title: Suppression of spermatogenesis with desogestrel and testosterone pellets is not enhanced by addition of finasteride.
abstract: Conversion of testosterone to dihydrotestosterone (DHT) by the action of 5alpha-reductase can amplify androgen action. This may be of particular importance in the presence of low testosterone concentrations and may contribute to maintenance of spermatogenesis in a proportion of men receiving male contraceptive regimens. We therefore investigated whether the addition of finasteride, a 5alpha-reductase inhibitor, to a prototype male hormonal contraceptive regimen consisting of desogestrel (150 microg orally daily) and repeated administration of testosterone pellets (2 x 200 mg per 12 weeks) would enhance suppression of spermatogenesis. Sixteen normal men were randomized to receive either the standard androgen/progestogen treatment alone (control group) or with finasteride (5 mg orally daily-FIN group) for 24 weeks. Both groups showed profound suppression of spermatogenesis with azoospermia being obtained in 6 of 8 subjects in the control group and in 5 of 7 in the FIN group. There were no significant differences between the groups with respect to sperm concentrations. Significant suppression of luteinizing hormone and follicle-stimulating hormone was achieved within 2 weeks of treatment in both groups, while testosterone concentrations were maintained in the normal physiological range. DHT concentrations fell in both groups but were significantly lower in the FIN group. Gonadotropin and testosterone concentrations were similar for both regimens throughout the study. This study demonstrates the potential for long-term suppression of spermatogenesis using a combination of an oral progestogen with repeated administration of a depot preparation of testosterone. However, these data do not support the involvement of 5alpha-reductase in maintaining residual spermatogenesis during gonadotropin suppression for hormonal male contraception.
authors.affiliation: Contraceptive Development Network, Centre for Reproductive Biology, University of Edinburgh, United Kingdom.
authors.forename: D
authors.initials: D
authors.lastname: Kinniburgh
authors.forename: R A
authors.initials: RA
authors.lastname: Anderson
authors.forename: D T
authors.initials: DT
authors.lastname: Baird
mesh_terms: D058891:5-alpha Reductase Inhibitors; D000328:Adult; D003267:Contraception / Q000379:methods; D003280:Contraceptives, Oral, Synthetic / Q000008:administration & dosage*; D017135:Desogestrel / Q000008:administration & dosage*; D013196:Dihydrotestosterone / Q000008:administration & dosage / Q000097:blood; D004359:Drug Therapy, Combination; D004791:Enzyme Inhibitors / Q000008:administration & dosage*; D018120:Finasteride / Q000008:administration & dosage*; D012739:Gonadal Steroid Hormones / Q000008:administration & dosage* / Q000097:blood; D006062:Gonadotropins / Q000097:blood; D006801:Humans; D008297:Male; D009845:Oligospermia / Q000139:chemically induced; D011446:Prospective Studies; D013091:Spermatogenesis / Q000187:drug effects*; D013739:Testosterone / Q000008:administration & dosage* / Q000097:blood
chemical_list: D058891:5-alpha Reductase Inhibitors; D003280:Contraceptives, Oral, Synthetic; D004791:Enzyme Inhibitors; D012739:Gonadal Steroid Hormones; D006062:Gonadotropins; D013196:Dihydrotestosterone; D013739:Testosterone; D018120:Finasteride; D017135:Desogestrel