1533 Cytomegalovirus as the Forme Fruste of Colorectal Cancer in a Young Female

Abstract

INTRODUCTION: Cytomegalovirus (CMV) infection is often seen in the GI tract among patients who are immunocompromised and most commonly affects the large bowel. Studies have shown CMV infection presenting as a colorectal cancer (CRC) like mass. We present a case of CMV presenting as the forme fruste of CRC. CASE DESCRIPTION/METHODS: A 31 year old Hispanic woman presented with a one week history of worsening abdominal pain, generalized weakness, hematochezia, and a 30 lb weight loss. She was a nonsmoker who had presented similarly 6 months prior to another institution and was diagnosed with CMV colitis by flexible sigmoidoscopy and biopsy of a rectal ulcer. Pathology revealed focal atypical epithelial proliferation, indefinite for dysplasia, and CMV immunostain was positive. The patient was treated with valganciclovir with improvement in symptoms, but later worsened. She denied change in bowel habits, history of anogenital warts, or HPV vaccination, but admits to a remote history of Chlamydia which was treated. History was also positive for chronic inactive HBV infection diagnosed 6 years prior to presentation. Significant labs were Hb 4.6 g/dL, MCV 65.9, Plt 466 K/uL, AST 43 U/L, ALP 111 U/L, HIV nonreactive, AFP 3.0 ng/ml, HBsAg reactive, HBV viral load of 613 IU/mL, HBcAb total reactive, HCV Ab nonreactive and CEA 44.6. CT abd/pelvis showed an inflammatory, ulcerated, rectal mass with wall thickening compatible with neoplasm (Figure 1). Large hypodensities were seen in both hepatic lobes consistent with metastases (Figure 2). Sigmoidoscopy showed an ulcerated partially obstructing mass in the rectum which was circumferential and friable and located at the anal verge and was approximately 10 cm in length. Biopsy of the mass showed scant adenocarcinoma admixed with ulcer and granulation tissue. Liver biopsy confirmed metastatic adenocarcinoma, colon primary. DISCUSSION: Potential previous exposure to oncogenic viruses such as HBV and HPV may have predisposed our patient to develop CRC at age 31. She had no other risk factors such as HIV infection, radiation exposure, or previous chemotherapy. Her underlying malignancy may have rendered her in an immunocompromised state that would have allowed CMV reactivation. Another possibility is exposure to multiple viruses caused immunocompromise allowing both CMV reactivation and CRC formation. CMV pseudo tumors are known to mimic CRC. Alarm symptoms such as weight loss and hematochezia in this patient warranted close follow up to complete resolution or alternative diagnosis.