PubMed · 4177336
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G Oclander. 1967. [Ovulostasis by sequential therapy].. https://pubmed.ncbi.nlm.nih.gov/4177336/
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Chlormadinone acetate was tested for the preparation of the "Chlormadinone Acetate Reference Standard (Control 881)". Analytical data obtained were as follows: loss on drying, 0.00%; infrared spectrum, 1740, 1715, 1658, 1604, 1587, 1256, 1244 cm-1; ultraviolet spectrum, lambda max = 284 nm; absorbance, E1cm1% (284 nm) = 539-549; optical rotation, [alpha]D20: -12.1 degrees; melting point, 214.6 degrees C; thin-layer chromatography, contaminants were not detected until 300 micrograms; high-performance liquid chromatography, one contaminant was detected. On the basis of the above results, this material was authorized as the National Institute of Hygienic Sciences Reference Standard (Control 881).
The choice of an optimal contraceptive method (OC) therapy is a significant problem in female SLE patients. In view of the influence of sex hormones on the evolution of SLE, oral contraceptive (OC) therapy has to be efficient, reversible and safe, without aggravating disease activity and causing metabolic and vascular side effects. Ethinyl estradiol-containing preparations, even at 30 micrograms/day, have been shown to trigger a crisis or unmask SLE, and they exert adverse metabolic and vascular effects. Therefore, combination estrogen-progestogen compounds must be avoided in women with SLE. Pure progestogen OC preparations do not stimulate SLE activity, but norsteroids have harmful metabolic effects and microprogestogens are not sufficiently reliable. In light of the decreased level of plasma androgens in female SLE patients, an attempt to modulate the hormonal milieu by lowering the estrogen to androgen ratio, while ensuring contraception was attempted using cyproterone acetate. This agent markedly lowered plasma estrogens and was effective and well tolerated, but its long-term effect on bone mineralization remains to be evaluated. Chlormadinone acetate, a 17-OH progesterone derivative, was proven effective and devoid of any metabolic or vascular side effects, and should be recommended as the safest routine OC therapy in women with SLE.
We investigated the mechanisms of the beneficial effect derived from progesterone therapy for sleep apnea syndrome (SAS). Nine patients with SAS were treated for 7 days with chlormadinone acetate (CMA), a respiratory stimulant known to increase not only CO2 and hypoxic chemosensitivity but also respiratory drive response for ventilatory loading. They were examined as to sleep events and ventilatory control during wakefulness before and during CMA treatment. Apnea-hypopnea index was significantly reduced from 51.1 +/- 5.7 to 43.6 +/- 8.1 episodes/h (p less than 0.05). The ratio of desaturation time with more than 4% SaO2 fall to total sleep time was diminished in seven of nine patients, and its mean value decreased from 44.9 +/- 8.6 to 28.7 +/- 8.1% (p less than 0.05). Both hypercapnic ventilatory response (HCVR) and load response during wakefulness were significantly increased, although isocapnic hypoxic ventilatory response (HVR) was not significantly enhanced by CMA. The degree of augmentation in awake load response as well as in HCVR was positively correlated with that of improvement in sleep-disordered breathing. Moreover, patients who did not show amelioration in oxygen desaturation were found to be incapable of increasing load response despite increased HCVR. We conclude that CMA therapy for sleep apnea syndrome is effective in the patients whose load response as well as respiratory control activity are augmented during wakefulness.