Clin J Gastroenterol (2013) 6:315–318 DOI 10.1007/s12328-013-0405-y
CASE REPORT
Mediastinal histoplasmosis presenting as dysphagia: a case report with literature review Dhara Chaudhari • Jason Mckinney Doris Hubbs • Mark Young
•
Received: 17 May 2013 / Accepted: 26 June 2013 / Published online: 7 July 2013 Ó Springer Japan 2013
Keywords Dysphagia Histoplasma Mediastinal lymphadenopathy Mediastinal histoplasmosis
histoplasmosis. Esophageal involvement can be secondary to isolated lymphadenopathy, fibrosing mediastinitis or as part of a disseminated process [1]. Esophageal involvement secondary to mediastinal histoplasmosis is rare and reported in 5–13 % cases [2]. Symptoms are due to impingement of the esophagus by enlarged lymph nodes. Patients may develop dysphagia, odynophagia, upper gastrointestinal bleeding, bronchoesophageal fistula, an esophageal abscess or traction diverticula. Diagnosis is made through different modalities. A barium esophagogram may display extrinsic compression. Computed tomography (CT) may show enlarged calcified mediastinal lymph nodes. Endoscopic ultrasound (EUS) can provide better visualization of lymph nodes and an opportunity to biopsy involved lymph nodes. Treatment options in general are antifungal agents to treat infection or surgery to relieve obstruction. We present a case of a female patient with dysphagia who was found to have mediastinal histoplasmosis. She was treated with thoracotomy and lymph node removal with evidence of Histoplasma on the lymph node biopsy specimen.
Introduction
Case
Mediastinal granulomas are fibrocaseous masses usually found in association with fungal infections such as
A 22-year-old female patient who recently relocated from Indiana with no past medical history, presented to the primary care clinic with a 4-month history of dysphagia to solid foods. She denied fever, weight loss, odynophagia, hematemesis or melena. Her childhood was without any major health problems. She denied smoking, alcohol or illicit drug abuse. Her family history was significant for non-Hodgkin’s lymphoma in her mother and maternal grandfather. A review of systems was negative. Her physical examination including vital signs was normal. Laboratory values revealed blood urea nitrogen 14 mg/dl
Abstract Histoplasmosis is an endemic infection of the Ohio and Mississippi River valleys. Clinical presentation of infection in immunocompetent hosts ranges from asymptomatic to minor flu-like symptoms; however, disseminated infection can occur in immunocompromised patients. Esophageal involvement in the form of dysphagia secondary to mediastinal histoplasmosis is rarely reported in the literature. We present a young female who complained of dysphagia and was found to have an esophageal stricture on barium esophagogram. Endoscopy revealed a submucosal nodule stricture situated 29 cm from the incisors. She underwent thoracotomy for lymph node removal. Histologic findings of the removed lymph node showed caseating granuloma with macrophages. The clinical findings together with the laboratory evaluation and biopsy features were suggestive of mediastinal histoplasmosis as the cause of the dysphagia.
