Medium dose cyproterone acetate (CPA; 10 mg daily p.o.) was administered to 10 fertile men for 12 weeks. Hormonal measurements and semen analyses were performed before, during (4th and 12th week) and after CPA treatment. At the hypothalamo-pituitary level CPA significantly reduced the hypophyseal storage and synthesis capacity for gonadotropins. Basal LH and FSH concentrations were suppressed by 30% and 40%, respectively; while basal prolactin was elevated by 75%. The episodic fluctuations of peripheral gonadotropins remained unaffected. At the testicular level CPA significantly decreased basal testosterone and dihydrotestosterone concentrations by 70% and 50%, respectively. The pulsatile pattern of androgen secretion was abolished. CPA also inhibited spermatogenesis and motility. No serious clinical side effects were observed. All changes appeared to be completely reversible. It is concluded that medium dose CPA induces progestational/anti-gonadotropic effects at the hypothalamo-pituitary level in addition to its antiandrogenic action at the testicular level.
PIP: Cyproterone acetate (CPA) was administered orally in 10-mg daily doses (medium dose) to 10 fertile men for 12 weeks to determine its efficacy as a male contraceptive. Before, during, and after CPA treatment, hormonal parameters were assayed as were semen samples. Gonadotropin secretion and storage were significantly affected by medium dose CPA; basal luteinizing hormone and follicle stimulating hormone concentrations dropped by 30 and 40%, respectively, whereas prolactin was elevated by 75%. Overall fluctuations associated with these pituitary gonadotropins were unaffected, however, over the course of time (in ratio). When testosterone and dihydrotestosterone levels were measured, a significant effect of CPA on the testicular level was apparent, for the concentrations of these 2 androgens diminished by 70 and 50%, respectively, and the pulsating pattern of androgen secretion was eradicated by CPA treatment. Semen samples were analyzed and revealed an effect of CPA on spermatogenesis and sperm motility. Both functions were inhibited with medium dose CPA. Side effects were minimal, and CPA's effects appeared to be completely reversed after cessation of treatment. The mechanism of action of CPA seems to be induction of progestational/antigonadotropic effects occurring at the hypothalamo-pituitary level, as well as its antiandrogenic effects at the testicular site.