抄録
The influence 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. In addition, the effect of gluco-corticoid on TRF-induced TSH release was investigated in vivo in dexamethasone treated rats. The TRF-induced 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 short term low doses or intermittent low doses administration of glucocorticoid. Little or no rise in plasma TSH occurred following TRF administration to patients with Cushing's syndrome. TSH response of TRF in rats receiving only one dose of dexamethasone (10 ug/100g B. W.) was (394. 8±15. 5 %) greater than control (162. 7±15 %). Successive administra-tion of dexamethasone for 15 days inhibited the TSH response (159. 3±14. 0 %) to the control level. It is possible to conclude from these observations that the mechanism of the glucocorticoid suppressive action on TSH secretion after shortterm, low doses of glucocorticoid administration may be an impaired secretion of endoge-nous TRF, which results in a supernormal TSH response induced by exogenous TRF. With longterm and high doses of glucocorticoid therapy, TSH secretion appears to be inhibited not only at the suprahypophyseal level but also at the pituitary level.