D. Chaudhari (&) D. Hubbs Department of Internal Medicine, East Tennessee State University, 1008 Quality Circle, Apt 79, Johnson City 37615, TN, USA e-mail: [email protected] J. Mckinney M. Young Department of Gastroenterology, East Tennessee State University, Johnson City, TN, USA
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(normal 8–23), creatinine 0.8 mg/dl (normal 0.80–1.30), total bilirubin 0.8 mg/dl (normal \1.0); alkaline phosphatase 120 IU/L; aspartate transaminase 24 IU/L (normal \35), alanine transaminase 30 IU/L (normal \35), alpha fetal protein 3.0 IU/ml, lactate dehydrogenase 267 IU/L (normal 200–450 IU/L), albumin 3.6 g/dl (normal 3.2–4.6 g/dl), total protein 6.9 g/dl (normal 6.4–8.3 g/dl), vitamin D 34.8 ng/ml (normal 20–80 ng/ml), negative carcinoembryonic antigen (CEA), and normal CA 19-9 level. A complete metabolic panel showed white blood count 9.29103/ll (normal 5–10.29103/ll ), hemoglobin 13.2 g/dl (normal 12.5–15.3 g/dl), platelet 3129103/ll (normal 150–4509103/ll ). A barium esophagogram was performed because of the dysphagia and revealed extrinsic compression at the lower third of the esophagus (Fig. 1) causing ‘hold up’ of a 13-mm barium tablet. CT with contrast of the chest revealed a 2.0 9 1.7 cm enlarged calcified lymph node with popcorn-type central calcification in the right subcarinal region (Fig. 2). Tuberculin skin test, hepatitis panel and human immunodeficiency virus were negative, and angiotensin-converting enzyme level was normal. Histoplasma complement fixation titer was elevated at 1:16 and immunohistochemistry was negative. An endoscopy showed a stricture situated 29 cm from the incisors with a small nodule above the stricture (Fig. 3). Endoscopic ultrasound was attempted but was not successful because of the patient’s non-compliance during the
Clin J Gastroenterol (2013) 6:315–318
procedure. The CT chest findings of calcified lymph node enlargement, the positive laboratory findings for histoplasma titer and the negative findings for other causes of enlarged lymph node such as tuberculosis, sarcoidosis, silicosis, together with the patient’s geographic area of residence over a long period, confirmed a diagnosis of mediastinal histoplasmosis. The patient’s symptoms of dysphagia continued to progress. Initially she was able to swallow chopped meat or chewed food but this gradually became difficult. She underwent thoracotomy which showed adherent adjacent tissue and allowed successful removal of the enlarged lymph node. A biopsy of the enlarged lymph node showed caseating granuloma with dystrophic calcification (Fig. 4). Since surgery, the patient has been improving gradually without any complaint of dysphagia.
Fig. 2 CT chest showing 2.0 9 1.7-cm calcified lymph node with popcorn-type central calcification in the right subcarinal region
Fig. 1 Barium esophagogram showing extrinsic compression
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Fig. 3 Endoscopy revealing submucosal nodule and stricture situated 29 cm from the incisors
Clin J Gastroenterol (2013) 6:315–318
Fig. 4 Biopsy slide of lymph node showing caseating granuloma with dystrophic granulation
Discussion Mediastinal granuloma is a fibrocaseous mass that occurs when a group of lymph nodes coalesce into a necrotic mass surrounded by thin fibrotic capsule. Causes include infectious etiologies such as histoplasma, tuberculosis, and noninfectious causes such as silicosis, sarcoid, Wegener’s granulomatosis or rheumatoid disease. Histoplasmosis is a disease endemic to the Ohio, and Mississippi River valleys caused by Histoplasma microconidia. Human infection is caused by soil contaminated with spores of H. capsulatum. The clinical course ranges from flu-like symptoms with low-level exposure to disseminated infection. Prior to development of immunity to H. capsulatum, hematogenous spread occurs to reticuloendothelial organs and lymph nodes leading to nodular accumulation of epithelioid cells [3]. The sequela of H. capsulatum is formation of granuloma and caseous necrosis with eventual development of calcification during healing. The common sites of involvement are hilar and mediastinal lymph nodes, lung, liver or spleen. Massive mediastinal lymphadenopathy may occur without overt manifestation of parenchymal involvement [3]. Presentation of mediastinal granulomatous lymphadenopathy may be asymptomatic, regional complications secondary to obstruction, or fibrosing mediastinitis leading to entrapment of vital organs [1]. Gastrointestinal histoplasmosis can occur as a part of disseminated disease or as a local complication of active or chronic inflammation. Although H. capsulatum can be identified in the gastrointestinal tract of 70–90 % patients with disseminated disease undergoing autopsy, it is rarely diagnosed because symptoms only appear in 3–12 % of patients during their lifetime [1]. The small bowel and colon are the most commonly involved sites in
317
