there was a unifying pathophysiological mechanism. Although this rare association casts doubt on a shared pathogenesis, further studies are needed to better define the relationship between MD and UC.
Bradley Anderson, MD* Seth Sweetser, MD*w *Department of Internal Medicine wDivision of Gastroenterology and Hepatology, Mayo Clinic College of Medicine, Rochester, MN
796 | www.jcge.com Copyright r 2015 Wolters Kluwer Health, Inc. All rights reserved. Copyright r 2015 Wolters Kluwer Health, Inc. All rights reserved.
J Clin Gastroenterol
Volume 49, Number 9, October 2015
Letters to the Editor
FIGURE 1. A, Endoscopic images demonstrating polypoid gastric mucosa with exuberant mucus, consistent with Me´ne´trier disease. B, Endoscopic mucosal resection demonstrating polypoid hyperplastic gastric mucosa with inflammatory infiltrate in lamina propria (arrow) and glandular cystic dilatation (asterisks).
REFERENCES 1. Nguyen VX, Nguyen CC, Leighton JA, et al. The association of Me´ne´trier disease with ulcerative colitis: a case report with implications on the pathogenesis of Me´ne´trier disease. Case Rep Gastroenterol. 2010;4:66–70. 2. Ojeda E, Ruiz J, Cosme A, et al. Menetrier disease associated with ulcerative colitis. Response to the treatment with octreotide. Review of the diagnostic criteria and etiopathogenesis. Gastroenterol Hepatol. 1997;20:175–179. 3. Rahimi A, Ebrahimi ND, Anbardan SJ, et al. Menetrier’s disease presenting with ulcerative colitis: a case report and review of the literature. Govaresh. 2013;18:191–196.
Copyright
r
4. Sasaki E, Toyonaga A, Murayama S, et al. A case report of Menetrier’s disease developed in a patient with ulcerative colitis. Nippon Shokakibyo Gakkai Zasshi. 1991;88:96–99. 5. Hemmings CT. Menetrier’s disease in a patient with ulcerative colitis: a case report and review of the literature. Pathology. 2007;39:282–283. 6. Belhocine K, Chaoui F. Menetrier disease and ulcerative colitis an unusual association. Gastroenterol Clin Biol. 2006;30:1105–1107. 7. Mirkovic D, Doder R, Ilic S, et al. Menetrier’s disease associated with ulcerative colitis. Vojnosanit Pregl. 2003;60: 747–751.
2015 Wolters Kluwer Health, Inc. All rights reserved.
8. Takagi H, Jhappan C, Sharp R, et al. Hypertrophic gastropathy resembling Menetrier’s disease in transgenenic mice overexpressing transforming growth factor alpha in the stomach. J Clin Invest. 1992;90:1161–1167. 9. Zimmer KP, Heine M, Weissen-Plenz G, et al. TGFa-associated MUC2 and MUC3 expression of the gastric epithelium in Me´ne´trier’s disease during remission of ulcerative colitis. Gut. 2011;60:1607–1608. 10. Loftus EV Jr. Clinical epidemiology of inflammatory bowel disease: incidence, prevalence, and environmental influences. Gastroenterology. 2004;126: 1504–1517.
www.jcge.com |
Copyright r 2015 Wolters Kluwer Health, Inc. All rights reserved.
