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Statins Protect Against Prostate Cancer: Presented at EAU

By Chris Berrie

BERLIN, GERMANY -- March 27, 2007 -- The use of statins, rather than other cholesterol-lowering agents, significantly reduced the incidence of prostate cancer in the population-based Finnish Prostate Cancer Screening (FPCS) trial.

Although the statins have been reported to have growth inhibitory effects on prostate cancer cells in vitro, the evidence from epidemiological studies has remained controversial. Indeed, some studies have shown a negative association between statin use and risk of prostate cancer.

Principal investigator Teemu Murtola, MD, researcher in urology, School of Public Health, University of Tampere, Tampere, Finland, indicated that the poor results for statins in previous trials could be due at least in part to variations in prostate-specific antigen (PSA) measurements between statin users and non-users.

The FPCS trial is part of a European randomised study of prostate cancer screening designed to determine whether or not prostate cancer screening with PSA reduces mortality, but the Finnish researchers "used the population in a slightly different way", Dr. Murtola said during his presentation here on March 23^rd at the 22^nd Annual Congress of the European Association of Urology (EAU).

In their study, Dr. Murtola and colleagues evaluated the association between use of cholesterol drugs and prostate cancer incidence, stage and grade, and included PSA values.

The researchers evaluated all the men participating in the FPCS trial from 1996 to 2004 (N = 23,320). Of these, 6,755 (29.0%) had used statins and 934 (4.0%) had used other cholesterol-lowering agents. A total of 3 screening rounds were completed, and information on the prescription medicine purchases in this study population was obtained from the prescription database of the Finnish Social Insurance Institution.

Overall, prostate cancer incidence was significantly lower for statin users than non-users (4.0% vs 8.0%, respectively). A significant dose-response relationship was seen for the total cumulative quantity of statin users and incidence of prostate cancer (P < .001).

For tumour staging, the incidence of all prostate cancer grades was decreased by statin use, with the greatest decreases seen in T2 (0.9% vs 2.5%) and T3 (0.2% vs 0.6%) cancers.

Statin use reduced the incidence of all World Health Organisation (WHO) tumour grades (G1: 1.7% vs 3.2%; G2: 2.0% vs 4.4%; G3: 0.3% vs 0.6%), as for the Gleason grade groupings (grades 2-6: 3.0% vs 6.1%; grade 7: 0.7% vs 1.4%; grades 8-10: 0.3% vs 0.6%).

In contrast, there were no significant differences seen for prostate cancer incidence, stage or grade between users and non-users of other cholesterol drugs (e.g. fibrates, resins).

While median PSA levels were lower and showed higher median free/total ratios among users of both statins and fibrates, no correlations were seen between the drug concentrations and PSA levels.

This analysis therefore shows a protective effect of statin use against prostate cancer in a population that includes a large number of latent cancers identified through this comprehensive screening.

Although the use of both statins and fibrates was associated with favourable PSA levels and free/total PSA ratios, the researchers believe that as this effect is not related to the dose of cholesterol agent used, it is probably due to a common metabolic factor across the statin users, and thus could be related instead to their hypercholesterolaemia or obesity.

Finally, Dr. Murtola added, "I also think that the results from this study should be made known to men who have a high cholesterol and possibly familial disposition to prostate cancer, to increase their compliance in their use of statins."


[Presentation title: Prostate Cancer and Serum PSA Among Users of Serum Lipid-Lowering Drugs in the Finnish Prostate Cancer Screening Trial. Poster 803]

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