title: Endocrine therapy for benign prostatic hyperplasia in the 90's.
abstract: Endocrine therapy by means of castration for benign prostatic hyperplasia was introduced already in the middle of the 19th century. The technique was never popularized and was abandoned following the introduction of safe surgical techniques. In the second half of this century, small series of various endocrine treatments have been reported, mainly using progestational agents. The hormone dependency of the prostate is unique, since testosterone itself is not very active on the prostate cells but has to be converted to 5 alpha-dihydrotestosterone, which is almost ten times as effective an androgen in the prostate cell. By blocking this conversion, highly specific antiandrogenic effect will be obtained in the prostate but not in other organs of the body. The first 5 alpha-reductase inhibitor, finasteride, has proven effective in reducing prostate DHT. In large clinical trials, it has shown to reduce prostate size, improve urinary flow and reduce symptom score, statistically significantly better than placebo. The effect is sustained over at least 3 years. In a double-blind, randomized, placebo-controlled study over 2 years, patients were similarly improved in the finasteride group, whereas they deteriorated in the placebo group. This indicates that finasteride is able to halt the progression of the natural course of benign prostatic hyperplasia. Benign prostatic hyperplasia, generally believed to be a stromal disease, is potentially dependent on estrogens for its development. By blocking aromatization of testosterone to estrogen in the prostate cells, a hypothetical beneficial effect on the disease process should be gained. Results from phase II-studies have been promising. However, in placebo-controlled studies, aromatase inhibitors did not perform better than placebo.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Urology, Karolinska Hospital, Stockholm, Sweden.
authors.forename: P
authors.initials: P
authors.lastname: Ekman
mesh_terms: D000735:Androstenedione / Q000031:analogs & derivatives* / Q000627:therapeutic use; D047072:Aromatase Inhibitors; D018849:Controlled Clinical Trials as Topic; D004311:Double-Blind Method; D004791:Enzyme Inhibitors / Q000627:therapeutic use; D018120:Finasteride / Q000627:therapeutic use*; D006801:Humans; D008297:Male; D010919:Placebos; D011470:Prostatic Hyperplasia / Q000188:drug therapy* / Q000503:physiopathology; D013738:Testolactone / Q000627:therapeutic use*
chemical_list: D047072:Aromatase Inhibitors; D004791:Enzyme Inhibitors; D010919:Placebos; D000735:Androstenedione; D018120:Finasteride; C048751:atamestane; D013738:Testolactone