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Research Article Free access | 10.1172/JCI107421

Thyroid Hormone Inhibition of the Prolactin Response to Thyrotropin-Releasing Hormone

Peter J. Snyder, Laurence S. Jacobs, Robert D. Utiger, and William H. Daughaday

Endocrine Section, Department of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104

Metabolism Division, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, 63110

Find articles by Snyder, P. in: PubMed | Google Scholar

Endocrine Section, Department of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104

Metabolism Division, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, 63110

Find articles by Jacobs, L. in: PubMed | Google Scholar

Endocrine Section, Department of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104

Metabolism Division, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, 63110

Find articles by Utiger, R. in: PubMed | Google Scholar

Endocrine Section, Department of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104

Metabolism Division, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, 63110

Find articles by Daughaday, W. in: PubMed | Google Scholar

Published September 1, 1973 - More info

Published in Volume 52, Issue 9 on September 1, 1973
J Clin Invest. 1973;52(9):2324–2329. https://doi.org/10.1172/JCI107421.
© 1973 The American Society for Clinical Investigation
Published September 1, 1973 - Version history
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Abstract

The influence of serum triiodothyronine (T3) and thyroxine (T4) concentrations on the release of prolactin in man was studied by determining the prolactin response to synthetic thyrotropin-releasing hormone (TRH) in hypothyroid and hyperthyroid patients before and after correction of their serum thyroid hormone abnormalities. The maximum increment in serum prolactin above the basal level (maximum Δ prolactin) was used as the index of response to TRH.

In 12 patients with primary hypothyroidism, the maximum Δ prolactin in response to TRH fell from 100.5±29.1 ng/ml (mean ±SEM) before treatment to 36.1±6.0 ng/ml (P < 0.01) during the 4th wk of treatment with 30 μg T3 + 120 μg T4 daily. The mean serum T3 level increased from 57±8 to 138±10 ng/100 ml, and the mean serum T4 level increased from 3.0±0.4 to 7.2±0.4 μg/100 ml during this treatment. In eight normal subjects the maximum Δprolactin in response to TRH was not significantly different during the 4th wk of treatment with 30 μg T3 + 120 μg T4 daily from the response before treatment. In 10 patients with hyperthyroidism, the maximum Δprolactin in response to TRH increased from 14.2±2.9 ng/ml before treatment to 46.9±6.7 ng/ml (P < 0.001) during antithyroid treatment. The mean serum T3 level fell from 313±47 to 90±8 ng/100 ml, and the mean serum T4 level fell from 20.8±2.5 to 6.8±0.6 μg/100 ml during this treatment.

These results show that changes from normal serum levels of T3 and T4 are associated with changes in prolactin responses to TRH; subnormal serum levels of T3 and T4 increase TRH-induced prolactin release, whereas substantially higher than normal serum levels of T3 and T4 inhibit this release.

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