Effect of cyproterone acetate on clinical, endocrine and pathological features of benign prostatic hypertrophy.

The absence of BPH in castrated or hypopituitary patients suggests that the disease is related to the amounts of secreted sex steroids—testosterone (T) and estrogen (E)—and perhaps to either GH or prolactin. We have, therefore, attempted medical castration with progestational anti-androgens. This study reports the objective effects of a progestational anti-androgen, cyproterone acetate (CPA), on the clinical symptoms of BPH and correlates these changes with the effects of the drug on sex steroid production and the action of androgens at the prostate cellular level. CPA was administered prior to TURP. Significant decreases occurred in plasma T, urinary TG, and E production rates, but not in plasma LH. CPA also decreased LH and HGH reserves. In vitro incubation of CPA with prostate minces from controls decreased binding of H³-DHT to prostate cytosol receptors. Histologic studies of prostate tissue from patients treated with CPA indicated atrophy and embryonal changes of glandular elements. Three of 4 patients treated with CPA voided spontaneously within 2 months of therapy. In summary, CPA decreased sex steroid synthesis by the testes without suppression of LH. CPA also appeared to block steroid-protein binding in the prostate. These hormonal and biochemical effects correlated with clinical improvement indicated by the ability to void in patients in retention prior to therapy.