Elevation of plasma immunoreactive luteinizing hormone releasing hormone in hyperprolactinemic-amenorrheic women on bromocriptine therapy.

There is evidence to suggest that abnormalities in the secretion of prolactin (PRL) in patients with the hyperprolactinemia-amenorrhea syndrome are due to hypothalamic dysfunction. In an attempt to further define the inhibitory effect of excessive PRL release on luteinizing hormone releasing hormone (LHRH) and luteinizing hormone (LH) secretory patterns in human plasma, four amenorrheic women with known hyperprolactinemia were studied before and during bromocriptine (BRCR) therapy. Ten-minute blood samples collected with a continuous withdrawal pump for two hours were analyzed for immunoreactive LHRH (IR-LHRH), LH and PRL using previously established radioimmunoassay procedures. Three patients showed a significant rise in mean IR-LHRH plasma levels coincident with a significant decrease in mean PRL concentrations five days to two weeks following BRCR therapy, whereas mean LH titers increased significantly in only one patient. One patient showed no increase in IR-LHRH or LH with BRCR therapy and failed to show a decrease in serum PRL to normal levels after five days of this treatment. A defect in the control of PRL release in these patients seemed to result from the inability of dopaminergic inhibition to be mediated effectively and seemed to be associated with altered secretion of LHRH.