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At least 433 records · Page 24Linked to original sources
PubMed1988

[Therapy of prostatic cancer with cyproterone acetate].

45 patients with recently detected prostatic cancer were treated with cyproterone acetate (CPA) at a dosage of 100 mg/die. 25 patients underwent primary orchiectomy and consecutive treatment with 200 mg CPA/die. In 44.4% of the 45 patients who underwent monotherapy with 100 mg CPA/die progression of cancer was observed 10.8 months after beginning of treatment on average 55.6% of these patients showed a remission or stabilisation. 7 patients died, 4 certainly due to prostatic cancer. In the 25 patients who underwent orchiectomy and treatment with 200 mg CPA/die, 92% showed a remission. One patient of this group died, but not as a result of cancer. Based on the present data it may be concluded that treatment of inoperable prostatic cancer with 100 mg CPA as monotherapy is not indicated in patients with poorly differentiated tumours. Combination therapy--in addition to other possibilities of contrasexual therapy in prostatic cancer--seems to be of high efficacy.

Aged↗
PubMedDate not supplied

Effects of combined hypophysectomy and cyproterone acetate on the adrenal chromaffin cells of the rat. Evidence for postnatal migration of adrenal chromaffin cells.

A light and electron-microscopic study was performed concerning the effects of hypophysectomy (HP) followed by cyproterone acetate (CA) treatment on the adrenal chromaffin cells of the rat. The latter drug is reported to interfere with steroid biosynthesis. When given following HP, CA was found to induce degeneration in the inner cells of the zona fasciculata and a marked fall in the blood corticosterone level. The adrenal chromaffin cells which were depleted after the administration of reserpine at the beginning of the experiment failed to recover two weeks later. In addition, some of the depleted chromaffin cells migrated towards the outer cells of the zona fasciculata, had the appearance of pheochromoblasts and showed features of increased synthetic activity. The results are discussed in the light of the generally accepted functional relationship between the cells of the adrenal cortex and the medulla and following a marked fall in the concentration of blood corticosterone, a chemobiotaxis is suggested between the chromaffin and adrenal cortical cells.

Adrenal Cortex↗
PubMed1981

Antiandrogenic effects of cyproterone acetate and chloromadinone acetate on the rat hypothalamus as revealed by electroencephalographic responses.

Bipolar stainless steel electrodes were implanted stereotaxically into given hypothalamic and cortical regions of the brain of 48 rats. The animals were divided into two groups of equal numbers and the electrical activity of the given regions was recorded electroencephalographically (EEG). The effect of the acute and chronic administration of cyproterone acetate (CPA) or chloromadinone acetate (CHA), in doses inducing sterility, on EEG activity were observed. Apart from slight inhibition in the preoptic region, no appreciable EEG changes were found after CPA, while CHA reduced the discharge frequency in both the preoptic and the posterior hypothalamus. These findings can be attributed to the presence of two different types of androgen receptors in the hypothalamus.

Androgen Antagonists↗
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↗
PubMedDate not supplied

[The response to gonadotropin-releasing hormone in hirsutism after treatment with cyproterone acetate].

The authors studied the response of the luteinizing hormone (LH), follicle-stimulating hormone (FSH), proclatin (PRL) and testosterone (T) to the intravenous injection of 100 microgram of synthetic gonadotropin-releasing hormone (GnRH) in hirsute women in the follicular phase, prior to and after the administration of cyproterone acetate (CPA). The GnRH stimulation before and after the CPA therapy induced a significant increase in plasma LH and FSH levels (P less than 0.01) and a significant drop in the plasma PRL concentration (p less than 0.05). Unchanged plasma T levels were observed during the test, prior to the CPA administration. Following the CPA application there was a significant increment of basal plasma PRL levels (p less than 0.05) and a significant drop of plasma FSH levels (p less than 0.01). No significant changes were observed, however, in LH and T levels. During the GnRH stimulation, after the administration of CPA, a significant decrease in T levels was noted (p less than 0.01). Considering basal concentrations of the hormones studied and the response to the LHR stimulation test, CPA was found to have no beneficial effect on the hypothalamic-pituitary dysfunction typical of androgenization in females.

