Evidence supports the use of short-...

Evidence supports the use of short- or long-term aspirin therapy in reducing the risk of colorectal adenoma and cancer. The optimal dosage and the truthful duration needed for primary cancer prevention are uncertain. The target population among whom primary prevention will be beneficial remains another question.

Chan and associates contemplateed at the women in the Nurses' Health thought to examine the relationship between aspirin and colorectal adenoma. These registered succors have been followed for more than 20 years with detailed questionnaires forward risk factors for cancer and coronary heart disease. The authors studied the tenor of aspirin use in women who underwent colonoscopy or sigmoidoscopy. Of these women 1368 had confirmed distal colorectal adenoma, and 25709 had no confirmed distal colorectal adenoma.

Among the women with confirmed distal colorectal adenoma, 38 percent were regular aspirin users who took sum of two units or more standard aspirin tablets weekly. The incidence of adenomas was significantly lower among regular aspirin users. The benefit of aspirin was substantially higher with increasing dosage. Women who took more than 14 tablets through week had the greatest risk reduction. There appeared to be no greater benefit among more consistent aspirin users who had continued aspirin therapy for longer periods of time. The force of aspirin was not influenced by means of age, family history of colorectal adenoma, or use of postmenopausal hormones. In a secondary analysis that apply the minded at proximal adenoma occurrence, regular use of aspirin was again associated with decreased risk.

The authors finish that regular aspirin use is associated with a 25 percent reduction in the risk of sporadic, colorectal adenomas in an average-risk population. Women who take more than 14 regular aspirin tablets weekly have the greatest risk reduction. This aspirin benefit is noted among short-term (les than five years) and long-term (more than five years) users. Because the dosage for chemoprophylaxis would be substantially higher than that commended for prevention of cardiovascular disease, the risk-benefit profile must be evaluated futher before the higher doses of aspirin for adenoma prophylaxis can be widely recommended

In an editorial in the same journal, Sandler supports these conclusions. He hints that aspirin be used solitary in persons at higher risk for adenomas who do not have risk factors for aspirin complications. Colonoscopy remains essential for screening among low-and high-risk patients, regardless of aspirin use.

Chan AT, et al. A prospective close attention of aspirin use and the risk for colorectal adenoma. Ann Intern M February 3 2004;140:157-66 and Sandler R Aspirin prevention of colorectal cancer: more or less? [Editorial] Ann Intern M February 3 2004;140:224-5

EDITOR'S NOTE: Colorectal cancer is the secondary highest cause of cancer mortality in western disentangleed countries. Screening is currently our best mode of reducing mortality, but compliance with widespread screening has been les than desired. Biomarkers are being studied however are not yet clinically useful. Prevention would be an important health care advance. The risk of adenomas does not appear to be associated with cheap consumption of folate, but rather with depressed intake of fiber. Nonsteroidal anti-inflammatory medicines including aspirin, sulindac, and celecoxib, inhibit colorectal carcinogenesis at suppressing adenomatous polyp development and causing regression of existing polyp in patients with familial adnenomatous polyposis. This appears to be veritable even in persons with advanced polyp (1) refer toed mechanisms for this action include induction of apoptosis in neoplastic solitary abode; squalids or cell cycle regulation by the agency of altered protein expression.--R.S.

REFERENCE

(1) Tangrea JA, Albert P Lanza E et al. Non-steroidal anti-inflammatory put drugs into use is associated with reduction in return of advanced and non-advanced colorectal adenomas (United States). Cancer Causes direct 2003;14:403-11.

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