Adenocarcinoma Complicating Ulcerative Colitis Presenting as Multiple Pseudopolyp-like Lesions

Abstract

A man with 9 years of ulcerative colitis presented with fever, weight loss, and a 6-cm retroperitoneal mass ocated adjacent to the transverse colon that was detected by a omputed tomography scan. Colonoscopies at year 4 and 7 of is disease revealed moderately active chronic pancolitis withut dysplasia. He was maintained on mesalamine and intermitent corticosteroids. During the previous 2 months, he experinced 10 bloody bowel movements per day, abdominal ramping, and 30-pound weight loss. On admission, physical examination revealed a thin man in mild istress with a firm mass noted in the periumbilical area. Abnormal aboratory test results included a white blood cell count of 35,000 ells/mm3, hematocrit of 28%, and a platelet count of 1,151,000 ells/mm3. A computed tomography–guided biopsy of the pericolic ass revealed poorly differentiated adenocarcinoma. Colonoscopy as attempted but was aborted at the level of the descending colon ecause of abdominal pain. However, the endoscopist noted multiple olypoid lesions, which were thought to represent inflammatory seudopolyps, throughout the left colon (Figure A). The patient underwent a total proctocolectomy and end leostomy. Grossly, a 10.5-cm firm tan/white mass was present n the transverse colon (Figure B, thick arrows). The remainder of he colonic mucosa was diffusely studded with numerous preominantly sessile nodules, which ranged in size from 0.1–2 cm Figure B, thin arrows). Pathology confirmed the presence of a oorly differentiated carcinoma with mixed glandular and squaous differentiation arising in a background of diffuse chronic olitis with high-grade dysplasia. In addition, 33 lymph nodes were ositive for metastatic carcinoma (American Joint Committee on ancer stage pT4a N2b). In addition to the main tumor mass, here were numerous mucosal nodules located both proximal and istal to the main tumor (Figure C, inset and arrows). The mucosal odules were composed of metastases cytologically identical to the rimary tumor without evidence of in situ neoplasia or mural nvolvement. On the basis of this pattern of involvement, the etastases were considered to be derived from luminal passage of umor cells to inflamed portions of colon. Sporadic colon cancer often metastasizes to peritoneum, local ymph nodes, or distant organs via the blood. However, little has een published regarding mechanisms of metastasis in inflammaory bowel disease–associated colon cancer, although the process is elieved to be similar to sporadic colon cancer. Exfoliated cancer ells might also spread as a result of surgery,1 fistula,2 or inflammation caused by obstruction.3 We speculate that this is a case of luminal metastasis in ulcerative colitis–associated colon cancer that was not previously reported and might represent an additional mode of metastasis that should be considered.