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Dysplasia in ulcerative colitis: histopathological diagnostic difficulties and surgical treatment

In this issue, Lindberg and colleagues have addressed the important question of the value of limited surgery in selected patients with ulcerative colitis complicated by dysplasia or invasive cancer. In doing so, they have reopened a long-standing debate. Crohn and Rosenberg [1], over eight decades ago, were among the first to establish the evidence for the association of dysplasia and colorectal carcinoma in patients with inflammatory bowel disease. The publication was since then followed by discussion and controversy particularly in the last 25 years. Dysplasia is strictly a histopathological diagnosis and in the large bowel, it is best defined as ‘unequivocal neoplastic change of the epithelium limited by the basement membrane’ [2]. The risk of developing cancer in ulcerative colitis is 6–10 times that of the general population. Risk factors favouring the development of dysplasia directly relate to the duration and extent of colitis, and others include a family history of colorectal cancer and the presence of primary sclerosing cholangitis [3]. There are technical factors in the diagnosis of dysplasia that need to be understood. These include the various classifications used by histopathologists, the significant interand intra-observer variation among histopathologists and the number of biopsies required to make a definitive diagnosis. These considerations lead to the question of what to do when dysplasia is diagnosed. The classic paper of Riddell et al. [2] emphasized the importance of histological classification and suggested clinical follow-up and treatment schedules. This was modified by a Japanese group [4] and later improved by a joint European, American and Japanese histopathological concordat resulting in the so-called Vienna Classification [5] which aimed to reconcile the various different terminologies and definitions prevalent in the literature. This classification is currently not widely used in practice presumably due to its recent introduction, but it would be beneficial for the time being if histopathologists used both the Riddell and Vienna classifications simultaneously in the hope that with the passage of time, this may lead to general agreement on the assessment of clinical risk and diagnostic reproducibility between each classification. Another controversial point in the diagnosis of dysplasia is the optimum number of biopsies required to make the diagnosis. It has been recommended that the diagnosis of dysplasia in ulcerative colitis should be based on the assessment of four random biopsies taken from every 10 cm of large bowel examined. Rubin et al. [6] have, however, advocated that for the detection of dysplasia with 90% confidence interval, an average of 33 biopsies per patient is needed. The workforce required for such a task with the currently available resources, including the shortage of histopathologists, is immense. Fortunately, recent work has shown that using targeted biopsies obtained by endoscopic magnification and chromoendoscopy, the number of biopsies required to make the diagnosis of dysplasia may not only decrease but the detection rate may also improve [7,8]. This will almost certainly become future practice. A further area requiring consideration is that the histological diagnosis of dysplasia is not a straightforward, standardized, rigid and infallible assessment. More than one study has shown a worrying degree of interand intra-observer variation among histopathologists that has led to the strong recommendation that two experienced histopathologists should examine the biopsies [9,10]. This practice is now widely used and the paper of Lindberg et al. in this issue would have benefited from this recommendation. Perhaps, the most controversial question raised by a diagnosis of dysplasia is its clinical implication. Is there an agreed clinical approach? The short answer is no. Action varies from none to minor destructive local procedures to proctocolectomy. It has been argued [11] that the rate of 20% of discovering a carcinoma in a patient with lowgrade dysplasia has resulted in an unnecessarily high rate of negative operations, with their morbidity and mortality. It is therefore not surprising to see two opposing schools of thought. The ‘doves’ include, for example, a study [12] of 60 cases of flat low-grade dysplastic lesions with no subsequent occurrence of carcinoma and the ‘hawks’ [13,14] include those who advocate proctocolectomy for multifocal low-grade dysplasia. The controversy is not only limited to flat lesions but has also extended to the dysplasia-associated mass lesion (DALM) which is further complicated by the difficulty in distinguishing between a sporadic adenoma vs an adenoma-like DALM. This problem may, however, have been settled of late by the work of Torres et al. [15] who studied 89 polypoidal lesions from 59 patients with inflammatory bowel disease (51 ulcerative colitis and eight Crohn’s diseases). The biopsy examinations were divided into