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Concordance of Insulin-Induced Hypoglycemia and Phenothiazine-Induced Prolactin Secretion in Man^*

MAIRE T BUCKMANj and PEAKE GLENNT, WITH THE EXPERT TECHNICAL ASSISTANCE OF BARRY DAVID

Medicine and Research Services, Veterans Administration Hospital, and the Department of Medicine, University of New Mexico School of Medicine Albuquerque, New Mexico 87131

Address requests for reprints to: Maire T. Buckman, M.D., Research Service (151), Veterans Administration Hospital, 2100 Ridgecrest Drive S.E., Albuquerque, New Mexico 87108.

Highly variable pituitary PRL responses have been reported after insulin-induced hypoglycemia in normal subjects. Thus, insulin hypoglycemia has not been widely utilized to ascertain hypothalamic-pituitary PRL reserve. To determine the clinical usefulness of measuring hypoglycemia-induced PRL secretion, serum PRL concentrations after standard insulin tolerance tests were compared to those after phenothiazine (perphenazine) administration in 12 normal subjects and in 24 euprolactinemic patients evaluated for possible hypothalamic-pituitary disorders. In normal subjects, mean PRL levels rose from 12.6 ± 1.0 to 42.6 ± 6.6 (1 SEM) ng/ml after insulin hypoglycemia and from 13.3 ± 1.7 to 52.2 ± 8.4 ng/ml after perphenazine ingestion. The mean maximum increment in PRL was 30.1 ± 6.7 ng/ml after hypoglycemia and 38.9 ± 8.8 ng/ml after perphenazine administration. In the 24 patients evaluated for hypothalamic-pituitary dysfunction, mean PRL concentration rose from 9.6 ± 1.3 to 32.0 ± 5.5 ng/ml after insulin administration and from 9.2 ± 1.1 to 35.2 ± 6.2 ng/ml after perphenazine ingestion. The mean maximum increment in PRL was similar after the two provocative tests: 22.4 ± 6.8 after insulin and 26.1 ± 7.6 after perphenazine administration. In 11 of 12 normal subjects and in 22 of 24 patients, the PRL responses to the two stimuli were concordant. In 3 individuals (8%), the responses were discordant in that the subjects had a normal perphenazine-induced response but no hypoglycemia-associated elevation in serum PRL concentration. The correlation coefficient (r) for the maximum serum PRL concentrations in the 36 subjects was highly significant at 0.52 (P < 0.005). Thus, in most individuals tested, the hypoglycemia-induced PRL response was similar to the perphenazineinduced response. Absence of a hypoglycemia-associated increase in PRL, however, does not establish diminished hypothalamic-pituitary PRL reserve. (JClin Endocrinol Metab 48: 213, 1979)

^* This work was supported in part by NIH Grants HD-05794-05 and RR-00997-02.

Recipient of V.A. Clinical Investigator Award

Received January 16, 1978.