Statin users diagnosed with prostate cancer were less likely to die from the disease compared with nonstatin users, according to results of a prospective, population-based study published online May 1 in The Prostate. The risk of recurrence or progression of prostate cancer was no different between statin users and nonusers, though.
In 2012, Nielsen et al reported in the New England Journal of Medicine that statin use in cancer patients was associated with reduced cancer-related mortality (N Engl J Med 2012;367[19]:1792-1802). The study included all patients in Denmark with a cancer diagnosis between 1995 and 2007, about 8 percent of whom were statin users, and compared mortality of users vs. nonusers. The mortality reduction was observed in 13 types of cancer, including prostate cancer.
Senior author Janet L. Stanford, PhD, of the Fred Hutchinson Cancer Research Center in Seattle, and colleagues explored the association between statin use and prostate cancer in a U.S. population through the Seattle-Puget Sound Surveillance, Epidemiology, and End Results (SEER) Program cancer registry. They identified 1,001 men diagnosed with prostate cancer between 2002 and 2005 who provided information about statin use in baseline in-person interviews. Patients were followed for more than five years.
Stanford et al determined cancer-specific deaths with SEER, and verified them by reviewing death certificates. They ascertained cancer recurrence and progression events through follow-up surveys.
About 28 percent of the patients were statin users. The statin users were older; had a higher body mass index; were more likely to take aspirin and nonaspirin nonsteroidal anti-inflammatory drugs; to have a history of diabetes; were less likely to have distant disease; and less likely to have a high prostate-specific antigen (PSA) value.
Of the 661 patients who completed the follow-up survey and 24 others with events ascertained in the SEER registry and medical records, 22 percent had recurrence or progression of prostate cancer. At nine years, the risk of overall recurrence or progression was 22 percent in the statin group and 21 percent in the nonstatin group.
Twelve percent of the 1,001 patients died (average follow-up 7.6 years), 4 percent due to prostate cancer. The risk of prostate cancer-specific mortality was 1 percent in the statin group vs. 5 percent in the nonstatin group. They found no association with other-cause mortality.
Stanford et al noted that the association between statin use and reduced mortality was more pronounced in their study compared with the Danish analysis. They proposed that the higher frequency of use of statins in the U.S. may suggest that in the Danish study, patients prescribed statins were sicker or had other health-related factors. “Unfortunately, data on potentially important confounders such as smoking status, body mass index, and cancer screening history were missing in the Danish study,” they wrote.
Statin drugs may have an anticarcinogenic effect on prostate cancer cells by inhibiting cell survival or proliferation, among other possibilities, they suggested. “If the results of our study are validated in other patient cohorts with extended follow-up for cause-specific death, an intervention trial of statin drugs in prostate cancer patients may be justified,” Stanford said in a release.
The study did not address changes in statin use after baseline although in the follow-up survey they found that less than 6 percent of patients had stopped using statins after their cancer diagnosis. The small number of prostate cancer-specific deaths did not allow for granular analyses on statin use, and potential confounding was possible despite the use of competing risk regression and other models.