Finasteride effects on hypoxia and angiogenetic markers in benign prostatic hyperplasia.

Author(s): Lekas AG, Lazaris AC, Chrisofos M, Papatsoris AG, Lappas D, Patsouris E, Deliveliotis C

Affiliation(s): Department of Urology, General Hospital of Nikea, Piraeus, Greece. alekas@med.uoa.gr

Publication date & source: 2006-08, Urology., 68(2):436-41.

Publication type: Randomized Controlled Trial

OBJECTIVES: To assess the effects of finasteride on angiogenetic and hypoxia markers in benign prostatic hyperplasia. METHODS: A total of 178 patients aged 51 to 85 years (mean 68.7) with benign prostatic hyperplasia and awaiting transurethral prostate resection were prospectively randomized into a group of patients receiving finasteride (group 1; 88 patients) and a group of patients who received no medication until transurethral prostate resection (group 2; 90 patients). Tissue specimens were immunohistochemically stained with monoclonal antibodies against CD34 for microvessel density (MVD), vascular endothelial growth factor (VEGF), and hypoxia inducible factor-1alpha (HIF-1alpha). RESULTS: Blood loss during transurethral prostate resection was significantly higher in group 2 compared with group 1 (P <0.001). The distribution of CD34 immunostaining was mainly at the suburethral prostate. MVD, VEGF, and HIF-1alpha values were significantly lower statistically (P <0.001) in group 1 compared with group 2. In the finasteride group (group 1), the positive correlation of the immunoreactivity of CD34 and HIF-1alpha, VEGF and HIF-1alpha, and VEGF and CD34 was statistically significant (P <0.001). In the same group, MVD and VEGF and HIF-1alpha expression correlated statistically with the treatment duration. CONCLUSIONS: Finasteride administration in benign prostatic hyperplasia results in statistically significant suppression of MVD, VEGF, and HIF-1alpha in a time-dependent manner.