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Sustained Elevation of Serum Prolactin by Metoclopramide: A Clinical Model of Idiopathic Hyperprolactinemia^*

DAVID L. HEALY and HENRY G. BURGER

Prince Henry’s Hospital Medical Research Centre and Department of Endocrinology,Melbourne, Victoria, Australia 3004

To investigate the potential usefulness of metoclopramide in inducing chronic hyperprolactinemia in the human and in providing a clinical model of idiopathic hyperprolactinemia, this drug was administered as 10-mg tablets every 8 h for 1 week to five women and four men volunteers. Within 24 h in the women, the mean serum PRL values rose from 19.4 ± 3.0 (SEM)-42.4 ± 6.5 ng/ml (P < 0.01). By 48 h in the men, the mean serum PRL increased from 8.7 ± 0.6-24.3 ± 5.2 ng/ml (P < 0.01). As long as metoclopramide was continued, elevated serum PRL levels were maintained; they returned to the normal range 24 h after cessation of the drug. No change in serum TSH values occurred during repeated metoclopramide ingestion.

Three days after commencing metoclopramide, the volunteers were challenged with a further 10-mg tablet of this drug and 200 µg TRH iv, and the results were compared with control tests using these agents. After the tablet of metoclopramide, there was no significant further elevation in serum PRL values in either sex.

During metoclopramide administration, the women showed a smaller increment in the mean serum PRL response to TRH (24.3 ± 4.9 ng/ml compared with 49.6 ± 6.6 ng/ml P < 0.01) and a smaller area of response of serum PRL (1514 ± 487 ng/ml/min compared with 3582 ± 776 ng/ml/min; P < 0.025) than in the control TRH test. The men showed a similar increment in the mean serum PRL, but a greater area of response of serum PRL (2712 ± 540 ng/ml/min compared with 1512 ± 295 ng/ml/min; P < 0.05) to TRH during metoclopramide exposure than to TRH alone.

It was concluded that 1) metoclopramide can sustain a state of hyperprolactinemia for at least 7 days; 2) in that circumstance, hypothalamic-pituitary responses to a further metoclopramide stimulation test mimic the response seen in patients with idiopathic hyperprolactinemia; and 3) responses to TRH in metoclopramidetreated normal women are diminished.(J Clin EndocrinolMetab 46: 709, 1978)

^* This study was supported by the National Health and Medical Research Council of Australia.

Postgraduate Medical Research Scholar of the NHMRC of Australia. To whom requests for reprints should be addressed.

Received June 21, 1977.

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