SAN DIEGO – Long-term use of aspirin, other nonsteroidal anti-inflammatory drugs, or statins affected neither the levels of prostate-specific antigen nor the velocity with which those levels changed, judging from a secondary analysis from a clinical trial.
"The prevention of prostate cancer by statins, aspirin, and other NSAIDs is an important topic given the widespread use of these drugs in the general population and particularly in the population of men at risk for prostate cancer," Steven P. Stratton. Ph.D., said in an interview during a conference sponsored by the American Association for Cancer Research and the Prostate Cancer Foundation.
"A lot of scientific papers have been published linking these drugs together with cancer prevention, but results are controversial. So definitive, prospective studies in prostate cancer have to be performed before we can know for sure," he said.
In an effort to investigate the effect of these medications on markers used to assess prostate cancer risk, Dr. Stratton and his associates analyzed a population of 699 men enrolled in a phase III chemoprevention trial that was designed to investigate the effects of selenium supplementation on prostate cancer incidence.
"The selenium didn’t work, but we also asked men in this study about their use of other commonly used drugs like statins and NSAIDs; and we measured the PSA on all of these men every 6 months for 5 years," said Dr. Stratton, who chairs the Scientific Review Committee and leads the Prostate Cancer Prevention Team at the University of Arizona Cancer Center, Tucson. "We used statistical models to see if there were relationships between drug use and PSA changes over time."
Men in the study had a PSA greater than 4 ng/mL and/or a suspicious digital rectal examination and/or a PSA velocity (PSAV) of greater than 0.75 ng/mL/year, but with a negative prostate biopsy. During the course of the trial, 73 of the study participants were diagnosed with prostate cancer.
After Dr. Stratton and his associates adjusted for variables including selenium use, age, race, body mass index, and pack-years of smoking, they found that the use of aspirin, NSAIDs, or statins did not demonstrate significant associations with PSA (P = .79, .68, and .79, respectively) or PSAV (P = .23, .43, and .84, respectively). Stratification between men who developed prostate cancer during the course of the study and those with repeated negative prostate biopsies did not alter the results.
"The study wasn’t long enough, nor was it designed to detect a cancer prevention effect of these drugs, but we can say with pretty good confidence that the drug use did not impact the PSA test – a problem called ‘detection bias’ – given that we saw no differences between men taking the drugs and those who did not," Dr. Stratton said. "This is important, because if the drug interfered with the PSA test – regardless of the impact on cancer – it could reduce the usefulness of the PSA test in men taking these drugs."
He acknowledged certain limitations of the study, including the fact that it was a secondary analysis using data from a clinical trial designed for another purpose. "Also, the data on medication use were based on self-reporting by the patients rather than an examination of their medical records or more stringent methods of data collection," he said.
Dr. Stratton said he had no relevant financial conflicts to disclose.