Introduction

Chemoprevention of prostate cancer (PCa) has been extensively investigated in the last decades. So far only 5-alpha-reductase-inhibitors (5-ARI) are supported by clinical evidence to have chemopreventive effect on PCa incidence, hence unclear in terms of prevention of aggressive PCa. Evidence for an effect of statins on PCa is conflicting. The interaction between dyslipidemia and carcinogenesis is still to be established. The aim of the study was to analyse the influence of statins intake on PSA values and PCa development.

Methods

A population-based analysis including 4314 men from the European Randomized Study of Screening for Prostate Cancer (ERSPC) database was conducted. Data about drug intake, age, family history and symptoms was obtained by a self-administered questionnaire. A transrectal ultrasound guided prostate biopsy was performed in men with a PSA-level > 3ng/ml. Tumor stage and grade were registered, incidence and mortality data were obtained through registry linkages. PCa incidence and grade, total PSA value, free-to-total PSA and overall survival were compared between statin users and non-users, respectively.

Results

Over a follow-up period of 9.6 years men with statin (n=761) exposure had insignificantly lower risk to be diagnosed with PCa ([stat+] hazard ratio (HR) 0.77, 95 % confidence interval (CI) 0.58 to 1.02. Statin users had less low risk PCa compared to non-users (p<0.05) at baseline visit while there was no difference in other PCa risk groups (according to d'Amico risk groups classification) or at follow-up visit. Interestingly, total PSA values were lower in statin users both for baseline (1.5 vs. 1.8 ng/ml, p<0.001) and follow-up-visits (after four years) (1.8 vs. 2.1ng/ml, p<0.001). Overall mortality was higher among statin users compared to non-users ([stat+] HR 1.67, 95% CI 1.36 to 2.04, however the competing risk analysis could demonstrate that PCa incidence was not influenced by overall-mortality.

Conclusions

In our study population we could demonstrate that statins intake did not alter overall PCa risk in a statistically significant manner. However, the finding of persistently lower PSA values in statin users is of potential clinical importance. It suggests that PSA cutoff values should be lowered in statin users otherwise it may introduce potential bias towards delayed PCa detection in this group, especially outside screening setting. On the other hand lower PSA values may suggest a durable protective effect of statins on PCa development.

Funding

None