Opioid regulation of luteinizing hormone in amenorrheic patients after therapy for induction of ovulation.
This study evaluated the activity of central opiate receptors modulating luteinizing hormone (LH) secretion before and during treatment with human menopausal gonadotropin (n = 8) or purified human urinary follicle-stimulating hormone (n = 6) in 14 patients with hypogonadotropic hypogonadism (n = 6) or secondary amenorrhea (n = 8). LH response to saline infusion and naloxone administration (4 mg intravenously) was assessed. As control, 6 normal ovulating women were studied. Before therapy, all amenorrheic patients showed no LH increase after naloxone injection. Gonadotropin treatment restored the naloxone-induced LH response at preovulatory and midluteal phases in ovulating patients with secondary amenorrhea. The same response was present in spontaneously ovulating women but was absent in the hypogonadotropic hypogonad patients, despite the gonadotropin therapy's efficiency. In conclusion, when the alteration of gonadotropin-releasing hormone synthesis and/or release is reversible, the opioid system actively participates in the regulation of the hypothalamus-pituitary-gonadal axis.
D000328:Adult; D000568:Amenorrhea / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology*; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood / Q000627:therapeutic use; D006801:Humans; D007006:Hypogonadism / Q000150:complications; D007986:Luteinizing Hormone / Q000097:blood / Q000378:metabolism*; D008596:Menotropins / Q000627:therapeutic use; D009270:Naloxone / Q000494:pharmacology; D010062:Ovulation Induction / Q000379:methods*; D010906:Pituitary Hormone-Releasing Hormones; D011957:Receptors, Opioid / Q000502:physiology*; D012965:Sodium Chloride / Q000494:pharmacology; D013268:Stimulation, Chemical
D010906:Pituitary Hormone-Releasing Hormones; D011957:Receptors, Opioid; D009270:Naloxone; D012965:Sodium Chloride; D008596:Menotropins; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone