Abstract

The association between inflammatory bowel disease (IBD) and the development of colorectal cancer (CRC) was first described over eight decades ago (1). However, it was not until the late 1970s that the true clinical significance of this association was appreciated. It is now accepted that both ulcerative colitis (UC) and Crohn’s disease (CD) are associated with an increased risk of CRC (2). It is believed that CRC arises from dysplastic precursor lesions. Unlike the typical dysplasia-carcinoma sequence, the dysplastic lesions are believed to arise in flat mucosa and do not assume a mass-like or polypoid lesion. A recent meta-analysis (3) of 116 published articles estimated the risk of CRC in UC to be 2% at 10 years, 8% at 20 years and 13% at 30 years. Aside from the duration of the disease, the extent (4), family history (5,6) and early onset of CRC (7), along with concomitant primary sclerosing cholangitis (PSC) (8,9), are risk factors for the development of CRC. Similar rates of CRC have recently been demonstrated in patients with CD (10). This epidemiological relationship has led to the practice of surveillance colonoscopy in groups at risk. The initial intent of entering patients into a dysplasia surveillance program was to stratify patients into high-risk groups in need of proctocolectomy and low-risk groups who could continue in the surveillance program. Dr Remo Panaccione

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