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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ABSTRACT: Prior studies suggest cigarette smoking is associated with 1.5- to twofold increased risk of colorectal adenomas and possibly a higher risk of serrated polyps. Further clarification of risk differences between adenomas and serrated polyps is needed with regard to co-occurrence and polyp location. We conducted a combined analysis of conventional adenoma and serrated polyp occurrence using individual-level data from 2,915 patients participating in three colonoscopy-based clinical trials. All participants had ≥1 adenomas removed at baseline and were followed for up to 4 years. Smoking habits and other lifestyle factors were collected at baseline using questionnaires. We used generalized linear regression to estimate risk ratios and 95 % confidence intervals. Smokers were at slightly increased risk of adenomas compared to never smokers [current: RR 1.29 (95 % CI 1.11-1.49) and former: RR 1.18 (1.05-1.32)]. Smoking was associated with greater risk of serrated polyps [current: RR 2.01 (1.66-2.44); former: RR 1.42 (1.20-1.68)], particularly in the left colorectum. Associations between current smoking and occurrence of serrated polyps only [RR 2.33 (1.76-3.07)] and both adenomas and serrated polyps [RR 2.27 (1.68-3.06)] were more pronounced than for adenomas only [RR 1.31 (1.08-1.58)]. Results were similar for other smoking variables and did not differ by gender or for advanced adenomas. Cigarette smoking has only a weak association with adenomas, but is associated with a significantly increased risk of serrated polyps, particularly in the left colorectum. Since a minority of left-sided serrated polyps is thought to have malignant potential, the role of smoking in initiation phases of carcinogenesis is uncertain.Cancer Causes and Control 12/2014; 26(3). DOI:10.1007/s10552-014-0513-0 · 2.96 Impact Factor
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ABSTRACT: M. Underner, S. Hadjadj, M. Beauchant, F. Bridoux, F. Debiais, J.-C. Meurice Introduction In addition to being a major cardiovascular risk factor, smoking promotes or worsens thyroid, digestive, renal and bone diseases. Background Smoking is positively associated with hyperthyroidism. It is associated with Graves’ disease and it especially increases the risk of the development of severe exophthalmos. In contrast, smoking might exert a protective action for thyroid carcinoma. Smoking increases the severity of hepatic lesions in patients with chronic hepatitis C. Smoking accelerates the progression of primary biliary cirrhosis and increases the risk of hepatocellular carcinoma. Smoking increases risk of both hyperplastic and adenomatous polyps. While Crohn’s disease is associated with smoking, ulcerative colitis is largely a disease of non smokers. Smoking increases risk of development of both renal cell carcinoma and chronic nephropathies, particularly in types 1 and 2 diabetes. Smoking is a risk factor for decreased bone density and is associated with a significantly increased risk of fracture. Smoking is related to the development of rheumatoid arthritis and may adversely influence its severity. Conclusions Smoking might be considered a risk factor for the development of several thyroid, digestive, renal and bone diseases. Consequently, smoking prevention and cessation programs must be strongly encouraged among the patients concerned.Revue des Maladies Respiratoires 12/2008; 25(10):1261-1278. DOI:10.1016/S0761-8425(08)75091-5 · 0.49 Impact Factor
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ABSTRACT: In recent years a lot of interest has been focused on a specific category of polyps, the so-called serrated polyps which until recently were categorized with the hyperplastic or mixed polyps and were thought to have no risk of malignant transformation. Recently though, the serrated pathway of carcinogenesis was discovered and destroyed this myth. It is believed that up to one third of all colorectal cancers arise through the serrated pathway; these cancers occur more often in the proximal colon and have specific molecular characteristics. Specific subtypes of serrated polyps (mainly the sessile serrated adenomas/polyps) are thought to be precursor lesions of these cancers. The prevention of these cancers is a challenge for gastroenterologists because their location and endoscopic characteristics renders them difficult to detect. Also, although there is a clear need for creating a specific post-polypectomy surveillance program for these lesions, to date there have been no guidelines for surveillance with a high level of evidence. In this article the main molecular, endoscopic, histological and epidemiologic characteristics of these lesions are presented, as well as recommendations for surveillance.Annals of Gastroenterology 01/2013; 26(3):212-219.