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Neuro-Chirurgie Jan 2023
Topics: Humans; Chlormadinone Acetate; Meningioma; Meningeal Neoplasms
PubMed: 36608450
DOI: 10.1016/j.neuchi.2022.101398 -
American Journal of Clinical Dermatology Sep 2011Acne vulgaris, hirsutism, seborrhea and female pattern hair loss (FPHL) are common disorders of the pilosebaceous unit (PSU). In some women with hyperandrogenemia, an... (Review)
Review
Acne vulgaris, hirsutism, seborrhea and female pattern hair loss (FPHL) are common disorders of the pilosebaceous unit (PSU). In some women with hyperandrogenemia, an excess of androgens at the PSU can lead to the development of these dermatological manifestations. These manifestations can cause many psychiatric and psychological implications, such as social fears and anxiety, and can adversely affect quality of life. High androgen levels at the PSU as a possible underlying cause of acne vulgaris, hirsutism, seborrhea and FPHL supports the rationale for using combined oral contraceptives for the management of these conditions in women. The purpose of this review is to describe these dermatological manifestations of the PSU and the management of these conditions through the use of the oral contraceptive ethinylestradiol/chlormadinone acetate (EE/CMA). EE/CMA 0.03/2 mg is a combined monophasic contraceptive pill with anti-androgenic properties. It is approved in Europe for contraception and has been investigated in phase III trials for the treatment of acne. EE/CMA was better than placebo and similar to another low-dose oral contraceptive (ethinylestradiol/levonorgestrel) in improving symptoms of acne in two phase III randomized controlled trials in patients with mild to moderate papulopustular acne. In addition, in trials investigating the contraceptive efficacy of EE/CMA, limited data suggest that there were also improvements in hirsutism, FPHL and seborrhea in small subgroups of patients. EE/CMA has a good safety profile. The most commonly reported adverse events are breast tenderness/pain, headache/migraine and nausea. Evidence in the literature indicates that the use of EE/CMA for the treatment of dermatological disorders under the control of androgens may be a valid treatment option. Further investigation is warranted.
Topics: Androgens; Chlormadinone Acetate; Contraceptives, Oral, Combined; Ethinyl Estradiol; Female; Hair Follicle; Humans; Quality of Life; Sebaceous Glands; Skin Diseases
PubMed: 21895044
DOI: 10.2165/1153874-S0-000000000-00000 -
Drugs 2004Ethinylestradiol/chlormadinone acetate 0.03/2mg (EE/CMA) is a combined monophasic contraceptive pill with antiandrogenic properties. In a large, noncomparative,... (Comparative Study)
Comparative Study
Ethinylestradiol/chlormadinone acetate 0.03/2mg (EE/CMA) is a combined monophasic contraceptive pill with antiandrogenic properties. In a large, noncomparative, multicentre trial (< or =24 cycles of treatment per woman) and two (6- and 12-cycle) postmarketing surveillance studies, EE/CMA was effective in preventing pregnancy. EE/CMA was significantly more effective than EE/levonorgestrel 0.03/0.15 mg/day in treating women with mild-to-moderate papulopustular acne of the face and related disorders in a randomised, single-blind, multicentre trial. EE/CMA was well tolerated in clinical trials and the postmarketing surveillance studies. Adverse events were those commonly reported with oral contraceptives. As expected, the most common menstrual disturbances were breakthrough bleeding, spotting and amenorrhoea.
Topics: Chlormadinone Acetate; Clinical Trials, Phase III as Topic; Contraceptives, Oral, Combined; Controlled Clinical Trials as Topic; Drug Therapy, Combination; Endometrium; Ethinyl Estradiol; Fallopian Tubes; Female; Germany; Humans; Pituitary Diseases
PubMed: 15025547
DOI: 10.2165/00003495-200464070-00005 -
The European Journal of Contraception &... 2005Chlormadinone acetate (CMA) is a derivative of naturally secreted progesterone that shows high affinity and activity at the progesterone receptor. It has an... (Review)
Review
Chlormadinone acetate (CMA) is a derivative of naturally secreted progesterone that shows high affinity and activity at the progesterone receptor. It has an anti-estrogenic effect and, in contrast to natural progesterone, shows moderate anti-androgenic properties. CMA acts by blocking androgen receptors in target organs and by reducing the activity of skin 5alpha-reductase. It suppresses gonadotropin secretion and thereby reduces ovarian and adrenal androgen production. CMA shows high contraceptive efficacy by inhibiting ovulation due to its ability to suppress or disrupt endogenous gonadotropin secretion and, by this, inhibits follicular growth and maturation. In addition, it suppresses endometrial thickness and increases the viscosity of cervical mucus. Pharmacokinetic studies have shown rapid and almost complete absorption after oral administration, and CMA is being bound to albumin rather than SHBG (Sex-Hormone-Binding-Globulin). Multiple dosing studies have demonstrated that steady state is reached by day 7 after oral administration with peak plasma concentrations in the region of 2 ng/ml. After a single dose of CMA the half-life time is around 34 hours and after multiple dose administration approximately 38 hours. Safety studies have indicated that CMA has no clinically relevant effect on a wide range of metabolic parameters in normal subjects. Further studies in groups at high thromboembolic risk have shown that CMA alone produces a relative risk of 0.8 which is not considered significant. These results indicated the potential for CMA to be combined with ethinylestradiol in an oral contraceptive which provides highly effective contraception and excellent cycle control.
