Abstract INTRODUCTION Histoplasmosis can cause severe, disseminated infection in immunocompromised individuals. Tumor necrosis factor-alpha inhibitors (anti-TNFs) and glucocorticoids, commonly used to treat Crohn’s disease (CD), are risk factors for disseminated infection. Gastrointestinal complications of disseminated histoplasmosis typically affect the ileocecal area, and can mimic CD with ulcerations, polypoid masses, bleeding, perforations, and painful oral lesions. We report a case of a 77-year-old female with previous diagnosis of CD who presented with fever and painful mouth lesions who developed a small bowel perforation related to disseminated histoplasmosis. Case Report A 77-year-old female with a history of ileocolonic CD diagnosed in 1980’s and prior right hemicolectomy reportedly for an inflammatory colonic mass presented with fevers every 2-3 days for 2 years and recurrent painful oral lesions (figure 1) for 1 year unresponsive to multiple courses of oral steroids. Her CD had previously been managed with oral budesonide continuously since diagnosis, infliximab and azathioprine for the past 8 years. Despite therapy, she continued to have diffuse abdominal pain, intermittent hematochezia, and iron deficiency anemia requiring transfusions on this regimen. One week prior to presentation, she underwent biopsy of the base of the tongue which revealed oral histoplasmosis. Her abdominal imaging on arrival showed mild inflammatory colitis. Colonoscopy revealed severe terminal ileum stenosis, and discrete, deep, punched-out colonic ulcers without surrounding inflammation (figure 2); biopsies confirmed histoplasmosis with otherwise normal colonic mucosa. She was started on amphotericin, posaconazole and began tapering steroids. Infliximab was held. Unfortunately, her course was complicated by focal bowel perforation in the proximal jejunum requiring emergent exploratory laparotomy with small bowel resection. Surgical pathology showed histoplasmosis within the submucosa of the small bowel. Post-operatively, she developed melena and required additional transfusions. Bleeding resolved with correction of coagulopathy and further endoscopic evaluation was deferred due to recent anastomosis. Once stabilized, she continued to have poor oral intake and severe malnutrition. She eventually elected to stop all life prolonging measures and was discharged to home hospice. CONCLUSION This case underscores the significant clinical overlap between CD and disseminated histoplasmosis, which can lead to misdiagnosis and adverse outcomes. Tissue diagnosis is essential, and infections such as histoplasmosis should be excluded prior to escalating immunosuppression. Although prior records confirming her CD were unavailable, chronic steroid use and anti-TNF therapy likely contributed to severe histoplasmosis that resulted in bowel perforation.
Missi et al. (Thu,) studied this question.
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