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Use of non-steroidal anti-inflammatory drugs and prostate cancer risk: A population-based nested-case control study

Posted on:2010-06-24Degree:Ph.DType:Dissertation
University:University of Manitoba (Canada)Candidate:Mahmud, SalaheddinFull Text:PDF
GTID:1444390002478884Subject:Health Sciences
Abstract/Summary:
Non-steroidal anti-inflammatory drugs (NSAIDs) have been shown to prevent the development of colon cancer, and there is evidence for a protective effect for other types of cancer including prostate cancer (PC). Despite strong laboratory evidence, the epidemiological studies that examined the relationship between NSAID use and PC have so far reported conflicting results. Most studies were limited by exposure and disease misclassification, limited information on dose and duration of use, and by the possibility of screening and other biases.;Ever-use of propionates (e.g., ibuprofen, naproxen) was associated with a modest reduction in PC risk (OR=0.90; 95%CI 0.84-0.95), whereas use of other NSAIDs was not consistently related to PC risk. In particular, we did not observe the hypothesized inverse associations with aspirin use. There was no clear evidence of a dose-response or duration-response relationships between any of the examined NSAID classes and PC risk. Most examined classes were inversely related to the risk of metastatic disease, but without clear evidence of a dose-response relationship.;Despite the study's limitations, our findings suggest modest benefits of at least some NSAIDs in reducing PC risk. Further research is required to address many important unresolved questions before any firm conclusions about the clinical utility of NSAIDs could be reached.;We conducted a nested a case-control study using the databases of the Saskatchewan Prescription Drug Plan (SPDP) and the Saskatchewan Cancer Registry to examine the effects of NSAID use on the risks of developing PC. Cases (N=9,007) were men aged 40 years or older diagnosed with histologically-confirmed prostatic carcinoma between 1985 and 2000. Using incidence density sampling, each case was matched to four controls on age, calendar time and duration of membership in the SPDP. Detailed histories of exposure to prescription NSAIDs and other drugs were obtained from the SPDP. Conditional logistic regression models were used to model the effects of NSAID use on PC risk while accounting for matching and for potential confounding by screening and other covariates.
Keywords/Search Tags:PC risk, NSAID, Cancer, Drugs, Nsaids, Evidence
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