Gastrointestinal: Unusual cause of ileocecal thickening in an immunocompromised patient: A histologic surprise

Gastrointestinal: Unusual cause of ileocecal thickening in an immunocompromised patient: A... A 40‐year‐old female presented with colicky abdominal pain for 1 year with fever and significant weight loss for 3 months. She was cachectic with body mass index of 14.3 kg/m2 and had pallor. Her hemoglobin was 8.4 g/dL with mean corpuscular volume of 75 fL. Mantoux skin test, chest roentgenogram, and liver and kidney function tests were normal. Her abdominal computed tomography revealed circumferential mural thickening in terminal ileum, ileocecal junction, and cecum (Fig. a). Colonoscopy revealed cecal ulcers with narrowing and ulceration of the ileocecal valve (Fig. b). Colonic biopsy showed granulation tissue with mixed inflammatory infiltrate and numerous budding yeast within histiocytes and outside that were highlighted on periodic acid–Schiff stain confirming the morphology of Histoplasma (Fig. a,b). Stain for acid fast bacilli and tissue biopsy for tuberculosis culture were negative. She had HIV‐positive status with CD4 count of 125/μL. She was initiated on injectable liposomal amphotericin B for 14 days followed by itraconazole 200 mg twice daily. Also, antiretroviral therapy (tenofovir, lamivudine, and efavirenz) was started. At 4 months of follow‐up, the patient has improved and gained 12 kg of weight.1(a) Computed tomography showing thickening of the cecum and (b) colonoscopy showing cecal ulcerations.2Photomicrograph showing inflammatory granulation tissue with numerous budding yeast forms predominantly within histiocytes and few organisms residing extracellularly on (a) HE (40×) and on (b) periodic acid–Schiff (40×) stain.Histoplasmosis is a common causative agent causing endemic mycosis in certain regions. Disseminated histoplasmosis is usually seen in patients with advanced acquired immune deficiency syndrome and is fatal if untreated. Isolated gastrointestinal histoplasmosis as the initial presentation in patients with acquired immune deficiency syndrome is uncommon and is underdiagnosed because of non‐specific presentation and low suspicion in non‐endemic areas. The clinical presentation is usually in the form of abdominal pain, fever, weight loss, and diarrhea. The ileocecal area is the usual site of involvement and macroscopically presents as polyps or plaques, ulcers, or growth mimicking malignancy/inflammatory bowel disease. Rare presentations are intestinal perforation and obstruction and gastrointestinal bleeding. Although culture is the gold standard for diagnosis, histopathology is sufficient as it is positive in > 85% of patients. As per Infectious Diseases Society of America, liposomal amphotericin B is the standard of care that is followed by the administration of oral itraconazole once patients are stabilized, which can be stopped once the CD4 count is > 150. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Gastroenterology and Hepatology Wiley

Gastrointestinal: Unusual cause of ileocecal thickening in an immunocompromised patient: A histologic surprise

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Publisher
Wiley
Copyright
© 2018 Journal of Gastroenterology and Hepatology Foundation and John Wiley & Sons Australia, Ltd
ISSN
0815-9319
eISSN
1440-1746
D.O.I.
10.1111/jgh.13994
Publisher site
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Abstract

A 40‐year‐old female presented with colicky abdominal pain for 1 year with fever and significant weight loss for 3 months. She was cachectic with body mass index of 14.3 kg/m2 and had pallor. Her hemoglobin was 8.4 g/dL with mean corpuscular volume of 75 fL. Mantoux skin test, chest roentgenogram, and liver and kidney function tests were normal. Her abdominal computed tomography revealed circumferential mural thickening in terminal ileum, ileocecal junction, and cecum (Fig. a). Colonoscopy revealed cecal ulcers with narrowing and ulceration of the ileocecal valve (Fig. b). Colonic biopsy showed granulation tissue with mixed inflammatory infiltrate and numerous budding yeast within histiocytes and outside that were highlighted on periodic acid–Schiff stain confirming the morphology of Histoplasma (Fig. a,b). Stain for acid fast bacilli and tissue biopsy for tuberculosis culture were negative. She had HIV‐positive status with CD4 count of 125/μL. She was initiated on injectable liposomal amphotericin B for 14 days followed by itraconazole 200 mg twice daily. Also, antiretroviral therapy (tenofovir, lamivudine, and efavirenz) was started. At 4 months of follow‐up, the patient has improved and gained 12 kg of weight.1(a) Computed tomography showing thickening of the cecum and (b) colonoscopy showing cecal ulcerations.2Photomicrograph showing inflammatory granulation tissue with numerous budding yeast forms predominantly within histiocytes and few organisms residing extracellularly on (a) HE (40×) and on (b) periodic acid–Schiff (40×) stain.Histoplasmosis is a common causative agent causing endemic mycosis in certain regions. Disseminated histoplasmosis is usually seen in patients with advanced acquired immune deficiency syndrome and is fatal if untreated. Isolated gastrointestinal histoplasmosis as the initial presentation in patients with acquired immune deficiency syndrome is uncommon and is underdiagnosed because of non‐specific presentation and low suspicion in non‐endemic areas. The clinical presentation is usually in the form of abdominal pain, fever, weight loss, and diarrhea. The ileocecal area is the usual site of involvement and macroscopically presents as polyps or plaques, ulcers, or growth mimicking malignancy/inflammatory bowel disease. Rare presentations are intestinal perforation and obstruction and gastrointestinal bleeding. Although culture is the gold standard for diagnosis, histopathology is sufficient as it is positive in > 85% of patients. As per Infectious Diseases Society of America, liposomal amphotericin B is the standard of care that is followed by the administration of oral itraconazole once patients are stabilized, which can be stopped once the CD4 count is > 150.

Journal

Journal of Gastroenterology and HepatologyWiley

Published: Jan 1, 2018

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