Adolescent↗
PubMed1983

[Treatment of hirsutism with cyproterone acetate and percutaneous estradiol].

One-hundred and fifty hirsute women (68 with type I or II polycystic ovary syndrome and 82 with idiopathic hirsutism) were treated for periods of 6 to 48 months with oral cyproterone (CPA), a drug with peripheral antiandrogenic, antigonadotrophic and progestative properties, and 17 beta-estradiol given percutaneously to ensure estrogenic impregnation. CPA was administered in daily doses of 50 mg from day 5 to day 25 of the menstrual cycle, and E 2 (3 mg/day) from day 16 to day 25. The dramatic regression of hirsutism observed after 3 to 6 months of treatment was paralleled by a marked decrease of plasma testosterone and delta 4-androstenedione levels and a decrease of the androgen-dependent skin testosterone 5 alpha-reductase. The CPA-percutaneous E 2 combination also has contraceptive properties. Beside its remarkable therapeutic effectiveness, it has the advantages of avoiding the adverse reactions reported with higher doses of CPA and the metabolic and vascular effects of synthetic estrogen administered orally.

Administration, Oral↗
PubMed1983

[Precocious puberty associated with Von Recklinghausen's disease. Developmental follow-up under cyproterone acetate treatment].

Authors describe a case of a boy aged 8-10/12 years with precocious puberty associated with Von Recklinghausen's disease. He was treated with cyproterone acetate (100 mg/m2/24 h oral doses) and controlled for a period of two years. He shows very few effects of puberal physical signs and improvement of his sexual behavioral area. They have evaluated growth evolution by different parameters and couldn't appreciate any improvement because of the advanced bone age (13-6/12 years) when treatment was started.

Adult↗
PubMed1983

[The mechanism of action of cyproterone acetate in the treatment of hirsutism].

Cyproterone acetate (CPA) in association with percutaneously offinistered estradiol has been used for the treatment of 150 hirsute patients for periods ranging from 6 months to 3 years. A spectacular clinical improvement ensued. Plasma testosterone (T) and androstenedione (A) fell from 69 +/- 24 to 33 +/- 8 and 210 +/- 103 to 119 +/- 25 ng/dl (mean +/- SD) respectively after 3 months of treatment and remained low thereafter. In contrast, T glucuronide (Tg) and 3 alpha-androstanediol (Adiol) remained high during the whole course of treatment: 37 +/- 9 and 115 +/- 43 micrograms/24 h respectively. In vitro T 5 alpha-reductase activity (5 alpha-R) in pubic skin decreased from 147 +/- 34 to 79 +/- 17 fmol/mg skin after 1 year of treatment. To elucidate the discrepancy between plasma and urinary androgens levels, T production rate (PR) and metabolic clearance rate (MCR) were measured with the constant infusion technique in 6 patients before and after 6 months of treatment. PR decreased from 988 +/- 205 to 380 +/- 140 micrograms/24 h (mean +/- SD). In contrast MCRT increased from 1275 +/- 200 to 1632 +/- 360 1/24 h; this increase in MCRT explains the striking plasma T concentration fall and the high TG and Adiol excretion relative to the decrease in PR. Antipyrine clearance rate (n = 8) increased from 36.3 +/- 5.2 to 51.5 +/- 7.4 ml/min whereas urinary/6 beta hydroxycortisol remained unchanged. In conclusion, CPA acts through several mechanisms:(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1983

[Cyproterone acetate. 15 cases of hirsutism treated for 1 year].

Fifteen women with idiopathic hirsutism (N = 11) or hirsutism with androgen excess (N = 4) were treated by Cyproterone acetate orally (50 mg from the 5 th to the 25 th day of the menstrual cycle) and Ethinyl Estradiol (day 15-25). Hirsutism was improved in 86% of cases with progressive improvement at 3, 6, 12 months. At 12 months, the clinical score for hirsutism was 56% of the original score. Disturbance of menstrual cycles was more frequent than reported with Hammerstein's pattern of treatment. Clinical and biological tolerance was good. delta 4 androstenedione decreased significantly at 6 months (respectively 2,26 ng/ml - 1,25 ng/ml). There was no significant decrease of plasma testosterone. Result of B 1-24 corticotropin test remained normal after 12 months of treatment.

