A study was performed to further evaluate pituitary-ovarian function in women receiving an oral contraceptive preparation. Basal hormone levels (follicle stimulating hormone, luteinizing hormone, estradiol and prolactin) and gonadotropic response to gonadotropic releasing hormone were studied in 12 healthy, regularly ovulating women in the early follicular and mid-luteal phases of their menstrual cycle (non-treatment control period). These same women were then given NORDETTE (ethinyl estradiol 30 microgram +d-Norgestrel 150 microgram) cyclically for 3 months. In the third month of treatment, the tests were repeated on day 21, i.e. after 21 active pills, and on day 28, i.e. after 21 active and 7 inactive tablets. On active preparation, basal luteinizing hormone, follicle stimulating hormone and estradiol and gonadotropin response to gonadotropin releasing hormone were significantly suppressed. However, by day 28 (after completion of the inactive tablets), basal gonadotropin and estradiol concentrations and the gonadotropic response to gonadotropic releasing hormone were not significantly different to their pretreatment levels. No consistent change in prolactin concentration occurred as a result of oral contraceptive therapy. These results indicate that the 'active' component of even a relatively low-dose pill causes considerable suppression of pituitary-ovarian function but that after 7 days of placebo, pituitary function and basal estradiol secretion have virtually returned to normal.
PIP: The pituitary-ovarian function of women receiving oral contraceptives (OCs) was studied by measuring basal levels of follicle stimulating hormone (FSH), luteinizing hormone (LH), estradiol, and prolactin, as well as gonadotrophic response to gonadotropin-releasing hormone (GRH). 12 healthy, regularly ovulating women were studied in the early follicular and midluteal phases of the menstrual cycle; this constituted the nontreatment control period. After establishing base lines, the same women were given an OC containing 30 mcg of ethinyl estradiol plus 150 mcg of D-norgestrel for 3 months. On Day 21 and 28 of the 3rd treatment month, hormone and gonadotrophic measurements were again performed, i.e., both immediately after the 3 weeks of OC ingestion and after the 7 days of noningestion. Overall it was discovered that the active component of even a relatively low-dose OC causes considerable suppression of pituitary-ovarian function, but after 7 days of placebo, the pituitary function and basal estradiol secretion virtually returned to normal. More specifically, on Day 21 measurement, LH, FSH, estradiol and gonadotrophic response were significantly suppressed (p.01). By Day 28, however, basal gonadotropin and estradiol concentrations and the gonadotrophic response to GRH were not significantly different than their pretreatment values. No consistent change in prolactin concentration was noted as a result of OC therapy.