Tamsulosin for the Treatment of Benign Prostatic Hypertrophy

Abstract

OBJECTIVE: To review the information necessary to assess the efficacy and safety of tamsulosin compared with other adrenergic antagonists for treatment of symptomatic benign prostatic hyperplasia. DATA SOURCES: A search was conducted of Cumulated Index Medicus, January 1993–August 1999, which was restricted to human trials and English-language journals. STUDYSELECTION AND DATAEXTRACTION: Efficacy studies were included if the design was randomized and included a control group. Drug safety was assessed using data from any patient series or controlled study. DATA SYNTHESIS: Tamsulosin, a uroselective α1A-adrenergic receptor antagonist, relaxes smooth muscle in the prostate and bladder neck, thereby enhancing bladder emptying. In randomized, controlled clinical trials using standardized instruments, tamsulosin improves obstructive voiding symptoms by at least 25% in 65–80% of patients with symptomatic benign prostatic hyperplasia. Tamsulosin also improves peak urinary flow rate by 1.4–3.6 mL/sec in various studies and reduces post-void residual urine volume. The usual dosage of tamsulosin was 0.4 or 0.8 mg orally once a day in the studies performed in the US and Europe; daily doses of 0.1–0.4 mg were used in studies performed in Japan. The beneficial effects of tamsulosin on voiding symptoms, peak urinary flow rate, and bladder emptying appear to be dose-related, up to a ceiling dose of 0.4 mg. The most common adverse effects are headache, asthenia, dizziness, and rhinitis-like complaints. Retrograde or delayed ejaculation occurs in 4.5–14.0% of patients and has required discontinuation of treatment in a minority of these patients. At the usual dose of 0.4–0.8 mg/d, tamsulosin does not appear to significantly reduce blood pressure, increase heart rate, or cause first-dose syncope; therefore, dosage titration is not necessary when initiating treatment. Use of nifedipine, enalapril, atenolol, furosemide, or digoxin does not require dosage modification when tamsulosin is initiated concomitantly; hypotension has not been reported with combined use of tamsulosin and these commonly used agents. CONCLUSIONS: Tamsulosin is an improvement over other a-adrenergic antagonists for the management of symptoms of benign prostatic hyperplasia. It is a more convenient alternative that does not require initial dosage titration, has a fast onset of action, and has a low potential to cause hypotension when used alone or in combination with commonly used antihypertensive agents. It is more costly than some of the other second-generation α-adrenergic antagonists.