Department of Endocrinology and Metabolic Diseases, Faculty of Medicine, Ibn-i Sina Hospital, Ankara University, Sihhiye, Ankara, Turkey,
Endocrine. 2014 Feb;45(1):136-43. doi: 10.1007/s12020-013-9933-y. Epub 2013 Mar 27.
Explicit data regarding the changes in adrenocortical reserves during hyperthyroidism do not exist. We aimed to document the capability (response) of adrenal gland to secrete cortisol and DHEA-S during hyperthyroidism compared to euthyroidism, and to describe factors associated with these responses. A standard-dose (0.25 mg/i.v.) ACTH stimulation test was performed to the same patients before hyperthyroidism treatment, and after attainment of euthyroidism. Baseline cortisol (Cor(0)), DHEA-S (DHEA-S(0)), cortisol binding globulin (CBG), ACTH, calculated free cortisol (by Coolen's equation = CFC), free cortisol index (FCI), 60-min cortisol (Cor(60)), and DHEA-S (DHEA-S(60)), delta cortisol (ΔCor), delta DHEA-S (ΔDHEA-S) responses were evaluated. Forty-one patients [22 females, 49.5 ± 15.2 years old, 32 Graves disease, nine toxic nodular goiter] had similar Cor(0), DHEA-S(0), CFC, FCI, and DHEA-S(60) in hyperthyroid and euthyroid states. Cor(60), ΔCor, and ΔDHEA-S were lower in hyperthyroidism. In four (10 %) patients the peak ACTH-stimulated cortisol values were lower than 18 μg/dL. When the test repeated after attainment of euthyroidism, all of the patients had normal cortisol response. Regression analysis demonstrated an independent association of Cor(60) with free T3 in hyperthyroidism. However, the predictors of CFC, FCI, and DHEA-S levels were serum creatinine levels in hyperthyroidism, and both creatinine and transaminase levels in euthyroidism. ACTH-stimulated peak cortisol, delta cortisol, and delta DHEA-S levels are decreased during hyperthyroidism, probably due to increased turnover. Since about 10 % of the subjects with hyperthyroidism are at risk for adrenal insufficiency, clinicians dealing with Graves' disease should be alert to the possibility of adrenal insufficiency during hyperthyroid stage.
目前尚无关于甲状腺功能亢进症期间肾上腺储备变化的明确数据。我们旨在记录与甲状腺功能正常相比,在甲状腺功能亢进症期间肾上腺分泌皮质醇和 DHEA-S 的能力(反应),并描述与这些反应相关的因素。对同一患者在甲状腺功能亢进症治疗前和甲状腺功能正常后进行标准剂量(0.25mg/i.v.)ACTH 刺激试验。评估基础皮质醇(Cor(0))、DHEA-S(DHEA-S(0))、皮质醇结合球蛋白(CBG)、ACTH、计算游离皮质醇(根据 Coolen 方程=CFC)、游离皮质醇指数(FCI)、60 分钟皮质醇(Cor(60))和 DHEA-S(DHEA-S(60))、皮质醇(ΔCor)和 DHEA-S(ΔDHEA-S)的反应。41 例患者[22 名女性,49.5±15.2 岁,32 例格雷夫斯病,9 例毒性结节性甲状腺肿]在甲状腺功能亢进和甲状腺功能正常状态下具有相似的 Cor(0)、DHEA-S(0)、CFC、FCI 和 DHEA-S(60)。甲状腺功能亢进时 Cor(60)、ΔCor 和 ΔDHEA-S 较低。在 4 名(10%)患者中,峰值 ACTH 刺激皮质醇值低于 18μg/dL。当在甲状腺功能正常后重复该测试时,所有患者的皮质醇反应均正常。回归分析表明,甲状腺功能亢进时 Cor(60)与游离 T3 之间存在独立关联。然而,CFC、FCI 和 DHEA-S 水平的预测因子是甲状腺功能亢进时的血清肌酐水平,以及甲状腺功能正常时的肌酐和转氨酶水平。甲状腺功能亢进期间,ACTH 刺激的皮质醇峰值、皮质醇和 DHEA-S 水平降低,可能是由于代谢增加所致。由于大约 10%的甲状腺功能亢进患者存在肾上腺功能不全的风险,因此处理格雷夫斯病的临床医生在甲状腺功能亢进阶段应警惕肾上腺功能不全的可能性。