Re R N, Kourides I A, Ridgway E C, Weintraub B D, Maloof F
J Clin Endocrinol Metab. 1976 Aug;43(2):338-46. doi: 10.1210/jcem-43-2-338.
In order to determine the mechanism by which glucocorticosteroids decrease the serum concentration of thyrotropin (TSH), we studied eight normal subjects before and after they received 16 mg of dexamethasone daily for 2 1/2 days. Serum levels of TSH and prolactin (PRL) were measured in the basal state and in response to the intravenous administration of 200 mug thyrotropin-releasing hormone (TRH); T4, free T4 (fT4), T3, and free T3 (fT3) were measured before TRH injection. Metabolic clearance rates of TSH corrected for body surface area (MCR-TSH/m2) were determined by the method of constant infusion to equilibrium; the production rates of TSH (PR-TSH/m2) were calculated. Dexamethasone produced a decrease in basal TSH from 2.2 to 0.8 muU/ml (P less than 0.02), a statistically insignificant elevation in MCR-TSH/m2 from 25.8 to 34.1 ml/min/m2, and a decrease in PR-TSH/m2 from 79 to 30 mU/day/m2 (P less than 0.01). Peak TSH response to TRH decreased from 16.4 to 5.8 muU/ml (P less than 0.005), as did TSH reserve from 1.58 to 0.54 mU - min/ml (P less than 0.005). Repetitive TRH testing alone did not account for these changes. Basal PRL, peak PRL after TRH, and PRL reserve did not change significantly after dexamethasone administration. Although Basal T4 and fT4 did not change significantly, dexamethasone did decrease T3 from 106 to 61 ng/dl (P less than 0.001) and fT3 from 174 to 76 pg/dl (P less than 0.05). Dexamethasone produced similar changes in patients with various thyroid disorders. In addition, when plasma cortisol was lowered by metyrapone administration in 25 euthyroid patients, the serum TSH concentration rose from 1.6 to 3.1 muU/ml (P less than 0.001). These data indicate that dexamethasone a) suppresses TSH secretion without increasing fT3 and fT4 and b) blunts the TSH, but not the PRL response, to TRH. Hence, one effect of the administration of dexamethasone in high dose is a direct suppression of pituitary TSH secretion. Furthermore, physiologic levesl of circulating cortisol also have a suppressive effect on serum TSH.
为了确定糖皮质激素降低血清促甲状腺激素(TSH)浓度的机制,我们对8名正常受试者进行了研究,在他们每日接受16毫克地塞米松,持续2.5天之前和之后均进行观察。在基础状态下以及静脉注射200微克促甲状腺激素释放激素(TRH)后,测量血清TSH和催乳素(PRL)水平;在注射TRH之前测量T4、游离T4(fT4)、T3和游离T3(fT3)。采用持续输注至平衡的方法,测定经体表面积校正的TSH代谢清除率(MCR-TSH/m²);计算TSH的生成率(PR-TSH/m²)。地塞米松使基础TSH从2.2降至0.8微单位/毫升(P<0.02),使MCR-TSH/m²从25.8升至34.1毫升/分钟/平方米,升高幅度无统计学意义,使PR-TSH/m²从79降至30毫单位/天/平方米(P<0.01)。TRH刺激后TSH的峰值反应从16.4降至5.8微单位/毫升(P<0.005),TSH储备从1.58降至0.54毫单位·分钟/毫升(P<0.005)。仅重复进行TRH检测无法解释这些变化。地塞米松给药后,基础PRL、TRH刺激后的PRL峰值以及PRL储备均无显著变化。虽然基础T4和fT4无显著变化,但地塞米松确实使T3从106降至61纳克/分升(P<0.001),使fT3从174降至76皮克/分升(P<0.05)。地塞米松在患有各种甲状腺疾病的患者中产生了类似的变化。此外,在25名甲状腺功能正常的患者中,通过给予甲吡酮降低血浆皮质醇后,血清TSH浓度从1.6升至3.1微单位/毫升(P<0.001)。这些数据表明,地塞米松a)在不增加fT3和fT4的情况下抑制TSH分泌,b)减弱对TRH的TSH反应,但不减弱PRL反应。因此,高剂量地塞米松给药的一个作用是直接抑制垂体TSH分泌。此外,循环皮质醇的生理水平对血清TSH也有抑制作用。