Colonoscopic Surveillance in Inflammatory Bowel Disease

Thomas A Ullman

Disclosures

Curr Opin Gastroenterol. 2005;21(5):585-588. 

In This Article

Background

The first description of CRC complicating ulcerative colitis predates the first descriptions of what would ultimately be called Crohn's disease. Interestingly, both of these firsts share Burrell B. Crohn as the first author.[1] After fits and starts in characterizing better the connection between colitis and cancer, modern epidemiologic techniques allowed investigators to assert unequivocally that longstanding, extensive ulcerative colitis leads to an increased risk for the development of CRC. Although not appreciated until analyses excluded patients with colectomies or with disease limited to their small bowel, Crohn's colitis, too, was ultimately found to carry an increased risk for CRC.[2] In addition to duration of disease and extent of disease, the presence of concomitant primary sclerosing cholangitis and a family history of colorectal cancer have been demonstrated to increase this risk further.[3] On the basis of a meta-analysis of 116 published reports, Eaden et al.[4] have estimated the cumulative risk of CRC to be 8% at 20 years and 18% at 30 years for patients with ulcerative colitis. Because this disease preferentially affects men and women well before middle-age, these probabilities are too great to be ignored. In the pre-endoscopic era, strong consideration was given to prophylactic colectomy for patients with longstanding ulcerative colitis.

In 1967, Morson and Pang[5] noted that dysplasia (then called 'pre-cancer') from nontargeted biopsies of the rectum was associated with cancer elsewhere in the colon of patients with ulcerative colitis. This discovery led to the currently held postulate of a field effect in ulcerative colitis, whereby the entirety of the mucosa is believed to be at increased risk and a dysplastic focus in one area meant heightened risk for CRC throughout the colon. Subsequent confirmation of the association between dysplasia and CRC and the advent of per ano fiberoptic endoscopy led to the practice of surveillance, wherein high-risk patients with ulcerative colitis underwent serial colonoscopies with multiple nontargeted biopsies. Patients with dysplasia were referred for colectomy, and dysplasia-free patients continued with colonoscopic examinations. It was theorized that a program of surveillance could simultaneously minimize CRC mortality and unnecessary prophylactic colectomies. This system of surveillance has evolved slightly over the last 30 years, although no clear CRC mortality benefit has been demonstrated with its use. Key limitations to surveillance practice include the following:

  1. Low rates of observer agreement for the histopathologic interpretation of biopsy specimens, even among experts[6,7]

  2. Sampling error: endoscopists fail to take a sufficient number of biopsies to exclude the presence of dysplasia or cancer[8]

  3. Patient drop-out and incomplete follow-up[9]

  4. Lack of consensus on the management of intermediate grades of dysplasia because of incompletely understood natural history.

From the endoscopist-clinician's perspective, research in three of these areas has led to paradigm shifts either ready for use in practice or nearing their application. They are the following:

  1. The need to give strong consideration for surgery for patients found to have flat low-grade dysplasia at surveillance

  2. The ability to treat small, sessile adenoma-like lesions as one would sporadic adenomas provided that the surrounding mucosa is dysplasia-free

  3. The institution of chromoendoscopy and other techniques to identify dysplasia in situ better and to minimize unnecessary nontargeted biopsies.

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