Androgen suppression therapy represents an alternative to invasive approaches for the management of symptomatic benign prostatic hyperplasia. Androgen withdrawal from the prostate has been associated with the activation of specific genes involved with programmed cell death, or apoptosis. Luteinizing hormone-releasing hormone agonists, androgen receptor antagonists, and 5α-reductase inhibitors interrupt androgenic stimulation of prostatic growth by different mechanisms of action; consequently, their effectiveness and side effects vary. Although finasteride selectively inhibits 5α-reductase type 2 in the prostate, a second isozyme exists in the liver and skin after puberty and may account for incomplete clinical efficacy and the virilization seen in 5α-reductase deficiency after puberty. Two phase III clinical trials indicate that finasteride is a safe drug but, unfortunately, baseline prostatic volume, flow rate, and symptom severity do not predict treatment response. All forms of androgen suppression produce variable clinical improvement, measured by prostate size reduction, urodynamic obstruction, and symptom scores; this suggests a heterogeneity in the androgen dependence, tissue pathology, and obstructive physiology of benign prostatic hyperplasia.
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