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Article
November 1977

Adrenogenital Syndrome (11-ß-Hydroxylase Deficiency) With Hyperprolactinemia: Reversal by Glucocorticoid Administration

Author Affiliations

From the Veterans Administration Wadsworth Hospital Center and the Department of Medicine, School of Medicine, University of California at Los Angeles (Dr Brautbar), and the Department of Pharmacology, Hadassah University Hospital, Medical Center, Jerusalem (Dr Ben-David).

Arch Intern Med. 1977;137(11):1608-1609. doi:10.1001/archinte.1977.03630230082022
Abstract

In a patient with adrenogenital syndrome (11-β-hydroxylase deficiency), prednisone administration resulted in a suppression of basal levels of prolactin (PRL), while at the same time the PRL responses to levodopa and thyrotropin releasing hormone were normal. Following withdrawal of prednisone, serum PRL returned to high basal levels, with continued normal response to levodopa, and no observable change in thyroid stimulating hormone or human growth hormone levels. Our data suggest that glucocorticoid withdrawal produces a rebound in PRL release, as shown by excessive serum PRL levels. A direct suppressive effect of corticoids on PRL release is suggested.

(Arch Intern Med 137:1608-1609, 1977)

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