Benign prostatic hyperplasia. Hormonal treatment.
Androgen withdrawal therapy appears to produce a 20% to 30% decrease in the volume of the hyperplastic prostate after 3 to 6 months of therapy. Longer periods of treatment do not result in further prostatic regression, but further growth of the gland is not apparent in men treated with finasteride for 4 years. Although biopsy studies indicate that epithelial regression occurs to a much more significant degree than stromal regression, this may simply reflect the relatively longer turnover of the stromal cell population. The significant placebo effect of oral medication in patients with BPH makes interpretation of clinical symptomatology and uroflow data difficult. Analysis of symptom improvement is further complicated by the relatively slow improvement of patients on hormonal therapy, as opposed to surgery, where relief is immediate. In addition to limited stromal involution and inadequate treatment duration, other biologic factors may limit the clinical efficacy of androgen withdrawal therapy. Most importantly, partial involution may not necessarily decrease urethral resistance. In addition, obstruction-induced detrusor dysfunction may persist after relief of outflow obstruction in some patients, as it does following surgery. Incomplete blockade of androgen action, as well as compliance issues, may also limit efficacy. Long-term studies validate a modest but significant clinical response rate of finasteride therapy with preservation of sexual function in most men. Of the available hormonal therapeutic agents, only finasteride appears to have an acceptable risk-benefit ratio. Other 5 alpha-reductase inhibitors in the "pipeline," such as episteride, may have similar benefits. In the long term, this class of drugs may have a much larger role in patients who present with the early signs of BPH, to prevent any further progression of the disease. Presently, no form of antiandrogen therapy is as effective as transurethral resection of the prostate in relieving symptomatology. Because of patient preferences, however, medical therapy will play an increasingly important role in the management of patients with BPH.
McConnell
J D
JD
Division of Urology, University of Texas Southwestern Medical Center, Dallas, USA.
D000726:Androgen Antagonists / Q000627:therapeutic use; D000728:Androgens / Q000502:physiology; D042944:Cholestenone 5 alpha-Reductase; D018120:Finasteride / Q000627:therapeutic use; D006801:Humans; D008297:Male; D010088:Oxidoreductases / Q000037:antagonists & inhibitors; D011470:Prostatic Hyperplasia / Q000503:physiopathology / Q000628:therapy*
D000726:Androgen Antagonists; D000728:Androgens; D018120:Finasteride; D010088:Oxidoreductases; D042944:Cholestenone 5 alpha-Reductase