Dysplasia in ulcerative colitis--clinical consequences?

The overall absolute risk of colorectal cancer (CRC) in longstanding extensive or total ulcerative colitis (UC) is estimated to be 10%-15%. The size of this risk is 6- to 10-times that expected in the background population. By performing complete colonoscopies with multiple biopsies from the entire colon and rectum at regular intervals, surveillance programmes for high-risk UC patients aim at detecting mucosal dysplasia in order to select CRC-prone individuals for prophylactic colectomy.

In many of the hitherto reported surveillance programmes, the UC patients surveyed have a much lesser risk of dying from CRC than do non-surveyed patients, although randomized studies are lacking. The inter- and intra-observer variability of dysplasia among pathologists is a major pitfall in the surveillance of these patients, as well as the influence of active inflammation, making dysplasia assessment difficult. The practical issues discussed here are, to a large extent, based on the recommendations from the Swedish Gastroenterological Association.

Screening colonoscopy should be performed approximately 8-10 years after onset of disease. After negative results for screening or surveillance colonoscopy, the intervals between colonoscopies should not exceed 2 years. Biannual investigations of between 8 and 20 years' duration have been adopted in the Swedish studies, with annual colonoscopies from that point. Findings of CRC, a dysplasia-associated lesion or mass (DALM) with high-grade dysplasia (HGD) or low-grade dysplasia (LGD), or HGD in flat mucosa, are considered as indications for proctocolectomy, as well as repeated, confirmed findings of multifocal LGD. The management of unifocal LGD in flat mucosa is controversial (e.g. proctocolectomy or increased surveillance). Polyps may be handled with snare polypectomy.

The safest way of handling UC patients at high risk of developing CRC is by performing regular colonoscopic surveillance. Dysplasia is a useful prognostic marker for subsequent cancer development but has its limitations. A combination of enhanced colonoscopic surveillance using markers that are more sensitive than dysplasia might be the optimal way to manage the increased CRC risk in these patients.