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PubMed1982

The effects of orchidectomy, estrogens, and cyproterone acetate on plasma testosterone, LH, and FSH concentrations in patients with carcinoma of the prostate.

The peripheral plasma concentrations of testosterone, luteinising hormone (LH) and follicle stimulating hormone (FSH) were determined in 46 patients (age 51-86 years) with cytologically confirmed prostatic carcinoma. Treatment consisted of subcapsular orchidectomy (15 cases) or estrogen medication (16 cases) or cyproterone acetate (15 cases). The determinations were made before and 2 weeks and 2 months after treatment was initiated. No correlation was found between the pretreatment levels of testosterone and gonadotrophins and the local extent of the primary tumor or the degree of malignancy. Nor was there any correlation between hormonal level, presence of metastases or patient age. Orchidectomy and estrogen medication both resulted in very low plasma testosterone levels, corresponding to 15% of the pretreatment values. This proportion was 28% in the group treated with cyproterone acetate. Orchidectomy was followed by significant increase in the levels of LH and FSH. Estrogen treatment resulted in suppression of the LH levels to 40% and of FSH to 14% of the pretreatment values. The corresponding decreases in response to cyproterone acetate were 65 and 35%. The results indicate that reduction in gonadotrophin secretion is the primary mechanism in the lowering of testosterone levels produced by treatment with estrogens or cyproterone acetate.

Aged↗

PubMedDate not supplied

Biochemical analysis of rat testis and epididymis after cyproterone acetate treatment.

Male rats were treated with cyproterone acetate (10 mg/day/rat) for 13, 26 and 39 days. A marked decrease in proteins, nucleic acid and phospholipid content was recorded in testis and epididymis after CA treatment. However, a significant increase in glycogen and cholesterol content in testis and epididymis was observed after CA treatment.

Animals↗

PubMed2003

Effects of the antiandrogens, vinclozolin and cyproterone acetate on gonadal development in the Japanese medaka (Oryzias latipes).

This study was focused on determining the effects of exposure to antiandrogens on the gonadal development of Japanese medaka (Oryzias latipes). Test compounds included the fungicide, vinclozolin and the clinical antiandrogen, cyproterone acetate. Newly hatched medaka were exposed to aqueous solutions of vinclozolin (2500 microg/l) and the vinclozolin fungicide formulation, Ronilan (1000 and 5000 microg/l) and cyproterone acetate (1 and 10 microg/l), for 3 months. Histological evaluation of the gonadal tissues of exposed fish indicated that the 5000 microg/l concentration of the vinclozolin formulation (Ronilan) induced a low incidence of intersex (i.e. testis-ova) and the 2500 microg/l concentration of vinclozolin-affected spermatogenesis in males. Also, the vinclozolin treatments induced moderate ovarian atresia. Cyproterone acetate also induced a low incidence of testis-ova, but in contrast to the vinclozolin treatment the amount of ovarian tissue in the testis-ova was equal to or greater than the amount of testicular tissue. In the cyproterone acetate treatments, both oogenesis and spermatogenesis were moderately inhibited at all test concentrations. The results of this study indicate that antiandrogens have the potential to alter testicular development and gametogenesis in fish. However, research is needed to determine the mechanisms by which antiandrogens affect fish.

Analysis of Variance↗

PubMedDate not supplied

A long-term study of the epididymal- and fertility-suppressing effects of cyproterone acetate in the mouse.

The influence of cyproterone acetate (CA) (0.1 mg/mouse/day) on the epididymis and male fertility was analyzed in a long-term study in the Swiss albino cc strain. CA inhibits epididymal function in all segments as measured by organ weights, protein content and beta-glucuronidase activity. This antiandrogen also suppresses male fertility. It is important to note that the low dose of CA, used in this study, does not affect spermatogenesis. The effects of CA on epididymis and fertility are reversible and the magnitude of recovery or the period (in days) required for a significant recovery after the discontinuation of CA were seemingly directly proportional to the duration of antiandrogen treatment.

