___________________________________________________________________________ Colorectal Cancer
Screening/Surveillance Recommendations for Hereditary Colorectal Cancer
area before neoplastic development, and risk of neoplasia is not increased in mucosa that has never been inflamed. Thus, histologic instead of macroscopic evidence of tissue changes from inflammatory bowel syndrome serves as a more accurate determinant for assessing colorectal cancer risk. In the context of surveillance, extent of disease should be defined histologi- cally [119]. Practice recommendations for the diagnosis and treatment of colorectal cancer in inflammatory bowel syndrome patients were developed and published by the American Gastroenterol- ogy Association [119]. The guideline format presents a series of clinically relevant questions raised by an expert panel, followed by the response based on analysis of the published research. Natural History of Dysplasia Colorectal cancer in inflammatory bowel syndrome develops from dysplasia in most cases, and although imperfect, dyspla- sia is considered the best marker of colorectal cancer risk in inflammatory bowel syndrome. Predicting the natural history of dysplasia is more difficult, because dysplasia is present in 75% to 90% of patients with inflammatory bowel syndrome and colorectal cancer, but colorectal cancer can develop in the absence of previous history of dysplasia. Not all patients with low-grade dysplasia progress through a phase of detectable high-grade dysplasia before developing cancer. Importantly, interpretation of dysplasia in mucosal biopsy specimens is highly subject to observer subjectivity. Therefore, pathologists with particular expertise in gastrointestinal disorders should review all cases diagnosed as indefinite, low-grade dysplasia, or high-grade dysplasia. Colectomy Strong evidence indicates that patients with inflammatory bowel syndrome and a non-adenoma-like dysplasia-associated lesion or mass should receive a colectomy. Patients with inflammatory bowel syndrome and an adenoma-like dysplasia- associated lesion or mass, without evidence of flat dysplasia elsewhere in the colon, can be managed safely by polypectomy and continued surveillance. There is also strong evidence that colectomy for flat high-grade dysplasia treats undiagnosed synchronous cancer and prevents metachronous cancer. However, current evidence is insufficient to assess the balance of benefits and harms. Surveillance Colonoscopy Surveillance colonoscopy is at least moderately effective in reducing colorectal cancer risk in patients with inflammatory bowel syndrome. It is recommended for patients with inflam- matory bowel disease who are at an increased risk of colorectal cancer. Patients most likely to benefit are those with extensive ulcerative colitis or Crohn disease.
Patients diagnosed with a hereditary colorectal cancer syn- drome or with a highly suggestive family or personal history require a more intensive and frequent screening and surveil- lance protocol than patients with average risk because of their high risk for colorectal and extracolonic malignancies. Table 3 provides a summary of recommendations for patients with specific hereditary colorectal cancer syndromes [112]. For each hereditary colorectal cancer syndrome, the left column lists malignancies associated with the syndrome, and the cor- responding right column describes screening or surveillance approach specific to the at-risk malignancy. Inflammatory Bowel Disease as Colorectal Cancer Risk Factor Patients with inflammatory bowel disease, which includes ulcerative colitis and Crohn disease, have an elevated risk of developing colorectal cancer. The extent that colorectal cancer risk is elevated depends on the extent and duration of disease, but earlier age at onset is not associated with greater risk. Older estimates of colorectal cancer risk in patients with ulcerative colitis indicated a 2% greater risk after 10 years, 7.7% to 8% after 20 years, and 15.8% to 18% after 30 years of disease [119]. More recent estimates are somewhat lower, the result of more widespread prescribing of chemoprotective aminosalicylates, earlier and more liberal use of colectomy for medically refractory disease, and higher rates of surveillance colonoscopy. Studies involving patients with either ulcerative colitis or Crohn disease have shown comparable risk in both diseases [119]. The extent of inflammatory bowel syndrome is defined as the point in time when histologically identified disease is most extensive. Most colorectal cancers develop in patients with pancolitis, and disease extent is a major risk factor for colorectal cancer in patients with inflammatory bowel syndrome [119]. Patients with left-sided disease (up to the splenic flexure) have an intermediate risk level, while proctitis, ulcerative proctosig- moiditis, and backwash ileitis have little to no influence on risk level. A family history of sporadic colorectal cancer in a first- degree relative doubles the risk of colorectal cancer, and risk increases nine-fold if the first-degree relative was younger than 50 years of age when first diagnosed with colorectal cancer. The extent of macroscopic and histologic inflammation is associated with increased risk of colorectal cancer, which can develop in areas of endoscopically normal but histologically active colitis. Colorectal cancer can occur in areas where colitis has remitted or where histologic findings show inactive colitis such as crypt distortion in the absence of active inflammation. Lack of endoscopic inflammation at the time of neoplastic detection does not mean absence of inflammation in the
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