Administration, Oral↗
PubMed1983

Treatment of idiopathic hirsute women with two combinations of cyproterone acetate.

The effect of two combinations, reverse sequential and monophasic, with cyproterone-acetate, have been studied in a group of 14 women suffering from idiopathic hirsutism. The results obtained prove that both combinations have ovulation blocking properties, by decreasing the FSH, LH, progesterone and oestrogen levels, but also have favourable effects in the treatment of hirsutism. The reverse sequential combination showed an increase in the prolactin figures, although these figures were within normal limits.

Adolescent↗
PubMed1984

[Different behavior of the rat vas deferens of castrated animals and those treated with cyproterone acetate].

The effects of castration and treatment with the antiandrogen cyproterone acetate (CPA) on the responses of the vas deferens of the rat induced by phenylephrine, KCl and BaCl2 has been studied. Both castration and CPA induced a spontaneous motility in the rat vas deferens. Castration produces a decrease of the response amplitude induced by phenylephrine and KCl and an increase of those induced by BaCl2 in animals killed 30 days after castration. CPA increases the response amplitude induced by phenylephrine and KCl without modifying those induced by BaCl2. These results suggest that the antiandrogen CPA produces modifications qualitatively different from castration.

Animals↗
PubMed1984

[Serum testosterone determination in the antiandrogen therapy of sexual deviations with cyproterone acetate (preliminary report of experiences)].

Total testosterone concentrations in the serum of patients treated with antiandrogens were measured by means of an industrially produced radioimmunological testosterone assay kit (VEB Sächsisches Serumwerk Dresden). Antiandrogen therapy using cyproterone acetate (Androcur) leads to a reduction in serum testosterone concentration which is significant at the p less than 0.01 level. The data suggest that testosterone concentrations vary inversely with increasing Androcur dosage; they are around 7 nmol/l at the doses conventionally administered. The testosterone concentrations obtained under depot-Androcur treatment suggest that intervals between injections should be less than 10 days.

Adolescent↗
PubMed1981

Effects of cyproterone acetate on growth and androgen metabolism of rat ventral prostate transplants.

Cyproterone acetate (CA0 (10 or 20 mg kg-1 daily for 5 days) injected into castrate rats supplemented with testosterone propionate (TP) caused a significant decrease in ventral prostate weights in situ; no inhibitory effects were noted in transplant weights. CA failed to significantly inhibit DNA in either the in situ prostate or transplant, but his anti-androgen caused a significant decrease in the formation of 3H-dihydrotestosterone and 3H-androstanediol from radioactive testosterone in the in situ organ. Histologically, CA caused a decrease in epithelial cell secretory activity.

Androgens↗
PubMed1981

Spermatogenesis and SRBC haemolysin formation in various inbred mouse strains treated with cyproterone acetate.

The synthetic steroid antiandrogen cyproterone acetate (CA) was administered subcutaneously to adult male mice of the inbred strains B10, B10.D2, B10.BR and C57BL/6 either as a single dose of 1 mg or as 10 daily doses of 0.5 mg. At 48 h after a single dose of CA, the thymus and spleen weights were markedly reduced and the morphology of the thymus was changed (depletion of cortex lymphocytes) in some strains. At 6 h and at 12 days after the 10th dose of CA, thymuses in males of all strains were markedly diminished with a histologically apparent involution affecting the cortex, as well as the medulla and reticuloepithelial tissue. Spleen weights in males of some strains were also significantly lower. SRBC haemolysin titres at 12 days after the 10th dose and spermatogenesis at 6 h and at 12 days after the 10th dose were significantly decreased in males of all strains; in none of the males was sterility produced by the CA doses used, however, Indications of the strain differences could only be seen in the onset and duration of the damage to the spleen and the corresponding decrease in haemolysin formation. The importance of the consequences of short-term administration of CA is discussed in terms of potential risks for long-term administration of CA in the regulation of male fertility.

Animals↗
PubMed1981

[Decrease of the sebum excretion rate and improvement of acne in acneic women treated with the association: cyproterone acetate-ethinyl estradiol (author's transl)].

