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  • Title: [Plasma concentrations of LH and of sex steroids during the normal menstrual cycle and during contraceptive treatment].
    Author: Bayard F, Louvet JP, Moatti JP, Smilovici W, Duguet L, Boulard C.
    Journal: J Gynecol Obstet Biol Reprod (Paris); 1975; 4(7):915-26. PubMed ID: 767402.
    Abstract:
    The authors have studied the long-term effects of combined oestrogen-progestogen on the secretion of gonadotrophins and on ovarian function. Estimation of the radio-immune levels of the plasma concentrations of the pituitary luteinizing hormone (LH), of oestradiol (E2), of progesterone (P) and of 20 alpha hydroxyprogesterone (20 alpha OHP) and of testosterone (T) served as a base for this study. A test cycle and 8 cycles in which a combination of 50 micrograms of ethinyl-oestradiol and 0.5 mg of norgestrel were administered were studied in 4 normal volunteer women. A pituitary stimulation test using 50 micrograms of gonadotrophin "releasing factor" (LH-RH) was given during the 7th cycle. Ovarian stimulation using human menopausal gonadotrophins (HMG) was given during the 8th cycle of treatment in 3 of the women and in 3 other subjects. Pituitary secretion of LH and ovarian secretion of E2 and P are partially inhibited. Pituitary response to the injection of LH-RH stays normal but 5 out 6 patients had no response to stimulation by gonadotrophins. These results allow us to conclude that the lowering of production of gonadotrophins during treatment with combination oestrogen and progestagens is responsible for inhibition of ovarian activity, and that there is a delay before the latter respond to stimulation by either endogenous or exogenous gonadotrophins. Plasma luteinizing hormone (LH), estradiol, progesterone, 20alpha-hydroxyprogesterone, and testosterone were radioimmunoassayed daily throughout a normal menstrual cycle, the 3rd, 6th, and 9th cycles during oral contraception with Stediril, and during stimulation with LH-releasing factor (LH-RF), human menopausal gonadotropin (HMG), and human chorionic gonadotropin (HCG). 6 women aged 23-30 took Stediril (50 mcg ethinyl estradiol and .5 mg norgestrel, combined) for 1 year. I n the control menstrual cycle, LH rose to a plateau in the follicular and luteal phases, and a high midcycle peak; estradiol rose progressively until its midcycle peak, then fell and rose again; testosterone varied with higher peaks at midcycle; progesterone began to rise on the day of the LH peak to a maximum 5-9 days after ovulation; 20alpha-hydroxyprogesterone resembled progesterone but at a lower magnit ude. During pill cycles, the subjects took 1 mg dectancyl every 6 hours starting the day before blood sampling to inhibit adrenal corticosteroids. LH, estradiol, and progesterone were very low and invariant from Days 9 to 18. 50 mcg LH-RH elicited a significant LH peak (90-370 ng/ml) within 15-30 minutes. 75 IU FSH did not stimulate formation of a corpus luteum in 3 subjects taking 4 mg dexamethasone per day, although 150 IU FSH caused a corpus luteum to develop in 1 of 3 not taking the corticosteroid. Thus LH, estradiol, and progesterone secretions were incompletely inhibited by Stediril.
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