Gonadotrophin-secretion in adrenocortical insufficiency: impact of glucocorticoid substitution.
In patients with deficient endogenous glucocorticoid production due to primary adrenal insufficiency (n = 4) or bilateral adrenalectomy (n = 2) a rise in LRH-stimulated concentrations of LH was seen following withdrawal of substitution therapy for 84 h. Consecutive re-administration of glucocorticoids (dexamethasone 2.0 mg/day for 3 days) resulted in increased basal concentrations of LH and FSH and a diminished secretory response of LH upon iv LRH (100 micrograms). Five patients substituted with glucocorticoids because of adrenocortical insufficiency presented upon the administration of exogenous ACTH1-24 with unchanged basal and LRH-stimulated concentrations of LH and FSH as compared to a placebo experiment. These data suggest that the withdrawal and subsequent re-administration of gluco-corticoid substitution alters basal and stimulated concentrations of gonadotrophins in patients with adrenocortical insufficiency, thus providing evidence for the importance of adequate glucocorticoid supply in the regulation of gonadotrophin secretion.
D000224:Addison Disease / Q000503:physiopathology; D000302:Adrenal Cortex / Q000503:physiopathology*; D000315:Adrenalectomy; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology*; D000328:Adult; D000368:Aged; D003907:Dexamethasone / Q000494:pharmacology*; D005260:Female; D005640:Follicle Stimulating Hormone / Q000378:metabolism*; D007987:Gonadotropin-Releasing Hormone / Q000494:pharmacology; D006801:Humans; D007986:Luteinizing Hormone / Q000378:metabolism*; D008297:Male; D008875:Middle Aged
D007987:Gonadotropin-Releasing Hormone; D003907:Dexamethasone; D000324:Adrenocorticotropic Hormone; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone