The association between cigarette smoking and colorectal polyp recurrence (United States)
ABSTRACT Although evidence exists linking smoking to precancerous colorectal adenomatous polyps, few studies have examined the association between cigarette smoking and recurrence of colorectal polyps. This association was investigated prospectively with data from the Polyp Prevention Trial.
Cigarette smoking data were collected through baseline interviews. The study was completed by 1872 men and women with presence of adenomas at baseline colonoscopy. Multiple logistic regression analysis was used to examine the association between cigarette smoking and polyp recurrence (adenomatous and hyperplastic) up to four years from baseline.
Adenoma recurrence was not related to cigarette smoking. Current smokers had increased odds of hyperplastic polyps at follow-up compared to never smokers (OR 2.88, 95% CI 2.06-4.01). Current smoking was associated with subsequent distal (OR 3.44, 95% CI 2.38-4.95) and rectal (OR 3.53, 95% CI 2.15-5.78) hyperplastic polyps, but not subsequent proximal hyperplastic polyps. Cigarette smoking was associated with subsequent multiple and small size (4 mm) hyperplastic polyps. Significant linear trends were observed between development of subsequent hyperplastic polyps and all smoking variables.
Although no association with recurrent adenomas was observed, cigarette smoking was significantly associated with hyperplastic polyp development, except for those in the proximal colon. This prospective study confirms that cigarette smoking has a significant effect on the development of hyperplastic colorectal polyps.
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- "Identification of risk factors for colonic adenomas is important in order to risk stratify individuals for colorectal neoplasia and to guide the most appropriate screening recommendations . Many studies have linked age, gender, smoking, family history, and other factors, with risk of adenoma occurrence       . Less well studied are potential modifying interactions among risk factors. "
ABSTRACT: Evidence independently links smoking, family history, and gender with increased risk of adenomatous polyps. Using data from the New Hampshire Colonoscopy Registry (2004-2006), we examined the relation of combined risk factors with adenoma occurrence in 5,395 individuals undergoing screening colonoscopy. Self-reported data on smoking, family history and other factors were linked to pathology reports identifying adenomatous polyps and modeled with multiple logistic regression. In adjusted models a >15 pack-year smoking history increased the likelihood of an adenoma (OR = 1.54, 95% CI 1.28-1.86), although </=15 pack-years did not (OR = 1.07, 95% CI 0.87-1.32). Gender-stratified models showed a significantly increased risk of adenoma at lower smoking exposure even for men (OR = 1.32; 95% CI:1.00-1.76), but not for women (OR = 0.85; 95% CI:0.61-1.14). An ordered logistic regression model of adenoma occurrence showed a smoking history of >/=15 pack-years associated with 61% higher odds of adenoma at successively larger size categories (95% CI 1.34-1.93). For individuals with a family history of colorectal cancer, smoking does not further increase the risk of adenomas. Smoking duration is linked to occurrence and size of adenoma, especially for men.Journal of Cancer Epidemiology 06/2010; 2010:509347. DOI:10.1155/2010/509347
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ABSTRACT: A method is presented to integrate the dynamics of DC power flow into calculations of transient energy functions of AC/DC power systems. This method treats the generator input power as a function of the parameters and the input, output variables of the DC damping power controller. By using this transient energy function, the accuracy of the stability prediction of AC/DC power systems is improved. The new transient energy function is validated using 12-bus and 30-bus test systems by comparing the stability results with those obtained from time simulation. The new transient energy function is used in a number of studies to establish its effectiveness.IEEE Transactions on Power Systems 12/2003; 18(4-18):1470 - 1477. DOI:10.1109/TPWRS.2003.818705 · 3.53 Impact Factor