Diagnosis and Management of HIV-Associated Colitis

A 63-year-old male with a history of untreated HIV presented to the emergency room with acute on chronic watery diarrhea, weight loss, fatigue, fever and chills. His vital signs were within normal limits and his abdomen was soft, nondistended and tender to palpation in 4 quadrants without peritonitis. He did not have leukocytosis on presentation. CD4 count was 310. CT scan showed inflammatory changes in the rectum and sigmoid colon. Comprehensive infectious workup was negative for any pathogens including cytomegalovirus (CMV), cryptosporidium, chlamydia, gonorrhea, C. difficile, cryptococcus, tuberculosis (TB) and herpes simplex virus (HSV). Colonoscopy was performed and showed a continuous area of nonbleeding ulcerated mucosa in the rectum, sigmoid, descending and transverse colon (Fig. 1). Pancolonic biopsies revealed active colitis with focal areas of basal plasmacytosis and crypt branching in left colon, suggestive of acute on chronic colitis and possible ulcerative colitis (UC). Gastroenterology and infectious disease were consulted and patient was started on IV methylprednisolone for presumed UC flare. Over the next few weeks, the patient proceeded to develop melena as well as increased lower abdominal and pelvic pain with intermittent fevers despite IV steroid treatment. The patient was trialed on IV infliximab also without significant improvement. After several weeks of steroid and biologic treatment, he developed increased abdominal pain with tachycardia and hemodynamic instability. His examination was significant for peritonitis with abdominal distension concerning for fulminant colitis. Colorectal surgery was consulted and proceeded to do an emergent total abdominal colectomy and end ileostomy. Intraoperatively he was found to have a small anterior distal rectal perforation. The decision was made to drain this area widely with rectal drain and fecal diversion and start him on IV antibiotic therapy. His final pathology from the index operation showed ulceration and acute colitis. There was no chronic crypt architectural distortion such as crypt dropout, disarray, crypt branching or basal plasmacytosis that are often seen in inflammatory bowel disease (IBD). There was also increased apoptotic bodies and mitoses that were not consistent with IBD. After reviewing the clinical presentation, his disease progression, and final pathology, the treating team diagnosed the patient with HIV-associated colitis.