Estrogen reduction by aromatase inhibition for benign prostatic hyperplasia: results of a double-blind, placebo-controlled, randomized clinical trial using two doses of the aromatase-inhibitor atamestane. Atamestane Study Group.

BACKGROUND: The concept of estrogen withdrawal by an aromatase inhibitor in the treatment of benign prostatic hyperplasia (BPH) was assessed in a prospective, randomized, double-blind, placebo-controlled multicenter trial. METHODS: Two hundred and ninety-two patients with clinical symptoms of BPH were randomly allocated to one of the following treatments for 48 weeks: placebo or the selective aromatase inhibitor, atamestane, at a daily dose of 100 mg or 300 mg. Both doses of atamestane significantly reduced serum concentrations of estradiol and estrone, and produced a slight, dose-dependent, counter-regulatory increase in peripheral androgen concentration. RESULTS: Clinical symptoms improved during treatment in all three groups. Even after 48 weeks, the effect of active treatment did not exceed the effect seen with placebo. Overall tolerance of 100 mg atamestane was excellent, but 300 mg showed a slightly increased incidence of side effects compared with placebo. CONCLUSIONS: The conclusion from this study is that the reduction in estrogen concentration using the selective aromatase inhibitor atamestane has no effect on clinically established BPH.

Influence of indomethacin and aspirin on the vesicosphincteric dynamics of prostatectomized patients.

The urodynamic and clinical effects of two known prostaglandin synthetase inhibitors--indomethacin and aspirin--were analysed using 59 prostatectomized patients as experimental subjects. We obtained clinical and urodynamic results within each group by comparing the situation before and after medication. A placebo group of 12 patients was used to get an idea of the natural evolution of the situation. A urodynamic workup was done 1 h and 30 min after the administration of the drugs and placebo and the clinical results were analysed on the 8th day of treatment, at which time a few patients were again studied urodynamically. The clinical results were again evaluated a short time after the treatment had been terminated. Marked clinical and urodynamic changes showed that bladder and urethral structures had been affected. Urodynamic modifications, were statistically analysed. We concluded that changes noted were at least partially due to prostaglandin synthesis inhibition and the resulting inhibition of prostaglandin action.