797
which after a while leads to formation of the biliary calculosis. Therefore, we believe that evaluation of 2 separate cohorts of patients with GB sludge and comparison of cohorts of patients who underwent cholecystectomy and those who retained their GBs would be more appropriate. Also, we believe that comparing cohorts of patients with GB sludge and patients with GB calculosis (without acute cholecystitis, acute cholangitis, and acute pancreatitis in any cohort at the begining of the study) would be more appropriate. Secondly, relationship between functional GB disorder and the development of biliary events, such as acute cholecystitis, acute cholangitis, and acute pancreatitis, in non-GB sludge cohort of patients is quite vague. The authors reported that, during the follow-up, biliary events occurred in 8 patients (11.4%) in the non-GB sludge cohort. Acute pancreatitis occurred in 6 of 8 (in 5 patients as solely a disease and in 1 patient as acute pancreatitis associated with acute cholecystitis) patients in the non-GB sludge cohort during the followup. It remains debatable whether, in this series, acute pancreatitis is a cause or a consequence of biliary disorders. Only 2 remaining biliary events of 70 patients (2.9%) in the non-GB sludge cohort make this even more questionable. Concluding, we believe that more open questions remain regarding the role of GB sludge and its relationship to subsequent biliary events. However, despite its limitations, this study represents a significant step toward gaining more clarity in this matter. Enver Zerem, MD, PhD*w Lidija Lincender-Cvijetic´, MD, PhD* Admir Kurtcˇehajic´, MDz Josip Samardzˇic´, MDy Omar Zerem, BSc8 *Department of Medical Sciences, The Academy of Sciences and Arts of Bosnia and Herzegovina, Sarajevo wDepartment of Gastroenterology University Clinical Center Tuzla zMedical Center “Plava Poliklinika” 8Medical Faculty, University of Tuzla Tuzla, Bosnia and Herzegovina yDepartment of Surgery, County Hospital “Dr Josip Bencˇevic´,” Slavonski Brod Croatia
REFERENCES 1. Lee YS, Kang BK, Hwang IK, et al. Long-term outcomes of symptomatic gallbladder sludge. J Clin Gastroenterol. 2015;49:594–598. 2. Zerem E, Omerovic´ S. Minimally invasive management of biliary complications
J Clin Gastroenterol
after laparoscopic cholecystectomy. Eur J Intern Med. 2009;20:686–689. 3. Zerem E, Omerovic´ S. Can percutaneous cholecystostomy be a definitive management for acute cholecystitis in high-risk patients? Surg Laparosc Endosc Percutan Tech. 2014;24:187–191. 4. Zerem E, Omerovic´ S, Omerovic´ M, et al. Is transpapillary gallbladder stenting better than percutaneous cholecystostomy for the treatment of symptomatic gallbladder disease in decompensated cirrhotic patients? J Clin Gastroenterol. 2015; 49:448–449. 5. Zerem E, Omerovic´ S, Latic´ F. Comments on the article about the evaluation of the results of percutaneous cholecystostomy versus cholecystectomy. Ann Surg. 2015;261:e114.
Me´ne´trier Disease and Ulcerative Colitis To the Editor: Me´ne´trier disease (MD) is a rare hyperplastic, protein-losing gastropathy of an unknown etiology which manifests with nausea, vomiting, abdominal pain, and lower extremity edema. A relationship between ulcerative colitis (UC) and MD has been suggested by reports of patients with both the diagnoses. Upon review of the literature, we identified 8 such cases.1–7 We sought to quantify and describe our experience of patients with concurrent MD and UC. Cases were identified in our electronic medical record using institutional software to search by International Classification of Diseases, 9th Revision codes between the dates of January 1, 1994 and May 15, 2014. Records eligible for the softwarebased search were limited to those patients between the ages of 18 and 99 at the time of both MD and UC diagnoses. From a database of over 7.4 million patients, we identified 2 patients with both MD and UC. These 2 patients were both men with a known history of mild UC (8- and 35-y durations) based on Montreal classification before MD diagnosis (established at ages 34 and 53, respectively). Neither patient had extraintestinal manifestations of UC. Both patients presented with symptoms of episodic nausea, vomiting, and B.A.: acquisition of data and drafting of manuscript; S.S.: drafting of manuscript and critical revision of the manuscript for important intellectual content. Data were presented in part at the American College of Gastroenterology Annual Scientific Meeting October 2014, in Philadelphia, PA. The authors declare that they have nothing to disclose.
