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Am Fam Physician. 2003;68(11):2269-2270

Laboratory studies of nonsteroidal antiinflammatory drugs (NSAIDs) have demonstrated some antiproliferative effects on lung tumor growth, thought to be caused by inhibition of cyclooxygenase-2 enzymes. Previous observational studies of NSAID use and the incidence of lung cancer have produced conflicting results regarding a possible protective effect with the use of NSAIDs. Muscat and colleagues performed a retrospective case-control analysis to determine the effect of NSAID use on the incidence of lung cancer.

The authors identified 1,038 patients with lung cancer from a review of pathology data at several large East Coast hospital centers. Control patients without cancer were identified from the admission roster of the same hospitals, and were matched for age, gender, and month of interview. Control patients were excluded from the study if they had any clinical indication for regular use of aspirin or other NSAIDs (e.g., rheumatoid arthritis, osteoarthritis), or if they had any contraindication to use of NSAIDs (e.g., peptic ulcer, bleeding disorder). Case and control patients were interviewed by study personnel for recollection of NSAID use, smoking status, and demographic data.

Overall, 21 percent of the control patients regularly used NSAIDs (i.e., took three or more tablets per week for one or more years). Use of NSAIDs by control patients did not vary significantly by gender, age, smoking, or educational status. Among patients with cancer, 17 percent reported regular NSAID consumption. Because smoking is the chief risk factor for lung cancer, the analysis was divided among smokers and those who had never smoked. Among smokers, after adjustment for other demographic variables, the risk of lung cancer among regular NSAID users was 32 percent less than that in patients who did not regularly consume NSAIDs. Comparing the few persons with lung cancer among those who never smoked (84 of 1,038 patients) with patients in the control group, no protective effect was found with regular use of NSAIDs. Among smokers, there was no evidence of a dose-response effect to use of NSAIDs; longer use or higher rates of consumption did not confer more protection against lung cancer.

The authors conclude that their study identifies a possible protective effect against lung cancer in smokers who regularly use NSAIDs. They acknowledge the limitations of this retrospective study and the lack of any benefit to NSAID use seen in some other large epidemiologic studies of lung cancer.

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