title: Endocrine therapies for BPH: scientific rationale, clinical results, and patient selection.
abstract: In 1993, medical therapy for BPH is a reality. Androgen deprivation therapy (LHRH agonists, antiandrogens, and 5 alpha-reductase inhibitors) has been shown to be effective by reducing the static component of BPH. Of these agents, the 5 alpha-reductase inhibitors have the greatest promise because of their low toxicity profile. Aromatase inhibitors, which function via a different mechanism, however, have not been demonstrated, as monotherapy, to be effective in the treatment of symptomatic BPH. It is still theoretically possible that aromatase inhibitors could have a role in the management of prostatism if they are utilized in conjunction with an antiandrogen or 5 alpha-reductase inhibitor. Although the early results for this endocrine therapies are encouraging, several issues relating to medical treatment remain unanswered. Not everyone with significant prostatism will respond to androgen deprivation therapy. How does the physician identify pre-treatment the patient most likely to achieve a significant improvement in voiding function with 5 alpha-reductase inhibitor therapy? At the present time, there is no method--based on symptoms, DRE findings, serum hormone and PSA levels, or histopathologic criteria--for recognizing the ideal patient for androgen deprivation therapy. Without question, it is a subjective decision. As a result, the benefits and risks of these medical approaches as well as those of the minimally invasive and surgical therapies must be discussed with the patient so that he can participate in the management decision. In this manner, the expectations and needs of the patient will be best served.
authors.affiliation: Department of Urology, Mayo Clinic, Rochester, MN 55905.
authors.forename: J E
authors.initials: JE
authors.lastname: Oesterling
authors.forename: M F
authors.initials: MF
authors.lastname: el Etreby
authors.forename: G J
authors.initials: GJ
authors.lastname: Gormley
authors.forename: J L
authors.initials: JL
authors.lastname: Imperato-McGinley
authors.forename: C G
authors.initials: CG
authors.lastname: Roehrborn
authors.forename: F H
authors.initials: FH
authors.lastname: Schröder
authors.forename: U W
authors.initials: UW
authors.lastname: Tunn
mesh_terms: D058891:5-alpha Reductase Inhibitors; D000726:Androgen Antagonists / Q000627:therapeutic use*; D000728:Androgens / Q000502:physiology / Q000627:therapeutic use*; D000735:Androstenedione / Q000031:analogs & derivatives / Q000627:therapeutic use; D000818:Animals; D047072:Aromatase Inhibitors; D002986:Clinical Trials as Topic; D007987:Gonadotropin-Releasing Hormone / Q000819:agonists; D006728:Hormones / Q000627:therapeutic use*; D006801:Humans; D008297:Male; D008954:Models, Biological; D018579:Patient Selection; D011467:Prostate / Q000473:pathology / Q000502:physiology; D011470:Prostatic Hyperplasia / Q000188:drug therapy*
chemical_list: D058891:5-alpha Reductase Inhibitors; D000726:Androgen Antagonists; D000728:Androgens; D047072:Aromatase Inhibitors; D006728:Hormones; D007987:Gonadotropin-Releasing Hormone; D000735:Androstenedione; C048751:atamestane