Evidence for an increased opioid inhibition of luteinizing hormone secretion in hyperprolactinemic patients with pituitary microadenoma.
The inhibiting role of endogenous opioid peptides on gonadotropin secretion was evaluated by the infusion of an opioid receptor antagonist, naloxone (1.6 mg/h for 4 h), in 10 hyperprolactinemic patients with pituitary microadenoma (prolactinoma) and 5 normal women during the early follicular phase of the cycle. In normal women, naloxone infusion induced no significant changes in any of the three pituitary hormones measured. Six prolactinoma patients with low normal levels of basal LH [10.0 +/- 1.0 mIU/ml +/- SE)] responded to naloxone infusion with an increment of circulating LH in the form of an amplified pulsatile pattern of release, which lasted for at least 2 h after the infusion. The other 4 patients with prepubertal levels of LH (4.9 +/- 0.8 mIU/ml) exhibited no LH response to naloxone. There were no significant changes in FSH or PRL levels in either group of patients. These findings suggest that an increased endogenous opioid inhibition of LH release occurs in patients with PRL-producing microadenoma.
D000236:Adenoma / Q000378:metabolism*; D000328:Adult; D004723:Endorphins / Q000502:physiology; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood; D005498:Follicular Phase; D006801:Humans; D007986:Luteinizing Hormone / Q000378:metabolism*; D009270:Naloxone; D010911:Pituitary Neoplasms / Q000378:metabolism*; D011388:Prolactin / Q000097:blood*
D004723:Endorphins; D009270:Naloxone; D011388:Prolactin; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone