Prostate-specific antigen levels in relation to consumption of nonsteroidal anti-inflammatory drugs and acetaminophen: results from the 2001-2002 National Health and Nutrition Examination Survey.

BACKGROUND

Inflammation has been implicated in prostate carcinogenesis; therefore, the use of nonsteroidal anti-inflammatory drugs (NSAIDs) has the potential of decreasing the risk of prostate cancer. However, to the authors' knowledge the precise correlation between oral NSAID use, serum prostate-specific antigen (PSA), and prostate cancer risk is unknown. To further characterize this association, the authors evaluated serum PSA levels with regard to NSAID and acetaminophen consumption in a large cross-sectional study of men in the US.

METHODS

PSA levels were determined in 1319 men aged >40 years in the 2001-2002 National Health and Nutrition Examination Survey (NHANES). Linear regressions were performed on log-transformed PSA levels, accounting for the complex survey design, to evaluate the relations between PSA and the use of NSAIDs and acetaminophen after adjusting for the effects of age, race, educational level, smoking status, body mass index, coexisting inflammatory conditions, and heart disease.

RESULTS

NSAID and acetaminophen consumption displayed a negative association with PSA levels, namely, individuals who reported using NSAIDs (19.8%) or acetaminophen (1.3%) regularly had lower PSA levels than individuals who did not take these drugs, although the impact of acetaminophen was not statistically significant. PSA levels among NSAID users were 0.9 times the levels among nondrug takers (P = .038), whereas PSA levels among acetaminophen users were 0.76 times the levels in nondrug takers (P = .14). Individuals who stated they took both NSAIDs and acetaminophen (0.99%) on a regular basis had higher PSA levels (1.8 times greater), although not statistically significantly so (P = .24), than individuals who stated they did not take either of these drugs regularly.

CONCLUSIONS

The findings of the current study suggest that regular NSAID consumption may reduce serum PSA levels. Whether this is indicative of a protective effect on prostate cancer risk or masks possible prostate injury resulting in reduced detection of prostate cancer is unclear. Given the widespread consumption of NSAIDs and the regular use of PSA for the assessment of prostate cancer risk, the potential implications of the current study's findings may be substantial and warrant further investigation.