1973The Journal of Clinical Endocrinology & MetabolismRequires access

Influence of Glucocorticoids on TRF-Induced TSH Response in Man

Makoto Otsuki, MASAHITO DAKODA, Shigeaki Baba

Open publisher page 201 citations

Abstract

The influences of glucocorticoid administration or increased serum corticoid concentration on TRF-induced TSH release was studied in patients receiving glucocorticoids and in patients with Cushing's syndrome. The TRFinduced TSH release was inhibited in patients who had received glucocorticoids for long periods or in high doses. These patients had received more than 60 mEq of cortisol per day for more than six months. Definite plasma TSH increases by TRF were observed in patients receiving shortterm, low doses or intermittent, low doses administration of glucocorticoid. Little or no rise of plasma TSH occurred following TRF administration to patients with Cushing's syndrome. From these observations it is possible to conclude that the mechanism of the glucocorticoid suppressive action on TSH secretion after short-term, low doses of glucocorticoid administration may be an impaired secretion of endogenous TRF, which results in a supernormal TSH response induced by exogenous TRF. With long-term and high doses of glucocorticoid therapy, TSH secretion appears to be inhibited not only at the suprahypophyseal level but also at the pituitary level.

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What this paper is about

The influences of glucocorticoid administration or increased serum corticoid concentration on TRF-induced TSH release was studied in patients receiving glucocorticoids and in patients with Cushing's syndrome. The TRFinduced TSH release was inhibited in patients who had received glucocorticoids for long periods or in high doses. These patients had received more than 60 mEq of cortisol per day for more than six months. Definite plasma TSH increases by TRF were observed in patients receiving shortterm, low doses or intermittent, low doses administration of glucocorticoid. Little or no rise of plasma TSH occurred following TRF administration to patients with Cushing's syndrome. From these observations it is possible to conclude that the mechanism of the glucocorticoid suppressive action on TSH secretion after short-term, low doses of glucocorticoid administration may be an impaired secretion of endogenous TRF, which results in a supernormal TSH response induced by exogenous TRF. With long-term and high doses of glucocorticoid therapy, TSH secretion appears to be inhibited not only at the suprahypophyseal level but also at the pituitary level.

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Available abstract

The influences of glucocorticoid administration or increased serum corticoid concentration on TRF-induced TSH release was studied in patients receiving glucocorticoids and in patients with Cushing's syndrome. The TRFinduced TSH release was inhibited in patients who had received glucocorticoids for long periods or in high doses. These patients had received more than 60 mEq of cortisol per day for more than six months. Definite plasma TSH increases by TRF were observed in patients receiving shortterm, low doses or intermittent, low doses administration of glucocorticoid. Little or no rise of plasma TSH occurred following TRF administration to patients with Cushing's syndrome. From these observations it is possible to conclude that the mechanism of the glucocorticoid suppressive action on TSH secretion after short-term, low doses of glucocorticoid administration may be an impaired secretion of endogenous TRF, which results in a supernormal TSH response induced by exogenous TRF. With long-term and high doses of glucocorticoid therapy, TSH secretion appears to be inhibited not only at the suprahypophyseal level but also at the pituitary level.

Key concepts: Glucocorticoid, Endocrinology, Internal medicine, Endogeny, Medicine, Secretion

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