266 Population level associations between COX-2 Inhibition by NSAID use and prostate cancer risk
266 - Population level associations between COX-2 Inhibition by NSAID use and prostat... Page 1 of 1
e266 Population level associations between COX-2...
266 - Population level associations between COX-2 Inhibition by NSAID use and prostat... Page 1 of 1
e266 Population level associations between COX-2 Inhibition by NSAID use and prostate cancer risk Veitonmäki T.P.C.1, Tammela T.L.J.2, Auvinen A.1, Murtola T.J.2 1University
of Tampere, School of Health Sciences, Tampere, Finland, 2University of Tampere, School of Medicine, Tampere, Finland
INTRODUCTION & OBJECTIVES: Some previous studies have suggested that inhibition of COX-2 enzyme could affect prostate cancer growth. In support of this, some epidemiological studies have linked usage of COX-2 inhibiting anti-inflammatory drugs (NSAIDs) with decreased prostate cancer risk. In this case-control study we quantified COX-2 inhibition by NSAID use, and estimated prostate cancer risk stratified by cumulative COX-2 inhibition. MATERIAL & METHODS: All newly diagnosed prostate cancer cases in Finland during 19952002 and matched controls (24,657 case control pairs) were identified from the Finnish Cancer Registry and the Population Register Center, respectively. Detailed information on physicianprescribed medication purchases during the study period was obtained from a comprehensive national prescription database of Social Insurance Institution. A total cumulative COX-2 inhibition value was calculated by multiplying the total cumulative mg amount of each NSAID used with the drug specific COX-1/COX-2 inhibition ratio values. Prostate cancer risk was analyzed with stratification by cumulative COX-2 inhibition using a conditional logistic regression model. The propensity to NSAID use among users of BPH medication, anti-diabetic medication, cholesterol-lowering medication and antihypertensive medication use was estimated with a logistic regression method. These were combined into a propensity score for each study participant. An age adjusted propensity score analysis was carried out for both overall and advanced prostate cancer risk. RESULTS: After adjustment for potential confounders ever-use of NSAIDs was associated with elevated overall prostate cancer risk (OR 1.31, 95%CI 1.26, 1.37) and advanced cancer risk (OR 1.63, 95%CI 1.47, 1.80). The risk increase was similar for all strata of cumulative COX-2 inhibition. The age-adjusted propensity score stratified analysis gave similarly elevated risk among NSAID users as the main analysis. CONCLUSIONS: NSAID usage is associated with increased risk of prostate cancer at the population level regardless of the quantity of COX-2 inhibition caused by the usage. These findings could not be entirely explained by systematic differences, such as more active PSA testing among NSAID users, as the risk increase was observed also in the propensity score analysis. A biological explanation such as chronic inflammation deserves further studies.