Topics: Androgen Antagonists; Area Under Curve; Chlormadinone Acetate; Clinical Trials as Topic; Contraceptives, Oral, Synthetic; Female; Half-Life; Humans; Intestinal Absorption
PubMed: 16356876
DOI: 10.1080/13625180500434889 -
IARC Monographs on the Evaluation of... Dec 1979
Topics: Animals; Carcinogens; Chemical Phenomena; Chemistry; Chlormadinone Acetate; Dogs; Female; Humans; Male; Mice; Pregnancy; Rats; Teratogens
PubMed: 94586
DOI: No ID Found -
Contraception Apr 2009Chlormadinone acetate (CMA) is a derivative of progesterone (17alpha-acetoxy-6-chloro-4,6-pregnadiene-3,20-dione), first synthesized in 1961 and is used as an orally... (Review)
Review
Chlormadinone acetate (CMA) is a derivative of progesterone (17alpha-acetoxy-6-chloro-4,6-pregnadiene-3,20-dione), first synthesized in 1961 and is used as an orally effective progestogen in hormone replacement therapy (HRT), and in combination with ethinyl estradiol (EE) in contraception since 1999. Chlormadinone acetate has a strong progestogenic effect - about one-third higher than that of progesterone - and may vary depending on the previous effect of an estrogen, i.e., estrogens may promote the formation of progesterone receptors and proliferation of the endometrium. Like progesterone, it is anti-estrogenic and has no partial androgenic effect (at the doses used for contraception and HRT). In contrast to progesterone, it has a slight glucocorticoid effect, a pronounced anti-androgenic effect and no anti-mineralocorticoid effect. No pregnancy-maintaining effect of CMA has been demonstrated in humans. The anti-androgenic effect of CMA is presumed to be the result of both its binding to androgen receptors - competitively inhibiting the effect of endogenous testosterone and dihydrotestosterone - and the competitive inhibition of 5alpha-reductase. In this respect, dosing of CMA is crucial; agonistic effects are observed when doses are increased from those optimal for an antagonistic effect. Chlormadinone acetate has a strong anti-gonadotropic effect, through negative feedback on gonadotropin secretion, and has been used for more than 20 years alone for contraception in arterial risk patients. The clinical and metabolic tolerability of CMA has been demonstrated in numerous clinical studies with duration of treatment of up to 2.5 years. The more recent application of CMA as an oral contraceptive in combination with EE (Neo Eunomin, Belara) has proven highly successful, with studies reporting excellent contraceptive efficacy, high tolerability and adherence due to a good side effect profile and positive effects on preexisting dysmenorrhea, skin and hair conditions.
Topics: Chlormadinone Acetate; Contraceptives, Oral, Synthetic; Female; Humans
PubMed: 19272496
DOI: 10.1016/j.contraception.2008.10.017 -
Canadian Medical Association Journal Jul 1972There is an apparent discrepancy between the effects on the hemostatic mechanism of synthetic progestins alone and synthetic progestins in combination with synthetic...
There is an apparent discrepancy between the effects on the hemostatic mechanism of synthetic progestins alone and synthetic progestins in combination with synthetic estrogens. Coagulation studies were carried out on 21 patients treated with chlormadinone acetate 0.5 mg. on a continuous daily basis for 12 weeks in order to determine its effects on hemostasis. Unlike the standard estrogen/progestin contraceptive agents, this synthetic progestin appears to have no effect on the coagulation system as determined by standard laboratory tests.
Topics: Blood Coagulation; Blood Coagulation Factors; Blood Platelets; Chlormadinone Acetate; Contraceptives, Oral; Female; Fibrinogen; Fibrinolysis; Hemorrhage; Hemostasis; Humans; Immunodiffusion; Uterus
PubMed: 4114470
DOI: No ID Found -
British Medical Journal Dec 1969
Topics: Chlormadinone Acetate; Contraceptives, Oral; Female; Humans; Pregnancy
PubMed: 4188179
DOI: 10.1136/bmj.4.5684.686-b -
Gynecological Endocrinology : the... Jul 2016Chlormadinone acetate (CMA) is a progesterone derivative (17α-acetoxy-6-chloro-4,6-pregnadiene-3,20-dione), first synthesized in 1961. It was used as progestin-based... (Review)
Review
Chlormadinone acetate (CMA) is a progesterone derivative (17α-acetoxy-6-chloro-4,6-pregnadiene-3,20-dione), first synthesized in 1961. It was used as progestin-based hormone replacement therapy; since 1999 it was first used for oral contraception combined with ethinyl estradiol (EE). CMA exerts a potent progestagenic effect, about one third higher than that observed with endogenous progesterone. CMA is also an anti-estrogen, showing no androgenic effects (at birth control dose). Unlike progesterone, it has a mild glucosteroidal effect with no anti-mineralocorticoid effect at all. These biological actions have allowed CMA to have a role for therapeutic use in dysmenorrhea, hyperandrogenism, and as a contraceptive agent. In addition, CMA has exhibited beneficial neuroendocrine effects on women's mood. CMA-EE combination has shown excellent contraceptive efficacy, high tolerability, and compliance due to its risk-benefit profile, having additional benefits on skin and hair, such as reduction of seborrhea and acne. Metabolic tolerance of CMA has been demonstrated in several clinical studies. Currently, CMA is formulated to be taken as oral caplets in a 21 caplets package containing 0.03 mg/EE and 2 mg CMA per pill with/without seven placebo additional pills. Another presentation has 24 caplets containing 0.02 mg/EE and 2 mg CMA plus four placebo pills.
Topics: Chlormadinone Acetate; Contraception; Contraceptives, Oral, Synthetic; Dysmenorrhea; Female; Humans; Latin America
PubMed: 27113551
DOI: 10.3109/09513590.2016.1153059 -
Contraception May 1972
Topics: Acetates; Adult; Body Weight; Chlormadinone Acetate; Female; Humans; Menstruation Disturbances; Pregnancy
PubMed: 4119578
DOI: 10.1016/0010-7824(72)90029-7