GRANULOMATOUS DISEASE IN AN IMMUNOCOMPROMISED PATIENT

Abstract

A 51 y/o female was referred to our IBD Clinic in late 2003. She had HIV since 1995 treated with HAART with no opportunistic infections. Early in 2003 a colonoscopy for evaluation of abdominal pain revealed an ascending colonic stricture and sigmoid aphthous ulcers. Crohn's Disease (CD) was diagnosed; oral steroids and two doses of infliximab were given. The patient had not admitted her HIV infection. Two weeks after treatment fever, chills, and weight loss developed. When we saw her, she had constant, dull, RLQ pain, but no vomiting, rectal bleeding, tenesmus, constipation, diarrhea, dysuria, arthralgia, or perianal pain. She looked chronically ill and malnourished. Abdomen was soft, depressible, with RLQ tenderness, and no guarding or rebound. Rectal exam was negative. CBC and chemistries were normal, sed rate was 98 mm/hr. Stools were negative for ova, parasites, Salmonella, Shigella, Cryptosporidium, and C. difficile toxins. CD4 counts were >200, PPD was negative. Chest and small bowel × Rays were normal. Colonoscopy showed an ascending colonic stricture and an irregular mucosal pattern with aphthous ulcers in the ascending and transverse colon. An enterocutaneus fistula and intrabdominal abscesses developed, treated with antibiotics and percutaneous drainage. A right hemicolectomy and fistulectomy were performed. Peritoneal involvement was noted. Histology revealed granulomas with caseous necrosis and multigiant cells in the mucosa, submucosa and mesenteric nodes. Special stains did not show microorganisms. A second stool work-up yielded no organisms including C. albicans and M. tuberculosis. Urine antigen and serum complement fixation titers for Histoplasma capsulatum were positive. The patient recovered from surgery and had gained twenty pounds three months after discharge. Itraconazole was started for disseminated histoplasmosis. This case illustrates the importance of infectious etiologies in the differential diagnosis of IBD, especially in those immunocompromised or on immunotherapy. Gastrointestinal histoplasmosis has a clinical, radiological, and endoscopic presentation similar to CD. Transmural granulomatous inflammation with colonic fistulization and perforation is an extremely rare complication in disseminated cases. Immunomodulator therapies for CD such as infliximab can activate and worsen the course of histoplasmosis. A heightened awareness for detection of opportunistic infections must be maintained for all patients undergoing immunotherapeutic regimes.Figure