Volume 49, Number 9, October 2015
abdominal discomfort. Only 1 had lower extremity edema, whereas both had hypoalbuminemia. Endoscopic evaluation, in both cases, (Fig. 1A) with endoscopic mucosal resection confirmed the diagnosis of MD with histopathology showing glandular cystic dilatation and foveolar hyperplasia (Fig. 1B). At MD diagnosis, each patient’s UC was in symptomatic remission while on differing UC maintenance regimens. In 1 case, 6mercaptopurine and adalimumab were used, whereas the second patient was maintained on mesalamine monotherapy. Following both MD diagnoses, cetuximab infusion treatments were initiated resulting in symptomatic resolution. Both patients remained on cetuximab therapy and underwent annual endoscopic surveillance for gastric neoplasia. The simultaneous occurrence of MD and UC seems rare and may be a coincidence. However, a pathophysiological explanation for their cooccurrence is based on transforming growth factor (TGF)-a overexpression. Both MD and UC exhibit TGF-a excess in gastric and colonic mucosa, respectively. In MD, TGF-a stimulates gastric mucosal hyperplasia through enhanced epidermal growth factor receptor activation.8 In UC, upregulation of TGF-a occurs during epithelial regeneration of inactive UC.9 Increased TGF-a expression with inactive UC may then induce MD which explains why UC was in remission in both our patients. The TGF-a mechanism is further supported by symptomatic improvement in cases of coexistent MD and UC after initiation of cetuximab, an epidermal growth factor receptor inhibitor.1 The rarity of concomitant MD and UC, despite the relative commonality of UC (estimated prevalence of 7.6 to 246 cases per 100,000 patient years10), suggests that these 2 diseases are likely independent pathologic processes. While certain biological pathways may overlap between MD and UC, one would expect more cases reported in the literature and at our institution if there was a unifying pathophysiological mechanism. Although this rare association casts doubt on a shared pathogenesis, further studies are needed to better define the relationship between MD and UC.
Bradley Anderson, MD* Seth Sweetser, MD*w *Department of Internal Medicine wDivision of Gastroenterology and Hepatology, Mayo Clinic College of Medicine, Rochester, MN
796 | www.jcge.com Copyright r 2015 Wolters Kluwer Health, Inc. All rights reserved. Copyright r 2015 Wolters Kluwer Health, Inc. All rights reserved.
J Clin Gastroenterol
Volume 49, Number 9, October 2015
Letters to the Editor
FIGURE 1. A, Endoscopic images demonstrating polypoid gastric mucosa with exuberant mucus, consistent with Me´ne´trier disease. B, Endoscopic mucosal resection demonstrating polypoid hyperplastic gastric mucosa with inflammatory infiltrate in lamina propria (arrow) and glandular cystic dilatation (asterisks).
REFERENCES 1. Nguyen VX, Nguyen CC, Leighton JA, et al. The association of Me´ne´trier disease with ulcerative colitis: a case report with implications on the pathogenesis of Me´ne´trier disease. Case Rep Gastroenterol. 2010;4:66–70. 2. Ojeda E, Ruiz J, Cosme A, et al. Menetrier disease associated with ulcerative colitis. Response to the treatment with octreotide. Review of the diagnostic criteria and etiopathogenesis. Gastroenterol Hepatol. 1997;20:175–179. 3. Rahimi A, Ebrahimi ND, Anbardan SJ, et al. Menetrier’s disease presenting with ulcerative colitis: a case report and review of the literature. Govaresh. 2013;18:191–196.
Copyright
r
4. Sasaki E, Toyonaga A, Murayama S, et al. A case report of Menetrier’s disease developed in a patient with ulcerative colitis. Nippon Shokakibyo Gakkai Zasshi. 1991;88:96–99. 5. Hemmings CT. Menetrier’s disease in a patient with ulcerative colitis: a case report and review of the literature. Pathology. 2007;39:282–283. 6. Belhocine K, Chaoui F. Menetrier disease and ulcerative colitis an unusual association. Gastroenterol Clin Biol. 2006;30:1105–1107. 7. Mirkovic D, Doder R, Ilic S, et al. Menetrier’s disease associated with ulcerative colitis. Vojnosanit Pregl. 2003;60: 747–751.
2015 Wolters Kluwer Health, Inc. All rights reserved.
8. Takagi H, Jhappan C, Sharp R, et al. Hypertrophic gastropathy resembling Menetrier’s disease in transgenenic mice overexpressing transforming growth factor alpha in the stomach. J Clin Invest. 1992;90:1161–1167. 9. Zimmer KP, Heine M, Weissen-Plenz G, et al. TGFa-associated MUC2 and MUC3 expression of the gastric epithelium in Me´ne´trier’s disease during remission of ulcerative colitis. Gut. 2011;60:1607–1608. 10. Loftus EV Jr. Clinical epidemiology of inflammatory bowel disease: incidence, prevalence, and environmental influences. Gastroenterology. 2004;126: 1504–1517.
www.jcge.com |
Copyright r 2015 Wolters Kluwer Health, Inc. All rights reserved.
797
