Ulcerative colitis (UC) patients are at increased risk of colorectal dysplasia and cancer. Few studies have examined the clinical outcomes of dysplastic polyps resembling sporadic adenomas that are removed with endoscopic polypectomy.
A centralized diagnostic index identified patients evaluated between 1994 and 2004 with UC and polypoid dysplasia who were followed from the time of polypectomy until the most recent colonoscopy. They were stratified into two groups by polyp occurrence, either within (adenoma-like dysplasia) or outside (sporadic adenoma) the most proximal endoscopic or histologic extent of colitis. The endpoints of interest were the development of subsequent colorectal neoplasia, flat dysplasia, or cancer. The cumulative probabilities of these endpoints were estimated using the Kaplan–Meier method, and the association with clinical factors assessed using Cox proportional hazards regression.
Ninety-five patients were found to have polypoid dysplasia; of these, 77 underwent polypectomy. The cumulative probability of subsequent colorectal neoplasia in polypectomy patients was 18% at 1 year and 69% at 5 years. After polypectomy, cumulative incidence of cancer or flat dysplasia was 2% at 1 year and 13% at 5 years. The proportional hazards models indicated that these outcomes were not significantly associated with polyp type, primary sclerosing cholangitis, family history of colorectal cancer, 5-aminosalicylate use, extent of colitis, or duration of disease.
While polypectomy may be safe for the management of adenomas occurring in most UC patients, the 5-year cumulative incidence of a combined endpoint (cancer or flat dysplasia) was 13%. Such patients should be followed closely. (Inflamm Bowel Dis 2011;)
1Division of Gastroenterology & Hepatology, Rochester, Minnesota
2Division of Biostatistics, Mayo Clinic, Rochester, Minnesota
*Division of Gastroenterology & Hepatology, 200 First St. S.W., Rochester, MN 55905
Received 10 January 2011; Accepted 20 January 2011
Published online 17 March 2011 in Wiley Online Library (wileyonlinelibrary.com).
§Presented in part at the 108th Annual Meeting of the American Gastroenterological Association, May 19–24, 2007, Washington, D.C. (Gastroenterology 2007;132(4 Suppl 2):A-37).
†Supported in part by Procter & Gamble Pharmaceuticals and the Mayo Foundation for Medical Education & Research. The study sponsor played no role in study design, data collection, data analysis, or data interpretation.
Additional Supporting Information may be found in the online version of this article.