histoplasmosis. Esophageal involvement can be secondary to isolated lymphadenopathy, fibrosing mediastinitis or as a part of disseminated process. Esophageal involvement associated with mediastinal histoplasmic lymphadenopathy is rare and only reported in 5-13 % of cases [2]. Dysphagia as an initial manifestation of mediastinal histoplasma is a rare presentation. Esophageal manifestations are a result of extrinsic compression due to an enlarged mediastinal lymph node [4]. The most commonly involved sites are subcarinal and tracheobronchial lymph nodes [3]. The submucosal nodules and erosions are usually caused by fibrotic changes in para-esophageal lymph nodes during healing of granulomatous inflammation causing extraluminal compression [5]. Several modalities are used in the diagnosis of mediastinal histoplasmosis. CT is helpful in indicating the nature and extent of calcification and involvement of contiguous structures [6]. The identification of nodal calcification usually indicates a benign process. Upper endoscopy can be helpful in revealing submucosal nodules, strictures or traction diverticula in patients with histoplasmosis [7]. In our patient, upper endoscopy showed a submucosal nodule and stricture situated 29 cm from the incisors. Endoscopic ultrasound (EUS) should be used in patients with esophageal strictures or masses where CT or endoscopy findings are inconclusive. EUS findings of a mediastinal granuloma show a large mass of matted lymph nodes adherent to the esophagus with thick esophageal walls in contrast to malignant lymph nodes which appear as hypoechoic, rounded, separated lymph nodes with distinct borders without adherence to the esophageal wall [8]. EUS also provides better resolution of para-esophageal lesions with greater sensitivity than CT for identifying calcified lymph nodes. The added advantage with EUS is the ability to obtain a fine-needle aspiration biopsy without invasion of vascular structures [8]. Additional tools for diagnosis of histoplasmosis include antigen test, serology, direct microscopic examination, and culture. A urine antigen test has higher sensitivity compared to serum in cases of disseminated disease [9]; however, its sensitivity is unknown for localized histoplasmosis especially with esophageal involvement [10]. Culture results take several weeks to provide results making them less useful in clinical settings [11]. A serologic test in the form of complement fixation and immunodiffusion should be performed in suspected histoplasmosis [12]; however, because of cross-reactivity with other fungal infections, positive histoplasma serology might be misleading in patients with other active infections. The most definitive diagnostic method is biopsy of the involved site. Microscopic examination reveals inflammatory cell infiltrates including lymphocytes, plasma cells, and macrophages, along with eosinophils or neutrophils. Hematoxylin and
123
318
eosin (H&E) staining usually shows a halo around the yeast due to retraction of the basophilic cytoplasm from the cell wall [1]. Go¨mo¨ri methenamine silver stain is used to identify histoplasma when a small amount of yeast is present which cannot be detected on H&E staining [13]. Treatment options for mediastinal histoplasmosis are antifungal medications, surgery or a combination. Amphotericin B is superior to itraconazole, with an 80 % response rate [14]; however, amphotericin has a higher toxicity profile and is not effective in case of inactive infection. Treatment modalities for esophageal manifestation secondary to mediastinal histoplasmosis are not clear since there has been no retrospective studies or prospective trials performed to evaluate therapeutic options in such patients. In symptomatic patients, itraconazole for 6–12 months has been suggested [14]. In patients with progressive symptoms, surgical excision is performed to relieve obstruction. Palliative esophageal stenting against medical or surgical therapy has also not been evaluated. Surgery seems a lucrative option compared to antifungal treatment based on literature reviewed. Surgical excision is performed in most cases either for the relief of obstruction or to rule out malignancy in cases of doubt. A possible explanation is that while infection is deemed inactive as measured by tests available, symptoms of mediastinal histoplasmosis are progressive based on the hypothesis that there might be an active process causing enlargement of the lymph nodes and obstructing the surrounding structures and leading to fibrosis. Despite the absence of studies comparing treatment options for esophageal manifestations in mediastinal histoplasmosis, one suggestion, although not proven, is that removing the lymph node by surgery might decrease the chances of developing fibrosing mediastinitis [3]. Acknowledgments We thank Dr. Kimberly Helms for providing the H&E-stained slide of lymph node biopsy.
123
Clin J Gastroenterol (2013) 6:315–318 Conflict of interest of interest.
