STUDY OBJECTIVE: Studies done both in laboratory animals and humans suggest that nonsteroidal antiinflammatory drug (NSAID) use may reduce the risk of developing lung cancer. Many epidemiologic studies exploring this association lacked sufficient power to draw definitive conclusions. We conducted a metaanalysis to examine the effect of NSAID use on the risk of lung cancer. DESIGN: We searched the literature using MEDLINE, CANCERLIT, related conference abstracts, and bibliographies of selected studies. The estimators of relative risk (RR) and associated variances, adjusted for the greatest number of confounders, were abstracted and included in the metaanalysis. Combined estimators of RR were calculated using either fixed or random-effect models. Metaanalyses were performed on 14 studies (the number of cases ranged from 81 to 2,560) that examined the association between lung cancer and NSAIDs. Further, subgroup analyses were performed on the nine studies that had adjusted for the effects of smoking. RESULTS: The combined estimate of RR was 0.79 (95% confidence interval [CI], 0.66 to 0.95) when all the studies were included in the analysis, and was 0.68 (95% CI, 0.55 to 0.85) when the analysis was limited to the subgroup of studies adjusted for smoking. The combined estimates for case-control studies and cohort studies within this subgroup were 0.63 (95% CI, 0.47 to 0.86) and 0.78 (95% CI, 0.62 to 0.98), respectively. We also observed that small cell lung cancer was more inversely associated with NSAID use (RR, 0.48; 95% CI, 0.30 to 0.75) than non-small cell lung cancer (RR, 0.66; 95% CI, 0.56 to 0.79). CONCLUSION: The findings of this study support an inverse association between NSAID use and risk of lung cancer, but do not suggest a causal relationship.
STUDY OBJECTIVE: Studies done both in laboratory animals and humans suggest that nonsteroidal antiinflammatory drug (NSAID) use may reduce the risk of developing lung cancer. Many epidemiologic studies exploring this association lacked sufficient power to draw definitive conclusions. We conducted a metaanalysis to examine the effect of NSAID use on the risk of lung cancer. DESIGN: We searched the literature using MEDLINE, CANCERLIT, related conference abstracts, and bibliographies of selected studies. The estimators of relative risk (RR) and associated variances, adjusted for the greatest number of confounders, were abstracted and included in the metaanalysis. Combined estimators of RR were calculated using either fixed or random-effect models. Metaanalyses were performed on 14 studies (the number of cases ranged from 81 to 2,560) that examined the association between lung cancer and NSAIDs. Further, subgroup analyses were performed on the nine studies that had adjusted for the effects of smoking. RESULTS: The combined estimate of RR was 0.79 (95% confidence interval [CI], 0.66 to 0.95) when all the studies were included in the analysis, and was 0.68 (95% CI, 0.55 to 0.85) when the analysis was limited to the subgroup of studies adjusted for smoking. The combined estimates for case-control studies and cohort studies within this subgroup were 0.63 (95% CI, 0.47 to 0.86) and 0.78 (95% CI, 0.62 to 0.98), respectively. We also observed that small cell lung cancer was more inversely associated with NSAID use (RR, 0.48; 95% CI, 0.30 to 0.75) than non-small cell lung cancer (RR, 0.66; 95% CI, 0.56 to 0.79). CONCLUSION: The findings of this study support an inverse association between NSAID use and risk of lung cancer, but do not suggest a causal relationship.
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