A randomized cross-over comparison of two low-dose oral contraceptives upon hormonal and metabolic parameters: I. Effects upon sexual hormone levels

Prodrug versus Drug Effects of 150 μg Desogestrel or 3-Keto-Desogestrel in Combination with 30 μg Ethinylestradiol on Hormonal Parameters: Relevance of the Peak Serum Level of 3-Keto-Desogestrel

“…This is in agreement with previous results show ing no alterations in the FSH and LH levels on the 6th day of intake of EE/DG and a triphasic formulation contain ing EE and levonorgestrel, but a progressive decrease thereafter [7], No significant change in gonadotropin release had also been observed during the first half of a pill cycle using low-dose preparations with EE and lynestrenol or norethisterone [11][12][13], During the first week of intake of a combination of 30 pg EE + 150 pg levonorges trel, no change in LH and a slight decrease in FSH occurred which was followed by a progressive depression of both gonadotropins [ 14], On the other hand, it has been shown that mestranol even at doses of 12.5 and 25 pg/day is capable of progressively reducing the serum levels of FSH and LH in patients with gonadal dysgenesis. The additional administration of 1 mg norethisterone, how ever, caused a strong rise in gonadotropin release indicat ing an antagonistic action of the progestogen upon estro gen-mediated suppression of the hypothalamic-pituitary axis [15], Similar findings using lOOpg EE with 25 mg dimethisterone but not with 2 mg chlormadinone acetate have been reported by Jaffe and Midgley [16], The present results confirm the antagonistic action of proges togens on the EE-induced suppression of LH and FSH release, as the decrease in LH and FSH on day 21/III was less pronounced with EE/KDG although the KDG levels were higher.…”

“…The effects of EE/DG and EE/ KDG on the serum levels of androgens were similar to those previously observed with EE/DG. with a combina tion of 30 pg EE and 75 pg gestodene or with a triphasic preparation containing EE and levonorgestrel [7,8,21,22], The mechanisms of suppression of adrenal androgens is not clarified. Low-dose oral contraceptives have been demonstrated not to decrease basal ACTH release [23], The slight suppresison of DHEA-S already after 2 days of intake of EE/KDG, which is amplified during further treatment, is possibly caused by a direct inhibition of adrenal androgen biosynthesis [24],…”

“…Previous studies revealed no significant differences in the levels of gonadotropins and androgens between the early follicular and mid-luteal phase [7,8], Therefore, the short-and long-term effects of the two estrogen/progestogen combinations on various hormonal parameters were compared with those during the midluteal phase.…”

Pituitary-ovarian activity when switching from various monophasic pills to a triphasic pill

“…Moreover, the ancillary contraceptive effects on cervical mucus and the endometrium would have probably prevented pregnancy even if luteinization of the ruptured follicle had occurred. These results are dearly different from those of Kuhl et aL [7] who showed that E 2 levels in 36% of women on triphasic pills were indicative of follicular activity, and that escape ovulation occurred in 2 of their 22 volunteers (manifested by raised serum progesterone levels on day 21). Since neither ultrasound scans nor laparoscopy were performed in their study to confirm follicular rupture, the inferred 'escape ovulation' may well have been luteiulzed unruptured follicles (LUFs).…”

Growth hormone responses to continuous and intermittent exercise in females under oral contraceptive therapy

“…Testing during the OCU phase occurred during days 7±11 of the menstrual cycle when total estrogen levels were expected to be higher than in the OCNU phase. It is unlikely that production of endogenous estrogen had been fully suppressed given that OC ingestion started on day 6 (Kuhl et al 1985).…”