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Journal of Clinical Endocrinology & Metabolism Vol. 48, No. 4 700-705
doi:10.1210/jcem-48-4-700
Copyright © 1979 by the Endocrine Society.
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Inappropriate Secretion of Thyrotropin: Discordance between the Suppressive Effects of Corticosteroids and Thyroid Hormone*

ROBERT C. SMALLRIDGE, LEONARD WARTOFSKY and RICHARD C. DIMOND

Kyle Metabolic Unit, Endocrine-Metabolism Service, Walter Reed Army Medical Center, and the Division of Medicine, Walter Reed Army Institute of Research, Washington, D.C. 20012

A 46-yr-old postmenopausal woman with acromegaly and hyperthyroidism had serum levels of TSH which were repeatedly measurable (2.0-3.4 µU/ml) and, therefore, inappropriately elevated. In addition, serum concentrations of the {alpha}-subunit were persistently elevated (10.7-18.8 ng/ml). Although there was a reciprocal relationship between serum T4 and TSH levels during treatment with antithyroid drugs, the concentration of {alpha}-subunit did not appear to vary with either T4 or TSH. Transsphenoidal surgery documented the presence of a pituitary adenoma but failed to cure either the acromegaly or the hyperthyroidism.

While she was hyperthyroid, {alpha}-subunit fell to <1 µU/ml after prednisolone, but was unaffected by the administration of T3. {alpha}-Subunit was minimally suppressed by prednisolone and was not affected by T3. Secretion of TSH, {alpha}-subunit, and GH were unresponsive to TRH stimulation. When the patient became hypothyroid on antithyroid drugs, TRH increased TSH from 22.5 to >40 µU/ml, increased {alpha}-subunit from 14.6 to 21.8 ng/ml, and increased GH from 9 to 25 ng/ml. The patient was subsequently treated with both pituitary irradiation and 131I. Eighteen months later, she was euthyroid with serum TSH levels of 1.0 µU/ml, {alpha}-subunit levels of 4.3 ng/ml, and GH levels of 9 ng/ml. These data indicate that the patient had a pituitary tumor that secreted GH, TSH, and {alpha}-subunit and that there was a discordance between the feedback inhibitory effects of glucocorticoids and T3 on TSH secretion, and suggest that the tumor had an altered receptor for thyroid hormone. (J Clin Endocrinol Metab 48: 700, 1979)

* Presented in part at the 53rd meeting of the American Thyroid Association, Cleveland, OH, September 7-10, 1977. The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or reflecting the views of the Department of the Army or the Department of Defense.

Received May 18, 1978.




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