TY - JOUR
T1 - The Effect of Finasteride in Men with Benign Prostatic Hyperplasia
AU - Finasteride Study Group
AU - Gormley, Glenn J.
AU - Stoner, Elizabeth
AU - Bruskewitz, Reginald C.
AU - Imperato-Mcginley, Julianne
AU - Walsh, Patrick C.
AU - Mcconnell, John D.
AU - Andriole, Gerald L.
AU - Geller, Jack
AU - Bracken, Bruce R.
AU - Tenover, Joyce S.
AU - Vaughan, E. Darracott
AU - Pappas, Frances
AU - Taylor, Alice
AU - Binkowitz, Bruce
AU - ng, Jennifer
PY - 1992/10/22
Y1 - 1992/10/22
N2 - Benign prostatic hyperplasia is a progressive, androgen-dependent disease resulting in enlargement of the prostate gland and urinary obstruction. Preventing the conversion of testosterone to its tissue-active form, dihydrotestosterone, by inhibiting the enzyme 5α-reductase could decrease the action of androgens in their target tissues; in the prostate the result might be a decrease in prostatic hyperplasia and therefore in symptoms of urinary obstruction. In a double-blind study, we evaluated the effect of two doses of finasteride (1 mg and 5 mg) and placebo, each given once daily for 12 months, in 895 men with prostatic hyperplasia. Urinary symptoms, urinary flow, prostatic volume, and serum concentrations of dihydrotestosterone and prostate-specific antigen were determined periodically during the treatment period. As compared with the men in the placebo group, the men treated with 5 mg of finasteride per day had a significant decrease in total urinary-symptom scores (P<0.001), an increase of 1.6 ml per second (22 percent, P<0.001) in the maximal urinary-flow rate, and a 19 percent decrease in prostatic volume (P<0.001). The men treated with 1 mg of finasteride per day did not have a significant decrease in total urinary-symptom scores, but had an increase of 1.4 ml per second (23 percent) in the maximal urinary-flow rate, and an 18 percent decrease in prostatic volume. The men given placebo had no changes in total urinary-symptom scores, an increase of 0.2 ml per second (8 percent) in the maximal urinary-flow rate, and a 3 percent decrease in prostatic volume. The frequency of adverse effects in the three groups was similar, except for a higher incidence of decreased libido, impotence, and ejaculatory disorders in the finasteride-treated groups. The treatment of benign prostatic hyperplasia with 5 mg of finasteride per day results in a significant decrease in symptoms of obstruction, an increase in urinary flow, and a decrease in prostatic volume, but at a slightly increased risk of sexual dysfunction. (N Engl J Med 1992;327:1185–91.), BENIGN prostatic hyperplasia is common in aging men. The resulting enlargement of the prostate gland can lead to urethral obstruction and even complete urinary retention.1 2 3 The standard treatment is surgical resection of the prostate,4 and there has been no effective medical therapy. Androgens are required to maintain the size and function of the prostate in men. The prostate does not become enlarged in boys castrated before puberty, and androgen deprivation leads to a reduction in the size of the prostate.5 , 6 The androgen primarily responsible for prostatic growth and enlargement is dihydrotestosterone. Men who have 5α-reductase deficiency7 , 8 and who therefore cannot…
AB - Benign prostatic hyperplasia is a progressive, androgen-dependent disease resulting in enlargement of the prostate gland and urinary obstruction. Preventing the conversion of testosterone to its tissue-active form, dihydrotestosterone, by inhibiting the enzyme 5α-reductase could decrease the action of androgens in their target tissues; in the prostate the result might be a decrease in prostatic hyperplasia and therefore in symptoms of urinary obstruction. In a double-blind study, we evaluated the effect of two doses of finasteride (1 mg and 5 mg) and placebo, each given once daily for 12 months, in 895 men with prostatic hyperplasia. Urinary symptoms, urinary flow, prostatic volume, and serum concentrations of dihydrotestosterone and prostate-specific antigen were determined periodically during the treatment period. As compared with the men in the placebo group, the men treated with 5 mg of finasteride per day had a significant decrease in total urinary-symptom scores (P<0.001), an increase of 1.6 ml per second (22 percent, P<0.001) in the maximal urinary-flow rate, and a 19 percent decrease in prostatic volume (P<0.001). The men treated with 1 mg of finasteride per day did not have a significant decrease in total urinary-symptom scores, but had an increase of 1.4 ml per second (23 percent) in the maximal urinary-flow rate, and an 18 percent decrease in prostatic volume. The men given placebo had no changes in total urinary-symptom scores, an increase of 0.2 ml per second (8 percent) in the maximal urinary-flow rate, and a 3 percent decrease in prostatic volume. The frequency of adverse effects in the three groups was similar, except for a higher incidence of decreased libido, impotence, and ejaculatory disorders in the finasteride-treated groups. The treatment of benign prostatic hyperplasia with 5 mg of finasteride per day results in a significant decrease in symptoms of obstruction, an increase in urinary flow, and a decrease in prostatic volume, but at a slightly increased risk of sexual dysfunction. (N Engl J Med 1992;327:1185–91.), BENIGN prostatic hyperplasia is common in aging men. The resulting enlargement of the prostate gland can lead to urethral obstruction and even complete urinary retention.1 2 3 The standard treatment is surgical resection of the prostate,4 and there has been no effective medical therapy. Androgens are required to maintain the size and function of the prostate in men. The prostate does not become enlarged in boys castrated before puberty, and androgen deprivation leads to a reduction in the size of the prostate.5 , 6 The androgen primarily responsible for prostatic growth and enlargement is dihydrotestosterone. Men who have 5α-reductase deficiency7 , 8 and who therefore cannot…
UR - http://www.scopus.com/inward/record.url?scp=0026806486&partnerID=8YFLogxK
U2 - 10.1056/NEJM199210223271701
DO - 10.1056/NEJM199210223271701
M3 - Article
C2 - 1383816
AN - SCOPUS:0026806486
SN - 0028-4793
VL - 327
SP - 1185
EP - 1191
JO - New England Journal of Medicine
JF - New England Journal of Medicine
IS - 17
ER -