Are adenomatous polyps rare in ulcerative colitis?

Field: Medicine (Health Sciences)

Sirs, I read with interest Kitiyakara et al.'s paper on the prevalence of adenomatous polyps in ulcerative colitis.1 They suggest that adenomatous polyps are less common in ulcerative colitis than in people without inflammatory bowel disease. They conclude that ‘the disease process [of ulcerative colitis] protects against the formation of dysplastic adenomatous polyp’. I would like to offer several other potential explanations for their findings. First, as the authors correctly point out, the reduced incidence of adenomatous polyps may be due to a protective effect of 5-ASA drugs. Secondly, patients with ulcerative colitis might have a genetic predisposition to develop fewer adenomas, as opposed to it being an effect of the disease process per se. Thirdly, the actual adenoma incidence might not be reduced, but harder to detect (and thus overlooked) in patients with ulcerative colitis, because the background mucosa in ulcerative colitis is inflamed and irregular in contour. In particular, the presence of multiple postinflammatory polyps (described in 25% of their ulcerative colitis cohort) can make detection of adenomatous polyps difficult. Fourthly, and in my view most likely, the apparent difference in adenomatous polyp detection might simply be due to the different categorization of dysplastic lesions in ulcerative colitis. The authors succinctly summarize the difficulties in mass lesion dysplasia classification in ulcerative colitis, and their own data (as with several other studies) fails to detect reliable immunohistochemical differences between dysplasia-associated lesion or mass (DALM) and adenomatous polyps. It may also be that flat dysplasia in ulcerative colitis (which, although difficult to detect, is usually endoscopically visible)2 is part of the same neoplastic spectrum as raised dysplasia, in a similar way to that of flat adenomas and polypoid adenomas. Thus it may simply be that the morphology of dysplastic lesions (and hence the terminology used) is altered, but not their incidence. From the data presented in the paper, 13 of 150 patients with ulcerative colitis developed dysplastic lesions (excluding one patient with a cancer), compared with 24 of 205 control patients. Assessed in this way, the reduced incidence in dysplasia is not statistically significant (odds ratio 0.72, 95% confidence intervals 0.35–1.46; P = 0.38, Fisher's exact test). As there are no reliable endoscopic, histological or immunohistochemical discriminators between colitic dysplasia and sporadic adenomatous dysplasia, it is difficult for clinicians to know how best to manage colitic patients in whom dysplasia is detected. The diagnosis of a DALM is often retrospective, and its prognostic relevance is thus subject to significant selection bias. Moreover, all studies in the literature have been retrospective, and the definition of a DALM varies from paper to paper. Our recent study from St Mark's Hospital (again retrospective),2 demonstrated that the key question may be whether a specific lesion is endoscopically resectable or not. Seventy-five per cent of nonresectable dysplastic lesions (regardless of the terminology used to describe the lesion) contained cancer at colectomy, whereas endoscopically resected lesions carried a cancer prognosis no different to that of the colitic surveillance cohort as a whole. Endoscopic resection of carefully selected dysplastic lesions has been advocated by several other recent studies.3–5 There is undoubtedly a need for a prospective study with clearly defined descriptors. Nevertheless, the authors should be commended for contributing useful additional data to this difficult subject.