Animals↗

PubMed1992

Androgens and androgen-receptors in prostate tissue from patients with benign prostatic hyperplasia: effects of cyproterone acetate.

Testosterone, 5 alpha-dihydrotestosterone and cyproterone acetate (CPA) were estimated in samples of prostate tissue, obtained from benign prostatic hyperplasia (BPH) patients who were or were not pretreated with CPA. Furthermore, these steroids were estimated in various fractions of the BPH tissue, and the number of nuclear androgen-receptor sites was determined. CPA-treatment caused a 4-fold, significant suppression of 5 alpha-dihydrotestosterone levels in total prostate tissue and its subfractions, without affecting testosterone levels or the androgen-receptor contents of the nuclear extracts. Nuclear concentrations of CPA were twice as high as those of 5 alpha-dihydrotestosterone. It is concluded that effects of CPA may have been caused through a combination of the following mechanisms: (1) suppression of peripheral androgen levels; (2) competition with androgens for (nuclear) androgen-receptors; and (3) suppression of prostatic 5 alpha-reductase.

5-alpha Reductase Inhibitors↗

PubMed1987

Inhibition of rat testicular 17 alpha-hydroxylase and 17,20-lyase activities by anti-androgens (flutamide, hydroxyflutamide, RU23908, cyproterone acetate) in vitro.

Flutamide, hydroxyflutamide, RU23908 and cyproterone acetate (CPA) inhibited rat testicular microsomal 17 alpha-hydroxylase and 17,20-lyase activities in vitro. The Km of [3H] progesterone for 17 alpha-hydroxylase was 45 +/- 0.62 nmol/l (+/- SEM, n = 12) and the Km of [3H] 17 alpha-hydroxyprogesterone for 17,20-lyase was 192 +/- 0.42 nmol/l (+/- SEM, n = 12). The Ki values for 17 alpha-hydroxylase, determined from Lineweaver-Burk plots were 102 +/- 3.2 mumol/l (+/- SEM, n = 6), 363 +/- 3.8 mumol/l (+/- SEM, n = 6), 118 +/- 1.4 mumol/l (+/- SEM, n = 6) and 123 +/- 2.1 mumol/l (+/- SEM, n = 6) for flutamide, hydroxyflutamide, RU23908 and CPA respectively. Flutamide and CPA were mixed-type inhibitors, whereas hydroxyflutamide and RU23908 were competitive inhibitors of 17 alpha-hydroxylase activity. Ki values for 17,20-lyase were 33 +/- 3.1 mumol/l (+/- SEM, n = 6), 112 +/- 3.1 mumol/l (+/- SEM, n = 6), 69 +/- 4.4 mumol/l (+/- SEM, n = 6) and 71 +/- 3.2 mumol/l (+/- SEM, n = 6) for flutamide, hydroxyflutamide, RU23908 and CPA, respectively. Inhibition was found to be competitive in each case. Although the characteristic action of anti-androgens is at the receptor level, these results demonstrate that anti-androgens may also have inhibitory effects on androgen biosynthesis which could prove to be of clinical significance.

Aldehyde-Lyases↗

PubMed1996

Carcinogenicity of cyproterone acetate in the mouse.

The synthetic progestin cyproterone acetate (CPA) has been shown to be a hepatocarcinogen in the rat, but little is known of its effects in mice. A 52 week CPA study in the mouse strain C57Bl/10J has been reported not to produce liver tumours, although CPA induced significant liver enlargement and induction of the mixed function oxidase CYP3A. The present study is a further investigation of the effects of CPA in mice of the C57Bl/10J strain dosed for 104 weeks. A group of 40 mice/sex were fed 800 p.p.m. CPA in the diet for 104 weeks with a control group of eight/sex. Mortality was high in females after 40 weeks due to hormonal effects in the uterus; no female and only four CPA-dosed males survived to 104 weeks. Liver cell hypertrophy with increased fat and glycogen and single cell or small multifocal areas of hepatocellular necrosis were universal. Proliferating cell nuclear antigen demonstrated an increase in proliferating cells within tumours and within the non-tumour bearing liver of CPA-dosed mice compared with normal livers of control mice. Hepatocellular tumours developed in 44% of males and 22% of females dosed with CPA, compared with none in the controls (the strain has a low, <10%, incidence of spontaneous liver tumours compared with other mouse strains). In addition, over 85% of both sexes dosed with CPA developed adenomatous polyps of the pyloric antrum and pancreatic islet cell hyperplasia, shown by immunostaining to be chiefly of insulin-secreting cells. Adrenocortical atrophy was also observed with other widespread effects in the endocrine system. The results suggest that the liver tumours, as in the rat, are likely to be related to effects on liver growth and mitogenesis. It is suggested that the tumours of the stomach and the pancreatic islet cell hyperplasia are manifestations of the effects of CPA in the endocrine system.

