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Evidence for an Increased Opioid Inhibition of Luteinizing Hormone Secretion in Hyperprolactinemic Patients with Pituitary Microadenoma^*

M. E. QUIGLEY, K. L. SHEEHAN, R. F. CASPER and S. S. C. YEN

Department of Reproductive Medicine, School of Medicine (T-002), University of California San Diego, La Jolla, California 92093

The inhibiting role of endogenous opioid peptides on gonadotropin secretion was evaluated by the infusion of anopioid receptor antagonist, naloxone (1.6 mg/ for 4 h), in 10 hyperprolactinemic patients with pituitary microadenoma (prolactinoma) and 5 normal women during the early follicular phaseof 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 mlU/ml ±SE)] responded to naloxone infusionwith 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 mlU/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.

^* This work was supported by Rockefeller Foundation Grant RF-75029 and NIH Research Grant HD-12303. A portion of the patient studies was performed in the Clinical Research Center, supported byNIH Grant RR-00827.

Research Fellow in Reproductive Endocrinology.

Research Fellow in Reproductive Endocrinology, supported by Medical Research Council of Canada.

To whom all correspondence and rewquests for reprints should be addressed.

Received July 19, 1979.