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  • Title: Effect of oral contraceptives on plasma androgenic steroids and their precursors.
    Author: Fern M, Rose DP, Fern EB.
    Journal: Obstet Gynecol; 1978 May; 51(5):541-4. PubMed ID: 148599.
    Abstract:
    Plasma dehydroepiandrosterone (DHEA), its sulfate ester (DHEAS), and androstenedione (A2), delta5-pregnenolone (delta5-P), and 17 alpha-hydroxypregnenolone were measured in women using estrogen-containing oral contraceptives and in female controls of similar age. All three androgenic steroids and their two C21 precursors were reduced in the oral contraceptive users compared with the controls. It is concluded that oral contraceptives cause a decrease in plasma DHEA, DHEAS, and A2, one possible mechanism for which is the inhibition of delta5-P synthesis from cholesterol. An attempt to confirm the effect of oral contraceptives (OCs) on the plasma dehydroepiandrosterone sulfate (DHEAS) and to explore the biochemical site of their action is presented. 89 women taking estrogen-containing OCs for 6 months or longer and 47 controls were studied. Both groups were of similar age, and with regular menstrual cycles. OCs used were Ovral (ethinyl estradiol, 50 mcg, norgestrel, .05 mg), Demulen 50 (ethinyl estradiol, 50 mcg; ethynodiol diacetate, 1 mg), and Ortho-Novum 1/50 (mestranol, 50 mcg; norethindrone, 1 mg). A single sample of plasma was made from the heparinized blood taken between 7-8 a.m. between Days 15-21 of a contraceptive treatment cycle in the experimental group and between Days 15-21 of a menstrual cycle in the control group. The results of the plasma DHEAS, DHEA, and androstenedione assays showed that all 3 OC preparations caused reductions in the androgenic steroids when compared with the controls. Results of statistical comparisons between the different OCs did not indicate if ethinyl estradiol or mestranol exerted a greater effect. Concentrations of delta-5-P and 17-delta-5-P were found to be lower in the experimental cases than in the controls. It is concluded that OCs cause a decrease in plasma DHEA, DHEAS, and androstenedione, with 1 possible mechanism being the inhibition of delta-5-P synthesis from cholesterol.
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