Adenomatous Polyps↗

PubMed1980

Pubertal development in girls with sexual precocity after discontinuation of treatment with cyproterone acetate.

Twenty-four girls with sexual precocity who had been treated with cyproterone acetate were followed for periods from 1 to 8 1/2 years after the discontinuation of therapy. It was found that their further pubertal development and the resumption or appearance of menstruation followed a natural course within the wide limits of physiological variability. It is concluded that puberty resumes its natural course following cessation of treatment with cyproterone acetate, and it is assumed that the reproductive ability of these patients will not be affected.

Adolescent↗

PubMed1984

Treatment of severe hirsutism resulting from hyperandrogenism with the reverse sequential cyproterone acetate regimen.

Women with severe hirsutism resulting from hyperandrogenism often respond poorly to suppressive therapy aimed at decreasing adrenal or ovarian androgen production. Antiandrogens, such as cyproterone acetate, prevent androgens from expressing their activity at target sites by inhibiting the formation of the androgen/cytosol binding protein complex. Seven severely hirsute hyperandrogenic women were treated for six months with the reverse sequential cyproterone acetate regimen. Pretreatment plasma testosterone (T) levels were elevated in all subjects, and sex hormone binding globulin (SHBG) binding capacity was depressed. A free testosterone index, as assessed by the T/SHBG ratio, was markedly elevated. A marked and significant decrease in T levels and the T/SHBG ratio occurred during the first two cycles of treatment (p less than 0.01). Hirsutism grading assessed by the semiquantitative method of Ferriman and Gallwey did not change significantly until four months after the beginning of therapy but improved by six months of treatment. There was a marked antigonadotropic effect in terms of suppression of LH and FSH. The reverse sequential cyproterone acetate regimen produces rapid normalization of the plasma T, SHBG and free testosterone index, but resolution of the hirsutism is slower and requires several months of therapy.

Adult↗

PubMed1975

The LH response to LH releasing hormone in children with true isosexual precocious puberty treated with cyproterone acetate.

Fourteen girls and one boy with isosexual precocious puberty were submitted to LHRH stimulation tests, during and without therapy with cyproterone acetate. In addition, fourteen girls with isosexual precocious puberty not receiving any therapy were tested and served as controls. It was found that cyproterone acetate induces suppression of the responsiveness of the pituitary gland to secrete LH on LHRH stimulation. Daily oral therapy was found to be more effective than the regimen of intramuscular depot injections. These findings demonstrate that cyproterone acetate has an antigonadotrophic effect.

Administration, Oral↗

PubMed1992

The position of cyproterone acetate (CPA), a steroidal anti-androgen, in the treatment of prostate cancer.

Cyproterone acetate is a steroidal anti-androgen that blocks the androgen-receptor interaction and reduces serum testosterone through its weak anti-gonadotropic action. It can be regarded as the only anti-hormone that causes complete androgen blockade as monotherapy. Many animal experiments and several clinical phase II and phase III trials have demonstrated that it deserves a place in the endocrine therapy of advanced prostate cancer, particularly for those patients who find orchidectomy unacceptable and who do not have known cardiovascular risks. Additionally, cyproterone acetate can be used safely to prevent disease flare when a luteinizing hormone releasing hormone analog is the drug of choice and to suppress hot flashes in response to LHRH agonists or after orchidectomy.

