INDUCTION OF PHARMACOLOGICAL HYPOGONADOTROPISM USING GONADOTROPIN-RELEASING HORMONE AGONISTS IN PATIENTS UNDERGOING CONTROLLED OVARIAN STIMULATION

Pharmacological hypogonadotropism was induced in 167 women using the gonadotropin-releasing hormone agonists (GnRH-A) buserelin acetate or triptorelin acetate. 84 patients (group 1) began treatment using 1.2 mg/ day buserelin acetate intranasally during the follicular phase (days 1-3); 41 patients (group II) began the same treatment, supported by 10 mg medroxyprogesterone acetate for 10 days, during the early luteal phase; 42 patients (group 3) received triptorelin acetate as an intramuscular depot injection, supported by 10 mg medroxyprogesterone acetate for 10 days, during the early luteal phase. Serum luteinizing hormone, follicle-stimulating hormone, oestradiol (E2), prolactin, and testosterone levels were monitored. Pituitary function was assessed by (1) measurement of endogenous luteinizing hormone fluctuation; (2) response to luteinizing hormone releasing hormone administration, and (3) response to oestradiol benzoate (E2 test). Complete pituitary desensitization was only assumed, if all three tests were negative. The LH-RH test and the E2 test were shown to be the most reliable indicator of pituitary function. E2 administration led to further reduction of gonadotropin secretion after pituitary desensitization. The desensitization time was 41.1 ± 11.7 days in group 1 and was significantly reduced to 20.7 ± 10.5 days in group 2 (p < 0.01); a further, non-significant shortening to 15.1 ± 3.0 days was observed in group 3. Changes in endocrine parameters demonstrated hypogonadotropic hypo-oestrogenism after initial pituitary stimulation. © 1990 S. Karger AG, Basel.