The authors declare that they have no conflict
References 1. Kahi CJ, Wheat LJ, Allen SD, Sarosi GA. Gastrointestinal histoplasmosis. Am J Gastroenterol. 2005;100(1):220–31. 2. Coss KC, Wheat LJ, Conces DJ, Brashear RE, Hull MT. Esophageal fistula complicating mediastinal histoplasmosis. Am J Med. 1987;83:343–6. 3. Gilliland MD, Scott LD, Walker WE. Esophageal obstruction caused by mediastinal histoplasmosis: beneficial results of operation. Surgery. 1984;95(1):59–62. 4. Moore T. Esophageal obstruction due to mediastinal granuloma. J Thorac Surg. 1959;37:127. 5. Christodoupoulos J, Klotz A. Esophageal obstruction due to granulomatous mediastinal lymphadenopathy. Gastroenterology. 1961;40:574. 6. Marshall JB, Singh R, Demmy TL, Bickel JT, Everett ED. Mediastinal histoplasmosis presenting with esophageal involvement and dysphagia: case study. Dysphagia. 1995; Winter; 10(1):53–8. 7. Sarosi G, Davies SF. Gastrointestinal involvement in histoplasmosis. Pract Gastroenterol. 1984;VIII:19–31. 8. Savides TJ, Gress FG, Wheat LJ, Ikenberry S, Hawes RH. Dysphagia due to mediastinal granulomas: diagnosis with endoscopic ultrasonography. Gastroenterology. 1995;109(2):366–73. 9. Felson B, Klatte EC. Complications of the arrested primary histoplasmic complex. JAMA. 1976;236(10):1157–61. 10. Garamella J, Stltzman F, Varco R, Jensen N. Subcarinal mediastinal granulomas causing esophageal obstruction. J Thorac Surg. 1955;30:187. 11. Wheat J, French ML, Kohler RB, et al. Laboratory tests for histoplasmosis: analysis of experience in a large urban outbreak. Ann Intern Med. 1982;(97) 5:680–5. 12. Fifer W, Woellner R, Gordon S. Mediastinal Histoplasmosis. Report of three cases with dysphagia as the presenting complaint. Chest. 1965;(47) 5: 518–6. 13. Ray A, Gahunia M. Histoplasmosis presenting as a hypopharyngeal mass in an immune compromised host. Pract Gastroenterol; 2010 pp. 41–6. 14. Wheat J, Sarosi G, Mckinsey D, et al. Practice guidelines for management of patients with histoplasmosis. Infectious diseases society of America. Clin Infect Dis. 2000;30(4):688–95.
CASE REPORT
Mediastinal histoplasmosis presenting as dysphagia: a case report with literature review Dhara Chaudhari • Jason Mckinney Doris Hubbs • Mark Young
•
Received: 17 May 2013 / Accepted: 26 June 2013 / Published online: 7 July 2013 Ó Springer Japan 2013
Keywords Dysphagia Histoplasma Mediastinal lymphadenopathy Mediastinal histoplasmosis
histoplasmosis. Esophageal involvement can be secondary to isolated lymphadenopathy, fibrosing mediastinitis or as part of a disseminated process [1]. Esophageal involvement secondary to mediastinal histoplasmosis is rare and reported in 5–13 % cases [2]. Symptoms are due to impingement of the esophagus by enlarged lymph nodes. Patients may develop dysphagia, odynophagia, upper gastrointestinal bleeding, bronchoesophageal fistula, an esophageal abscess or traction diverticula. Diagnosis is made through different modalities. A barium esophagogram may display extrinsic compression. Computed tomography (CT) may show enlarged calcified mediastinal lymph nodes. Endoscopic ultrasound (EUS) can provide better visualization of lymph nodes and an opportunity to biopsy involved lymph nodes. Treatment options in general are antifungal agents to treat infection or surgery to relieve obstruction. We present a case of a female patient with dysphagia who was found to have mediastinal histoplasmosis. She was treated with thoracotomy and lymph node removal with evidence of Histoplasma on the lymph node biopsy specimen.
