Abstract

INTRODUCTION: Cytomegalovirus is an extremely common pathogen that usually causes a mild, self-limiting disease in the immunocompetent host. The risk of active CMV disease increases in states of immunosuppression (AIDS, transplant recipients, cancer, IBD, use of immunosuppressive agents). CMV infection in transplant recipients has a predilection for the gastrointestinal tract. CASE DESCRIPTION/METHODS: A 46 yo African American male with history renal transplant in 2002 presented to the hospital for worsening creatinine. He was previously doing well on immunosuppression with sirolimus, cyclosporine, and prednisone. His baseline creatinine was 2.2-2.6 mg/dL. On admission his Cr was 5.8. He underwent a renal biopsy that was suspicious for antibody-mediated rejection. He received high dose IV steroids, plasmapheresis, and IVIG. His Cr improved to 4 and he was discharged on tacrolimus, mycophenolate, and a tapering prednisone dose. He returned to the hospital 3 weeks later with dyspnea and peripheral edema. He also had 2 episodes of hematochezia the day prior. His Cr increased to 7.2 and his hemoglobin dropped from 8.9 g/dL to 6.9. He was started on dialysis. His hemoglobin initially improved with a transfusion but 3 days later dropped to 6.9. GI was consulted. Colonoscopy revealed a 7 × 7 mm ulcer at the ileocecal valve. Biopsies confirmed CMV colitis. He was evaluated by infectious disease for treatment. DISCUSSION: CMV infection of the GI tract is relatively common in organ transplant recipients and can involve the upper or lower GI tract. It can result in mucosal injury, ulcerations, hemorrhage, GI dysmotility, or perforations. CMV colitis can present with fever, abdominal pain, diarrhea, hematochezia, toxic megacolon, or perforation. Lower GI bleeding is the most common initial presentation. Endoscopic findings of CMV colitis are categorized into 3 groups: well-demarcated ulcers, diffuse infiltrative ulcers, and pseudomembranous patterns. Sometimes hemorrhagic colitis is seen with multiple punctuate lesions. CMV reactivation can be elicited by high intensity immunosuppression and disease can lead to allograft dysfunction and rejection. Patients at risk for CMV infection should be started on antiviral prophylaxis. With symptoms of disease, a prompt diagnosis is necessary in order to start antiviral therapy with IV ganciclovir or oral valganciclovir. A delay in treatment can result in high morbidity and mortality and therefore clinicians need to have a high index of suspicion.

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