Dysplasia

Abstract

Ulcerative colitis and Crohn’s disease are associated with an increased risk for developing colorectal cancer (CRC). The size of the risk is not exactly known. A cumulative incidence of below 1 % in the first 8–10 years, rising in annual increments of 0.5–1.0 % thereafter to reach 5–10 % after 20 years has been reported. In a population-based study from Canada, Crohn’s disease and ulcerative colitis had similar increased risk ratios compared to population controls of 2.6. Independent risk factors for CRC in ulcerative colitis are the duration of the disease and the anatomic extent. Additional risk factors include primary sclerosing cholangitis (PSC), a positive family history or CRC, and the degree of endoscopic and histologic activity. As early as 1949, Warren and Sommers postulated that, like for sporadic CRC, a structural precursor to carcinoma existed in ulcerative colitis [1]. In 1967, microscopic “precancerous” changes were described in the mucosa of colectomy specimens of patients operated for carcinoma in ulcerative colitis [2]. Similar changes were reported in Crohn’s disease. The identification of such early lesions, called dysplasia, opens the possibility for early detection and secondary prevention of colorectal cancer with surveillance programs for patients with IBD. This implies however a precise definition of “dysplasia” and identification of reliable criteria for the detection of dysplasia during colonoscopy and microscopy.