Mechanism of persistent thyrotropin suppression in euthyroid patients with Graves′ disease after treatment
- VernacularTitle:Graves病患者甲状腺激素水平正常后sTSH长期抑制机制的探讨
- Author:
Jie MIAO
;
Yongju ZHAO
;
Shu WANG
;
Xiaohua JIANG
;
Zefei ZHAO
;
Liqun GU
;
Xuejiang GU
;
Guang NING
- Publication Type:Journal Article
- Keywords:
Graves′ disease;
Drug therapy;
Thyrotropin;
Antibodies;
thyrotropin receptor
- From:
Chinese Journal of Endocrinology and Metabolism
2008;24(2):170-173
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the mechanism of persistent thyrotropin suppression in euthyroid patients with Graves′ disease after antithyroid drugs (ATD) treatment. Methods A prospective clinical study was performed in 122 patients with newly diagnosed Graves′ disease. All the patients were treated with 30 mg methimazole or 300 mg propylthiouracil daily, to whom L-T4was added, aiming at normalizing FT3 and FT4 but avoiding elevated TSH level. When the patients were clinically and biochemically euthyroid for at least 3 months, their blood levels of thyroid hormones, TSH, TSH receptor antibody(TRAb) and thyroid peroxidase antibody(TPOAb) were detected again and the cases were divided into two groups according to negative or positive TRAb. Results After treatment as long as (7.1±1.1) months, stable euthyroid status was restored for 3 months. When the patients reached the euthyroid state, 64 of them still had detectable TRAb levels, and 58 became negative TRAb. The two groups had similar levels of FT3 and FT4, but patients with positive TRAb had lower TSH level than patients with negative TRAb[0.044 mIU/L(0.001-4.163 mIU/L) vs 1.749 mIU/L(0.079-4.646 mIU/L),P＜0.01]. In addition, the TSH level was negatively correlated with TRAb level (r=-0.539, P＜0.01), and not with FT3, FT4 levels or other factors. Conclusion The present study showed that elevated TRAb level is associated with persistent suppression of TSH in patients with Graves′ disease after being rendered euthyroid. This finding may be due to the binding of TRAb to pituitary TSH receptor.
