Presentation Authors: Lukas Gstrein*, Christopher Millan, Ashkan Mortezavi, Zurich, Switzerland, Stephen Wyler, Aarau, Switzerland, Lukas Manka, Braunschweig, Germany, Andreas Huber, Rainer Grobholz, Franz Recker, Aarau, Switzerland, Tullio Sulser, Daniel Eberli, Zurich, Switzerland, Maciej Kwiatkowski, Aarau, Switzerland
Introduction: Chemoprevention of prostate cancer (PCa) has been extensively investigated in the last decades. Sofar only 5-alpha-reductase-inhibitors (5-ARI) are supported by clinical evidence to havechemopreventive effect on PCa incidence, hence unclear in terms of prevention of aggressive PCa.Evidence for an effect of ASA on PCa is conflicting. The exact interaction pathways between ASA andcarcinogenesis are still to be established. The aim of the study was to analyze the influence of ASAintake on PSA values and PCa development.
Methods: A population-based analysis including 4314 men from the European Randomized Study of Screeningfor Prostate Cancer (ERSPC) database was conducted. Data about drug intake, age, family history andsymptoms was obtained by a self-administered questionnaire. A transrectal ultrasound guidedprostate biopsy was performed in men with a PSA-level > 3 ng/ml. Tumor stage and grade wereregistered; incidence and mortality data were obtained through registry linkages. PCa incidence andgrade, total PSA value, free-to-total PSA and overall survival were compared between ASA users andnon-users, respectively.
Results: Median follow-up time was 9.6 years. In all, n = 789 (18.3%) men used aspirin [ASA+]. Although overall PCa incidence was significantly lower among aspirin users ([ASA+] 54 (6.8%) vs. [ASA-] 338 (9.6%), p 0.015), the multivariate cox-regression analysis did not show the decreased risk to be diagnosed with PCa ([ASA+] hazard ratio (HR) 0.84, 95% confidence interval (CI) 0.62 - 1.16; p = 0.297) to be statistically significant. Total PSA values were significantly lower in aspirin users for both baseline (1.6 vs. 1.8 ng/ml, p = 0.007) and follow-up-visits after four years (1.75 vs. 2.1 ng/ml, p < 0.001). Multivariate cox-regression analysis predicted significantly higher overall mortality among ASA users compared to non-users ([ASA+] HR 1.46, 95% CI 1.10 to 1.94).
Conclusions: In our study population we could demonstrate that ASA intake did not alter overall PCa risk in a statistically significant manner. However, the finding of persistently lower PSA values in ASA users is of potential clinical importance. It suggests that PSA cutoff values should be lowered in ASA users otherwise it may introduce potential bias towards delayed PCa detection in this group, especially outside a screening setting. On the other hand, lower PSA values may suggest a protective effect of ASA on PCa development