Background Men with benign prostatic hyperplasia can be treated with α1-adrenergic–antagonist drugs that relax prostatic smooth muscle or with drugs that inhibit 5α-reductase and therefore reduce tissue androgen concentrations. However, the effects of the two types of drugs have not been compared. Methods We compared the safety and efficacy of placebo, terazosin (10 mg daily), finasteride (5 mg daily), and the combination of both drugs in 1229 men with benign prostatic hyperplasia. American Urological Association symptom scores and peak urinary-flow rates were determined at base line and periodically for one year. Results The mean changes from base line in the symptom scores in the placebo, finasteride, terazosin, and combination-therapy groups at one year were decreases of 2.6, 3.2, 6.1, and 6.2 points, respectively (P<0.001 for the comparisons of both terazosin and combination therapy with finasteride and with placebo). The mean changes at one year in the peak urinary-flow rates were increases of 1.4, 1...

https://www.nejm.org/doi/pdf/10.1056/NEJM199608223350801

The efficacy of terazosin, finasteride, or both in benign prostatic hyperplasia. Veterans Affairs Cooperative Studies Benign Prostatic Hyperplasia Study Group.

Prostate volume predicts outcome of treatment of benign prostatic hyperplasia with finasteride: Meta-analysis of randomized clinical trials*

1 We have systematically reviewed the presence, functional responses and regulation of alpha(1)-, alpha(2)- and beta-adrenoceptors in the bladder, urethra and prostate, with special emphasis on human tissues and receptor subtypes 2 Alpha(1)-adrenoceptors are only poorly expressed and play a limited functional role in the detrusor Alpha(1)-adrenoceptors, particularly their alpha(1A)-subtype, show a more pronounced expression and promote contraction of the bladder neck, urethra and prostate to enhance bladder outlet resistance, particularly in elderly men with enlarged prostates Alpha(1)-adrenoceptor agonists are important in the treatment of symptoms of benign prostatic hyperplasia, but their beneficial effects may involve receptors within and outside the prostate 3 Alpha(2)-adrenoceptors, mainly their alpha(2A)-subtype, are expressed in bladder, urethra and prostate They mediate pre-junctional inhibition of neurotransmitter release and also a weak contractile effect in the urethra of some species, but not humans Their overall post-junctional function in the lower urinary tract remains largely unclear 4 Beta-adrenoceptors mediate relaxation of smooth muscle in the bladder, urethra and prostate The available tools have limited the unequivocal identification of receptor subtypes at the protein and functional levels, but it appears that the beta(3)- and beta(2)-subtypes are important in the human bladder and urethra, respectively Beta(3)-adrenoceptor agonists are promising drug candidates for the treatment of the overactive bladder 5 We propose that the overall function of adrenoceptors in the lower urinary tract is to promote urinary continence Further elucidation of the functional roles of their subtypes will help a better understanding of voiding dysfunction and its treatment

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α1‐, α2‐ and β‐adrenoceptors in the urinary bladder, urethra and prostate

The efficacy of terazosin, finasteride, or both in benign prostatic hyperplasia

We examined the influence of androgens on benign prostatic hyperplasia, using nafarelin acetate, a potent luteinizing-hormone-releasing hormone agonist, to achieve reversible androgen deprivation in men with benign prostatic hyperplasia. Nine patients with bladder-outlet obstruction due to benign prostatic hyperplasia were treated with subcutaneous nafarelin acetate (400 micrograms per day) in an open trial for six months. In all patients, serum testosterone decreased to castrate levels. Objective observations included uroflowmetry, measurement of residual urine volume, determination of prostatic size by ultrasonography, and prostatic biopsy. In all patients, the prostate regressed to a mean (+/- SEM) of 75.8 +/- 3 percent of the initial size (range, 52 to 86; P less than 0.005); the regression reached a plateau after four months. Morphologic analysis of biopsy specimens showed regression of glandular epithelium. Three of nine patients had clinical improvement with treatment. Six months after the cessation of treatment, plasma testosterone levels had returned to normal and the size of the prostate had increased to 99 +/- 5.5 percent of the initial size. These findings suggest that androgens have an important supportive role in established benign prostatic hyperplasia and that testicular suppression will benefit some patients. However, this form of treatment could be applicable only in carefully selected patients who were not surgical candidates, and it would need to be maintained indefinitely.

H.R. Müller

Papers

Light Microscopic Stereological Analysis of the Normal Human Prostate and of Benign Prostatic Hyperplasia