Introduction
Case
Mediastinal granulomas are fibrocaseous masses usually found in association with fungal infections such as
A 22-year-old female patient who recently relocated from Indiana with no past medical history, presented to the primary care clinic with a 4-month history of dysphagia to solid foods. She denied fever, weight loss, odynophagia, hematemesis or melena. Her childhood was without any major health problems. She denied smoking, alcohol or illicit drug abuse. Her family history was significant for non-Hodgkin’s lymphoma in her mother and maternal grandfather. A review of systems was negative. Her physical examination including vital signs was normal. Laboratory values revealed blood urea nitrogen 14 mg/dl
Abstract Histoplasmosis is an endemic infection of the Ohio and Mississippi River valleys. Clinical presentation of infection in immunocompetent hosts ranges from asymptomatic to minor flu-like symptoms; however, disseminated infection can occur in immunocompromised patients. Esophageal involvement in the form of dysphagia secondary to mediastinal histoplasmosis is rarely reported in the literature. We present a young female who complained of dysphagia and was found to have an esophageal stricture on barium esophagogram. Endoscopy revealed a submucosal nodule stricture situated 29 cm from the incisors. She underwent thoracotomy for lymph node removal. Histologic findings of the removed lymph node showed caseating granuloma with macrophages. The clinical findings together with the laboratory evaluation and biopsy features were suggestive of mediastinal histoplasmosis as the cause of the dysphagia.
D. Chaudhari (&) D. Hubbs Department of Internal Medicine, East Tennessee State University, 1008 Quality Circle, Apt 79, Johnson City 37615, TN, USA e-mail: [email protected] J. Mckinney M. Young Department of Gastroenterology, East Tennessee State University, Johnson City, TN, USA
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316
(normal 8–23), creatinine 0.8 mg/dl (normal 0.80–1.30), total bilirubin 0.8 mg/dl (normal \1.0); alkaline phosphatase 120 IU/L; aspartate transaminase 24 IU/L (normal \35), alanine transaminase 30 IU/L (normal \35), alpha fetal protein 3.0 IU/ml, lactate dehydrogenase 267 IU/L (normal 200–450 IU/L), albumin 3.6 g/dl (normal 3.2–4.6 g/dl), total protein 6.9 g/dl (normal 6.4–8.3 g/dl), vitamin D 34.8 ng/ml (normal 20–80 ng/ml), negative carcinoembryonic antigen (CEA), and normal CA 19-9 level. A complete metabolic panel showed white blood count 9.29103/ll (normal 5–10.29103/ll ), hemoglobin 13.2 g/dl (normal 12.5–15.3 g/dl), platelet 3129103/ll (normal 150–4509103/ll ). A barium esophagogram was performed because of the dysphagia and revealed extrinsic compression at the lower third of the esophagus (Fig. 1) causing ‘hold up’ of a 13-mm barium tablet. CT with contrast of the chest revealed a 2.0 9 1.7 cm enlarged calcified lymph node with popcorn-type central calcification in the right subcarinal region (Fig. 2). Tuberculin skin test, hepatitis panel and human immunodeficiency virus were negative, and angiotensin-converting enzyme level was normal. Histoplasma complement fixation titer was elevated at 1:16 and immunohistochemistry was negative. An endoscopy showed a stricture situated 29 cm from the incisors with a small nodule above the stricture (Fig. 3). Endoscopic ultrasound was attempted but was not successful because of the patient’s non-compliance during the
Clin J Gastroenterol (2013) 6:315–318
procedure. The CT chest findings of calcified lymph node enlargement, the positive laboratory findings for histoplasma titer and the negative findings for other causes of enlarged lymph node such as tuberculosis, sarcoidosis, silicosis, together with the patient’s geographic area of residence over a long period, confirmed a diagnosis of mediastinal histoplasmosis. The patient’s symptoms of dysphagia continued to progress. Initially she was able to swallow chopped meat or chewed food but this gradually became difficult. She underwent thoracotomy which showed adherent adjacent tissue and allowed successful removal of the enlarged lymph node. A biopsy of the enlarged lymph node showed caseating granuloma with dystrophic calcification (Fig. 4). Since surgery, the patient has been improving gradually without any complaint of dysphagia.