37 women have received during a total of 429 cycles (mean 12 cycles/patients) an association containing cyproterone acetate 2 mg and ethinyl estradiol 0.05 mg. A marked improvement in the clinical symptoms (acne 35 cases) has been observed. The sequential determination of the sebum excretion rate has been made in the same time (150 measurements) and revealed an important, early and durable decrease in the sebum excretion rate. The respective role of the CA and EE has been analysed in a second trial. It seems that the antiandrogen might play a role in the clinical improvement and in the reduction of the sebaceous flow.

Acne Vulgaris↗
PubMed1981

Cyproterone acetate treatment of females with hyperandrogenism.

Five females with idiopathic hirsutism, ten with adrenogenital syndrome, four with acne vulgaris, and three with Stein-Leventhal syndrome were treated for nine months with large or small doses of cyproterone acetate (100 or 2 mg daily, respectively) in combination with oestrogen. The drug had a good effect on the acne vulgaris and moderated the hirsutism. In the various patient groups the serum testosterone level was decreased to between 58.6% (+/- 28.7% S.E.) and 10.8% (+/- 8.2% S.E.) of the basal value. No essential difference in effectiveness was observed between the large and small doses. Based on study of the side-effects, it is recommended that laboratory liver tests are used for control.

17-Ketosteroids↗
PubMed1978

Treatment of acne with cyproterone acetate and ethinyl estradiol.

Tablets containing 2 mg cyproterone acetate and 0.05 mg ethinyl estradiol in a calendar package of 21 days were used as an oral contraceptive to treat acne. The series comprised 20 patients. The women were 18--43 years of age, and all had acne which had previously been resistant to therapy. The treatment was continued for 6 months. Serum testosterone, 17-OHCS, 17-KS, serum ALAT and gamma-GT were recorded prior to the treatment at 3 and 6 months. Ten patients responded well to the treatment, 5 responded moderately well, 3 experienced no change, and 2 became worse. The serum testosterone level fell during the therapy and the ALAT level rose, though only one pathological ALAT value was recorded.

17-Hydroxycorticosteroids↗
PubMed1999

Cleavage of poly(ADP-ribose) transferase during p53-independent apoptosis in rat liver after treatment with N-nitrosomorpholine and cyproterone acetate.

The aim of this work was to study the role of the tumor suppressor p53 and of poly(ADP-ribose) transferase (pADPRT) in the control of hepatocyte apoptosis in two different in vivo models, i.e., during the process of tumor initiation by the genotoxin and cytotoxin N-nitrosomorpholine (NNM) and after withdrawal of the hepatomitogen cyproterone acetate (CPA). Treatment with NNM induces apoptosis followed by necrosis and regenerative DNA synthesis. At the first wave of apoptosis 12 h after NNM application, no p53 expression could be detected by immunohistochemical analysis and immunoblotting. However, 24 h after treatment, numerous p53-positive hepatocyte nuclei were detected, whereas hepatocytes in early and later stages of apoptosis were always negative. Simultaneously with the increased p53 levels, p21 protein was induced. This was accompanied by a block in replicative DNA synthesis, as detected by proliferating-cell nuclear antigen immunostaining. Concomitantly with the increase in apoptosis, dramatic degradation of the nuclear enzyme pADPRT was observed, as evidenced by immunoblotting and activity blotting. The decrease in pADPRT enzymatic activity observed 12 h after treatment coincided with the greatest extent of pADPRT cleavage. One prominent cleavage product was 64 kDa, suggesting that granzyme B was involved in pADPRT degradation. In the second in vivo model we used, i.e., withdrawal of treatment with the hepatomitogen CPA, apoptosis of excessive hepatocytes but no necrosis occurs. Again, no induction of p53 expression could be detected in the liver even at the maximum level of apoptosis, whereas a strong correlation between induction of apoptosis and cleavage of pADPRT to a 64-kDa fragment was observed. These results from whole-animal experiments strongly suggest that the induction of apoptosis in rat liver after genotoxic and cytotoxic damage and during regression of hyperplasia is driven by a p53-independent pathway but is accompanied by cleavage of pADPRT.

Animals↗