Androgen Antagonists↗

PubMedDate not supplied

Effects of low doses of cyproterone acetate on sperm morphology and some other parameters of reproduction in normal men.

Cyproterone acetate was given to three healthy men in a dosage of 10 mg per day for 8-14 weeks. The effects on sperm count, morphology, motility and vitality was followed weekly and compared with the effects of 25 mg daily in another case. Sperm morphology included the study of live spermatozoa separately. The effects on serum levels of FSH, LH, testosterone and oestrogens was also studied. With respect to sperm count and morphology a dose-effect relationship is indicated. Abnormalities within tails and midpieces of live spermatozoa appear early and may predict sterility before azoospermia develops. FSH and oestrogens were comparatively more depressed than LH and testosterone. The results indicate that cyproterone acetate may have an androgenic (or gestagenic) effect on the hypophyseo-hypothalamic level in addition to an antiandrogenic effect on gonads and their accessory organs.

Adult↗

PubMed1995

Nuclear matrix condensation and c-myc and c-fos expression are specifically altered in culture rat hepatocytes after exposure to cyproterone acetate and phenobarbital.

Regenerative or hyperplastic growth promotes carcinogenesis and can be induced by many nongenotoxic carcinogens. The mitogenic potential of the rodent liver tumor promoters, cyproterone acetate and phenobarbital was investigated in primary rat hepatocyte cultures. Two premitotic markers were analyzed, the expression of two immediate-early genes (c-fos and c-myc) and the decrease in the nuclear quinacrine dihydrochloride fluorescence indicative for a G0-G1 cell cycle shift. C-fos expression and decrease in nuclear fluorescence could be induced by both chemicals, phenobarbital being the lesser potent, whereas c-myc expression was only inducible by cyproterone acetate. In situ hybridization with c-myc revealed that both chemicals enhanced c-myc mRNA levels in individual cells, however the number of responding hepatocytes was increased by cyproterone acetate only. The chemical-induced premitotic changes in hepatocytes were highly specific in terms of affected genes and ploidy levels of responding hepatocytes.

Animals↗

PubMed2001

Comparison of the effect on acne with a combiphasic desogestrel-containing oral contraceptive and a preparation containing cyproterone acetate.

OBJECTIVE: To investigate the effect of a combiphasic oral contraceptive containing ethinylestradiol and desogestrel (combiphasic EE/DSG) on acne, compared with a preparation containing ethinylestradiol and cyproterone acetate (EE35/CPA). METHODS: An open, randomized, group-comparative, multicenter study was carried out, with 172 women randomized to treatment with either combiphasic EE/DSG (25 microg desogestrel and 40 microg ethinylestradiol for 7 days followed by 125 microg desogestrel and 30 microg ethinylestradiol for 15 days) or EE35/CPA (2.0 mg cyproterone acetate and 35 microg ethinylestradiol for 21 days). Assessments were performed at pretreatment and after cycles 3 and 6. RESULTS: The number of comedones, papules, pustules and nodules significantly decreased in both groups over the 6-month study. Compared with pretreatment (= 100%), the relative numbers of comedones, papules, pustules and nodules at cycle 6 significantly decreased to 37%, 38%, 19% and 12.5% in the combiphasic EE/DSG group and to 24%, 36%, 17% and 1% in the EE35/CPA group, respectively. All reductions were statistically significant (p < or = 0.003) at both cycles 3 and 6, except for nodules at cycle 6 with combiphasic EE/DSG, which probably resulted from differences between the treatment groups at baseline. There were no statistically significant differences between the two treatments. In both groups, the majority of women with severe acne shifted to a less severe acne category. CONCLUSIONS: Combiphasic EE/DSG progressively reduced the number and severity of acne lesions during the six cycles of treatment. The reduction in acne with the combiphasic oral contraceptive was comparable to a preparation containing the antiandrogen cyproterone acetate.

Acne Vulgaris↗

PubMed1994

[Long-term therapy of central precocious puberty in girls with the gonadoliberin analog D-Trp-6-LHRH after prior therapy with cyproterone acetate].