Fig. 2 CT chest showing 2.0 9 1.7-cm calcified lymph node with popcorn-type central calcification in the right subcarinal region
Fig. 1 Barium esophagogram showing extrinsic compression
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Fig. 3 Endoscopy revealing submucosal nodule and stricture situated 29 cm from the incisors
Clin J Gastroenterol (2013) 6:315–318
Fig. 4 Biopsy slide of lymph node showing caseating granuloma with dystrophic granulation
Discussion Mediastinal granuloma is a fibrocaseous mass that occurs when a group of lymph nodes coalesce into a necrotic mass surrounded by thin fibrotic capsule. Causes include infectious etiologies such as histoplasma, tuberculosis, and noninfectious causes such as silicosis, sarcoid, Wegener’s granulomatosis or rheumatoid disease. Histoplasmosis is a disease endemic to the Ohio, and Mississippi River valleys caused by Histoplasma microconidia. Human infection is caused by soil contaminated with spores of H. capsulatum. The clinical course ranges from flu-like symptoms with low-level exposure to disseminated infection. Prior to development of immunity to H. capsulatum, hematogenous spread occurs to reticuloendothelial organs and lymph nodes leading to nodular accumulation of epithelioid cells [3]. The sequela of H. capsulatum is formation of granuloma and caseous necrosis with eventual development of calcification during healing. The common sites of involvement are hilar and mediastinal lymph nodes, lung, liver or spleen. Massive mediastinal lymphadenopathy may occur without overt manifestation of parenchymal involvement [3]. Presentation of mediastinal granulomatous lymphadenopathy may be asymptomatic, regional complications secondary to obstruction, or fibrosing mediastinitis leading to entrapment of vital organs [1]. Gastrointestinal histoplasmosis can occur as a part of disseminated disease or as a local complication of active or chronic inflammation. Although H. capsulatum can be identified in the gastrointestinal tract of 70–90 % patients with disseminated disease undergoing autopsy, it is rarely diagnosed because symptoms only appear in 3–12 % of patients during their lifetime [1]. The small bowel and colon are the most commonly involved sites in
317
histoplasmosis. Esophageal involvement can be secondary to isolated lymphadenopathy, fibrosing mediastinitis or as a part of disseminated process. Esophageal involvement associated with mediastinal histoplasmic lymphadenopathy is rare and only reported in 5-13 % of cases [2]. Dysphagia as an initial manifestation of mediastinal histoplasma is a rare presentation. Esophageal manifestations are a result of extrinsic compression due to an enlarged mediastinal lymph node [4]. The most commonly involved sites are subcarinal and tracheobronchial lymph nodes [3]. The submucosal nodules and erosions are usually caused by fibrotic changes in para-esophageal lymph nodes during healing of granulomatous inflammation causing extraluminal compression [5]. Several modalities are used in the diagnosis of mediastinal histoplasmosis. CT is helpful in indicating the nature and extent of calcification and involvement of contiguous structures [6]. The identification of nodal calcification usually indicates a benign process. Upper endoscopy can be helpful in revealing submucosal nodules, strictures or traction diverticula in patients with histoplasmosis [7]. In our patient, upper endoscopy showed a submucosal nodule and stricture situated 29 cm from the incisors. Endoscopic ultrasound (EUS) should be used in patients with esophageal strictures or masses where CT or endoscopy findings are inconclusive. EUS findings of a mediastinal granuloma show a large mass of matted lymph nodes adherent to the esophagus with thick esophageal walls in contrast to malignant lymph nodes which appear as hypoechoic, rounded, separated lymph nodes with distinct borders without adherence to the esophageal wall [8]. EUS also provides better resolution of para-esophageal lesions with greater sensitivity than CT for identifying calcified lymph nodes. The added advantage with EUS is the ability to obtain a fine-needle aspiration biopsy without invasion of vascular structures [8]. Additional tools for diagnosis of histoplasmosis include antigen test, serology, direct microscopic examination, and culture. A urine antigen test has higher sensitivity compared to serum in cases of disseminated disease [9]; however, its sensitivity is unknown for localized histoplasmosis especially with esophageal involvement [10]. Culture results take several weeks to provide results making them less useful in clinical settings [11]. A serologic test in the form of complement fixation and immunodiffusion should be performed in suspected histoplasmosis [12]; however, because of cross-reactivity with other fungal infections, positive histoplasma serology might be misleading in patients with other active infections. The most definitive diagnostic method is biopsy of the involved site. Microscopic examination reveals inflammatory cell infiltrates including lymphocytes, plasma cells, and macrophages, along with eosinophils or neutrophils. Hematoxylin and
