Colorectal Cancer in IBD
نویسندگان
چکیده
Patients with long-standing ulcerative colitis and Crohn’s disease have an increased risk of developing colorectal cancer and patients with small intestinal Crohn’s disease are at increased risk of small bowel adenocarcinoma. Colorectal cancer appearing on the ground of inflammatory bowel disease is the result of a process which is believed to begin from no dysplasia progressing to indefinite dysplasia, low-grade dysplasia, high-grade dysplasia and finally to invasive adenocarcinoma, although colorectal cancer can arise without proceeding through each of these steps. Ulcerative colitis patients with total proctocolectomy and ileal pouch analanastomosis have a rather low risk of dysplasia in the ileal pouch, although the anal transition zone should be monitored periodically, especially if chronic pouchitis is present with associated severe villous atrophy. Concerning the risk factors predisposing to colorectal cancer in the setting of ulcerative colitis or Crohn’s disease, it seems that the risk increases with longer duration and greater anatomic extent of colitis, the degree of inflammation, and the presence of primary sclerosing cholangitis and family history of colorectal cancer. Concerning the mechanisms of carcinogenesis, it is now well established that the molecular alterations responsible for sporadic colorectal cancer, namely chromosomal instability, microsatellite instability and hypermethylation, also play a role in colitis-associated colon carcinogenesis. Chemoprevention strategies include the administration of agents such as aminosalicylates, ursodeoxycholic acid, and possibly folic acid and statins, the exact role of which remains to be further elucitated. Colorectal cancer (CRC) can develop on the grounds of inflammatory bowel disease (IBD), being the most common cancer among such patients. The three most important highrisk conditions for CRC are IBD and the hereditary syndromes of familial adenomatous polyposis and hereditary nonpolyposis colorectal cancer syndrome (1). The aim of this review is to discuss the epidemiology, risk factors and mechanisms of carcinogenesis in patients with IBD under the light of the current literature. The topics discussed are the epidemiological features of CRC in IBD, the established risk factors predisposing to colon carcinogenesis, and the molecular mechanisms involved in tumor development. Finally there is a brief discussion on the promising role of chemical agents that are currently under investigation in the prevention of CRC in patients with IBD. Colorectal Cancer in IBD Incidence of CRC in ulcerative colitis. The exact magnitude of the risk of cancer in ulcerative colitis (UC) is difficult to quantify due to biases and methodological errors. Early estimates of CRC incidence complicating UC often included a great proportion of patients who had more severe disease. Later population-based studies included more patients with left-sided disease or patients who had undergone colectomy and may thereby underestimate the true risk. IBD-related CRC is estimated to be responsible for less than 2% of all CRC appearing annually. In general, the risk of CRC begins to increase 8 or 10 years after the establishment of diagnosis (2-7). Depending on the study and country, the risk of developing CRC in patients with UC fluctuates between 0.9 to 8.8-fold and between 0.8 and 23-fold in patients with 2727 Correspondence to: Professor John K. Triantafillidis, Iera Odos 354, Haidari, Athens, Greece Tel: +3
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