Levine A C, Kirschenbaum A, Gabrilove J L
Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA.
Mt Sinai J Med. 1997 Jan;64(1):20-5.
It has long been suspected that sex steroids play a key role in the pathogenesis of benign prostatic hyperplasia (BPH). Prostatic diseases do not occur in males castrated before puberty or in males with heritable disorders of androgen production or action. Both estrogens and androgens have been shown to induce BPH in experimental animals.
Clinical studies utilizing hormonal therapies to treat BPH were reviewed. Studies that used total medical castration therapy via the use of a long-acting gonadotropin-releasing hormone (GnRH agonist), partial androgen blockade via the use of the 5 alpha-reductase inhibitor finasteride, and estrogen blockade (via the use of aromatase inhibitors) were analyzed.
Both the GnRH agonists and finasteride result in prostatic size reduction and alleviate symptoms in some patients. Both therapies are more effective in men with larger prostates (> 40 cc). Finasteride is less efficacious in terms of size reduction than the GnRH agonists but also has fewer side effects. To date, clinical trials with aromatase inhibitors have not yielded dramatic positive results in the treatment of BPH.