123
318
eosin (H&E) staining usually shows a halo around the yeast due to retraction of the basophilic cytoplasm from the cell wall [1]. Go¨mo¨ri methenamine silver stain is used to identify histoplasma when a small amount of yeast is present which cannot be detected on H&E staining [13]. Treatment options for mediastinal histoplasmosis are antifungal medications, surgery or a combination. Amphotericin B is superior to itraconazole, with an 80 % response rate [14]; however, amphotericin has a higher toxicity profile and is not effective in case of inactive infection. Treatment modalities for esophageal manifestation secondary to mediastinal histoplasmosis are not clear since there has been no retrospective studies or prospective trials performed to evaluate therapeutic options in such patients. In symptomatic patients, itraconazole for 6–12 months has been suggested [14]. In patients with progressive symptoms, surgical excision is performed to relieve obstruction. Palliative esophageal stenting against medical or surgical therapy has also not been evaluated. Surgery seems a lucrative option compared to antifungal treatment based on literature reviewed. Surgical excision is performed in most cases either for the relief of obstruction or to rule out malignancy in cases of doubt. A possible explanation is that while infection is deemed inactive as measured by tests available, symptoms of mediastinal histoplasmosis are progressive based on the hypothesis that there might be an active process causing enlargement of the lymph nodes and obstructing the surrounding structures and leading to fibrosis. Despite the absence of studies comparing treatment options for esophageal manifestations in mediastinal histoplasmosis, one suggestion, although not proven, is that removing the lymph node by surgery might decrease the chances of developing fibrosing mediastinitis [3]. Acknowledgments We thank Dr. Kimberly Helms for providing the H&E-stained slide of lymph node biopsy.
123
Clin J Gastroenterol (2013) 6:315–318 Conflict of interest of interest.
The authors declare that they have no conflict
References 1. Kahi CJ, Wheat LJ, Allen SD, Sarosi GA. Gastrointestinal histoplasmosis. Am J Gastroenterol. 2005;100(1):220–31. 2. Coss KC, Wheat LJ, Conces DJ, Brashear RE, Hull MT. Esophageal fistula complicating mediastinal histoplasmosis. Am J Med. 1987;83:343–6. 3. Gilliland MD, Scott LD, Walker WE. Esophageal obstruction caused by mediastinal histoplasmosis: beneficial results of operation. Surgery. 1984;95(1):59–62. 4. Moore T. Esophageal obstruction due to mediastinal granuloma. J Thorac Surg. 1959;37:127. 5. Christodoupoulos J, Klotz A. Esophageal obstruction due to granulomatous mediastinal lymphadenopathy. Gastroenterology. 1961;40:574. 6. Marshall JB, Singh R, Demmy TL, Bickel JT, Everett ED. Mediastinal histoplasmosis presenting with esophageal involvement and dysphagia: case study. Dysphagia. 1995; Winter; 10(1):53–8. 7. Sarosi G, Davies SF. Gastrointestinal involvement in histoplasmosis. Pract Gastroenterol. 1984;VIII:19–31. 8. Savides TJ, Gress FG, Wheat LJ, Ikenberry S, Hawes RH. Dysphagia due to mediastinal granulomas: diagnosis with endoscopic ultrasonography. Gastroenterology. 1995;109(2):366–73. 9. Felson B, Klatte EC. Complications of the arrested primary histoplasmic complex. JAMA. 1976;236(10):1157–61. 10. Garamella J, Stltzman F, Varco R, Jensen N. Subcarinal mediastinal granulomas causing esophageal obstruction. J Thorac Surg. 1955;30:187. 11. Wheat J, French ML, Kohler RB, et al. Laboratory tests for histoplasmosis: analysis of experience in a large urban outbreak. Ann Intern Med. 1982;(97) 5:680–5. 12. Fifer W, Woellner R, Gordon S. Mediastinal Histoplasmosis. Report of three cases with dysphagia as the presenting complaint. Chest. 1965;(47) 5: 518–6. 13. Ray A, Gahunia M. Histoplasmosis presenting as a hypopharyngeal mass in an immune compromised host. Pract Gastroenterol; 2010 pp. 41–6. 14. Wheat J, Sarosi G, Mckinsey D, et al. Practice guidelines for management of patients with histoplasmosis. Infectious diseases society of America. Clin Infect Dis. 2000;30(4):688–95.