A group of five girls with central precocious puberty (CPP) (four girls with idiopathic CPP and one girl with organically conditioned CPP) were treated for a mean period of 17 months (12-20 months) with an agonist of gonadoliberine (aGnRH) D-Trp-6-LHRH(Triptorelin), 60-100 micrograms/kg by the i.m. route, every four weeks. The calendar age (CA) of the girls was at the onset of aGnRH treatment 7.3 +/- 0.7 years, the bone age (BA) 9.6 +/- 1.0 years. Previously Cyproterone acetate treatment administered for an average period of 26 months (4-56 months) was gradually discontinued in the course of 12 weeks. After 12 months aGnRH treatment the growth rate slowed down from 8.1 #/- 2.1 to 6.2 +/- 1.7 cm/year (NS). The bone age increment per calendar year declined at the end of the first year of treatment from 1.7 +/- 0.8 to 0.94 +/- 0.4 (NS). Prediction of the adult height did not change in the course of one year (before aGnRH therapy 158.6 +/- 5.3 after one year's treatment 159.0 +/- 5.3 cm). In all girls premature maturing was arrested already during the original Cyproterone acetate treatment. With the exception of a single patient during aGnRH therapy progression was not recorded. In this girl with the idiopathic form of CPP the authors observed during regular Triptorelin administration, starting from the fourth month, clinical and biochemical manifestations of secondary therapeutic failure after termination of hitherto administered Cyproterone acetate treatment-"escape from treatment". Clinical and hormonal indicators improved after addition of Cyproterone acetate. This patient lacks typical symptoms suggesting McCune-Albright's syndrome.

Child↗

PubMed1983

Cyproterone acetate in treatment of post-orchidectomy hot flushes. Double-blind cross-over trial.

12 patients with troublesome hot flushes after orchidectomy (as a primary treatment for prostatic carcinoma) were treated with cyproterone acetate or placebo in a double-blind cross-over trial. The frequency of hot flushes was significantly reduced during the three weeks that cyproterone acetate (100 mg three times a day) was given. 5 patients complained of lassitude while on cyproterone acetate, but in none was it necessary to discontinue treatment.

Aged↗

PubMed1975

Effect of antiandrogen cyproterone acetate on the action of testosterone on mouse kidney.

The loss of endogenous testosterone in castrated male mice leads to a marked decrease in seminal vesicle and kidney tissue weight. 21 days' administration of exogenous testosterone abolished the effect of castration on the seminal vesicles and kidney tissue. The antiandrogen cyproterone acetate produced significant changes in the target tissue for androgens, i.e. in the seminal vesicles. In every case it blocked the action of both exogenous and endogenous testosterone on the seminal vesicles, but failed to block the "renotropic" action of testosterone, expressed as relative kidney weight. Contrary to its effect on the seminal vesicles, it did not influence relative kidney weight in normal animals. It likewise did not block the effect of exogenous testosterone on kidney tissue. The mechanism of the action of cyproterone acetate in androgen-dependent tissues is known to consist in inhibition of androgen binding to specific cell receptors in the target tissues. Some of the specific androgen receptors in mouse kidney are evidently different in character from those in the accessary sex glands, that being the reason why cyproterone acetate has an antiandrogenic, but not an antirenotropic effect. In agreement with experiments on rats, adrenal weight also decreases in mice after the administration of cyproterone acetate.

Animals↗

PubMed1985

[Therapy of virginal prostatic cancer with cyproterone acetate].

52 patients with virginal carcinoma of the prostate were treated with 100 mg cyproterone acetate during an observation period of 12 to 68 months (average 38.2 months). In 7 patients (13.5%) the therapy had to be stopped because of gastrointestinal intolerability. Of 45 patients in whom a relevant clinical statement was possible 44.4% showed a progression of the disease after a period of 3 to 30 months (on average 10.8 months). 95% of these patients had carcinomas with a higher degree of malignity (GII or GIII). From this is concluded that the monotherapy of the medium- to undifferentiated carcinoma of the prostate with cyproterone acetate is to be refused in this dosage.

Aged↗