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Adenomas can be found in 30 40% of patients when another colonoscopy is performed within 3 5 years after the initial examination Periodic colonoscopic surveillance is therefore recommended to detect these metachronous adenomas, which either may be new or may have been overlooked during the initial examination Most of these adenomas are small, without high-risk features and of little immediate clinical significance The probability of detecting advanced neoplasms at surveillance colonoscopy depends on the number, size, and histologic features of the polyps removed on initial (index) colonoscopy Patients with 1 2 small (< 1 cm) tubular adenomas (without villous features or high-grade dysplasia) should have their next colonoscopy in 5 10 years Patients with 3 10 adenomas, an adenoma > 1 cm, or an adenoma with villous features or high-grade dysplasia should have their next colonoscopy at 3 years Patients with more than 10 adenomas should have a repeat colonoscopy at 1 2 years and may be considered for evaluation for a familial polyposis syndrome (see below)
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Butterly LF et al Prevalence of clinically important histology on small adenomas Clin Gastroenterol Hepatol 2006 Mar;4(3): 343 8 [PMID: 16527698] Lauwers GY et al The serrated polyp comes of age Gastroenterology 2006 Nov;131(5):1631 4 [PMID: 17067594] Levine JS et al Adenomatous polyps of the colon N Engl J Med 2006 Dec 14;355(24):2551 7 [PMID: 17167138] Rockey DC et al Analysis of air contrast barium enema, computed tomographic colonography, and colonoscopy: prospective comparison Lancet 2005 Jan 22 28;365(9456):305 11 [PMID: 15664225] Schoen RE et al Yield of advanced adenoma and cancer based on polyp size detected at screening flexible sigmoidoscopy Gastroenterology 2006 Dec;131(6):1683 9 [PMID: 17188959] Winawer SJ et al Guidelines for colonoscopy surveillance after polypectomy: a consensus update by the US Multi-Society Task Force on Colorectal Cancer and the American Cancer Society Gastroenterology 2006 May;130(6):1872 85 [PMID: 16697750]
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There is an increased risk (up to 50%) of adenocarcinoma due to synchronous adenomatous polyps or mixed hamartomatous-adenomatous polyps Genetic defects have been identified to loci on 18q and 10q (MADH4 and BMPR1A) Genetic testing is available PTEN multiple hamartoma syndrome (Cowden disease) is characterized by hamartomatous polyps and lipomas throughout the gastrointestinal tract, trichilemmomas, and cerebellar lesions An increased rate of malignancy is demonstrated in the thyroid, breast, and urogenital tract
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Giardiello FM et al Peutz-Jeghers syndrome and management recommendations Clin Gastroenterol Hepatol 2006 Apr;4 (4):408 15 [PMID: 16616343] Schreibman IR et al The hamartomatous polyposis syndromes: a clinical and molecular review Am J Gastroenterol 2005 Feb;100(2):476 90 [PMID: 15667510]
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ifestations vary among families, depending in part on the type or site of mutation in the APC gene Desmoid tumors are locally invasive fibromas, most commonly intra-abdominal, that may cause bowel obstruction, ischemia, or hemorrhage They occur in 15% of patients and are the second leading cause of death in FAP Malignancies of the central nervous system (Turcot s syndrome) and tumors of the thyroid and liver (hepatoblastomas) may also develop in patients with FAP Genetic counseling and testing should be offered to patients with a diagnosis of FAP established by endoscopy and to first-degree family members of patients with the disease; testing should be done also to confirm a diagnosis of attenuated disease in patients with 20 or more adenomas Genetic testing is best performed by sequencing the APC gene to identify disease-associated mutations, which are identified in approximately 90% of cases of typical FAP Mutational assessment of MYH should be considered in patients with negative test results and in patients with suspected attenuated FAP First-degree relatives of patients with FAP should undergo genetic screening after age 10 years If the assay cannot be done or is not informative, family members at risk should undergo yearly sigmoidoscopy beginning at 12 years of age Once the diagnosis has been established, complete proctocolectomy with ileoanal anastomosis or colectomy with ileorectal anastomosis is recommended, usually before age 20 years Ileorectal anastomosis affords superior bowel function but has a 10% risk of development of rectal cancer, and for that reason frequent sigmoidoscopy with fulguration of polyps is required Sulindac and COX-2 selective agents (celecoxib) have been shown to decrease the number and size of polyps in the rectal stump but not the duodenum Upper endoscopic evaluation of the stomach, duodenum, and periampullary area should be performed every 1 3 years to look for adenomas or carcinoma Large (> 2 cm) periampullary adenomas require surgical resection
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Burt R et al Genetic testing for inherited colon cancer Gastroenterology 2005 May;128(6):1696 716 [PMID: 15887160] Galiatsatos P et al Familial adenomatous polyposis Am J Gastroenterol 2006 Feb;101(2):385 98 [PMID: 16454848] Maple JT et al Genetics of colonic polyposis Clin Gastroenterol Hepatol 2006 Jul;4(7):831 5 [PMID: 16797242]
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3 Hereditary Nonpolyposis Colorectal Cancer (HNPCC)
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HNPCC (also known as Lynch syndrome) is an autosomal dominant condition in which there is a markedly increased risk of developing colorectal cancer as well as a host of other cancers, including endometrial, ovarian, renal or vesical, hepatobiliary, gastric, and small intestinal cancers It is estimated to account for up to 3% of all colorectal cancers Affected individuals have a 60 80% lifetime risk of developing colorectal carcinoma and an over 30% lifetime risk of endometrial cancer Unlike individuals with familial adenomatous polyposis, patients with HNPCC develop only a few adenomas, which may be flat and more often contain villous features or high-grade dysplasia In contrast to the traditional polyp cancer progression (which may take over 10 years), these polyps are believed to undergo rapid transformation from normal tissue adenoma cancer It has been believed that HNPCC tends to develop at an earlier age than sporadic colorectal cancers (mean age: 44 years); however, in a recent study of HNPCC families, the median age at diagnosis of colorectal cancer (excluding probands) was 61 years very similar to sporadic cancer Compared with patients with sporadic tumors of similar pathologic stage, those with HNPCC tumors have improved survival Synchronous or metachronous cancers occur within 10 years in up to 45% of patients HNPCC is caused by a defect in one of several genes that are important in the detection and repair of DNA base-pair mismatches: MLH1, MSH2, MSH6, and PMS2 Germline mutations in MLH1 and MSH2 account for more than 90% of the known mutations in families with HNPCC Mutations in any of these mismatch repair genes result in a characteristic phenotypic DNA abnormality known as microsatellite instability In over 95% of cancers in patients with HNPCC, microsatellite instability is readily demonstrated by expansion or contraction of DNA microsatellites (short, repeated DNA sequences) Microsatellite instability also occurs in 15% of sporadic colorectal cancers, usually due to aberrant methylation of the MLH1 promoter resulting in decreased gene expression A thorough family cancer history is essential to identify families that may be affected with HNPCC so that appropriate genetic and colonoscopic screening can be offered Owing to
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