Introduction

Patients with inflammatory bowel disease (IBD) are at an increased risk for colorectal cancer (CRC) [1-4], but the quantisation of the risk of CRC in this specific population varies widely in different studies. However, CRC complicating ulcerative colitis (UC) and Crohn's disease (CD) only accounts for 1-2% of all cases of CRC in the general population. Most cases of CRC are either sporadic (65-85%) or familial (10-30%; Fig. 1) [3-4].

CRC is considered a serious complication of the disease and accounts for approximately 15% of all deaths in IBD patients [5]. The mortality in patients diagnosed with CRC who are also diagnosed with IBD is higher than for sporadic CRC [6]. However, much more is known about the risk in UC. The incidence of colorectal cancer in patients with ulcerative colitis is higher than in the general population. In a meta-analysis, the overall prevalence of CRC in any UC patient, based on 116 studies, was estimated to be 3.7%. The incidence rate corresponded to cumulative probabilities of 2% by 10 years, 8% by 20 years and 18% by 30 years [7].

The major risk factors for the development of CRC include young age at onset of IBD [1], extensive disease [8] and long disease duration [5]. It is biologically plausible that the excess cancer risk is secondary to chronic inflammation and it is recognised that duration of colitis is an important risk factor for CRC. Rutter et al. [9] showed for the first time that increasing severity of colonic inflammation is associated with an increase in the rate of colorectal neopla-sia in UC. Patients with disease extending to the hepatic flexure or more proximally have the greatest risk of CRC [10-12]. Most studies have found that the risk of CRC increases after 15 to 20 years; approximately one decade later than in pancolitis in patients with colitis confined to the left colon [8]. Patients with ulcerative proctitis and proctosigmoiditis are probably not at increased risk for CRC [13]. An increased risk of CRC has been observed in patients with UC complicated by primary sclerosing cholangi-tis. In these cases, cancer was more likely to be in the right colon, suggesting a possible role of bile acids in oncogenesis [14].

The evidence for other potential risk factors is scarce. Smoke [15], folate depletion [16-17] and a positive family history of colon cancer [18] may affect the occurrence of CRC. A hypothesis has been put forward according to which UC, CD and CRC occur in predisposed patients because of a mixture of genetic and environmental factors. One study has shown that relatives of patients with both IBD and CRC have an 80% increased risk of CRC [19]. In our study, there is no statistically significant difference between IBD and control cases of family members as far as prevalence of malignant colorectal, digestive extra-colonic or extra-digestive tract tumours [20]. Another recent study has investigated the prevalence of all malignancies in first-degree relatives of CD patients. The result showed a higher prevalence of breast cancer in female relatives, mainly in mothers, of CD patients compared with controls. The presence of breast cancer was not associated with any specific phenotype of the CD [21].

As in UC, Crohn's disease of the colon carries an increased risk of CRC. Ekbom et al. [1] found a relative risk of 5.6% for CRC among patients with CD, whereas in another Swedish patient cohort study, Persson et al. [22] did not find that the population relative risk increased. Similarly, Fireman et al. [23] from Israel and Jess et al. [24] in the Danish cohort, did not find an increased risk of CRC among their

Fig. 1. Distribution of CRC

patients with CD. Although analyzing subgroups within the CD study meant that there were few cancers identified, when patients with CD of >10-year duration were analyzed, the relative risk for CRC was 4.8%. For those patients with at least 10 years of disease and no surgery within the first 10 years, the relative risk was 8.3%. Thus, even among this reportedly negative study, when variables such as disease duration and possibly disease extent (based on no surgery) are analysed, the relative risk increases [5]. In the study of Gillen et al. [25], however, it appears that the malignant potential in CD and UC is of the same order of magnitude. Cancer developed in inflamed areas in both diseases, and was thus located in the right colon in 49% of patients with CD compared with 36% with UC, reflecting the difference in inflammatory sites in the two cases. Adenocarcino-mas develop only in affected segments of the small intestine, and are difficult to diagnose at an early stage because the radiological appearance is similar to that of stricturing CD.

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