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首页> 外文期刊>Thyroid: official journal of the American Thyroid Association >Differential evolution of thyroid peroxidase and thyrotropin receptor antibodies in graves' disease: thyroid peroxidase antibody activity reverts to pretreatment level after carbimazole withdrawal.
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Differential evolution of thyroid peroxidase and thyrotropin receptor antibodies in graves' disease: thyroid peroxidase antibody activity reverts to pretreatment level after carbimazole withdrawal.

机译:严重疾病中甲状腺过氧化物酶和促甲状腺激素受体抗体的差异进化:撤消卡咪唑后,甲状腺过氧化物酶抗体活性恢复到治疗前水平。

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摘要

In this study, we compared the evolution of thyroid peroxidase antibody (TPOAb) and thyroid-stimulating antibody (TSAb) activities before, during, and after treatment of Graves' disease (GD) with carbimazole. TPOAb and TSAb were measured in sera from 75 patients with GD, during an 18-month block-replace regimen and after drug withdrawal (12, 24, and 36 months). At diagnosis, TPOAb were present in 85% of the patients versus 99% for TSAb. During the treatment, TPOAb values and prevalence significantly decreased, as observed with TSAb. After drug withdrawal, TPOAb levels increased once again to reach the pretreatment values, whereas TSAb remained unchanged. TPOAb values and prevalence at drug withdrawal were not significantly different between patients who remained euthyroid and those who had a relapse of hyperthyroidism. In contrast, TSAb values and prevalence were higher at drug withdrawal in relapse patients. In conclusion, TPOAb and TSAb changes are similar during GD treatment by carbimazole but diverge after drug withdrawal. TPOAb might reflect autoimmune perturbations independently of the clinical status and of the thyroid-stimulating activity.
机译:在这项研究中,我们比较了用卡巴咪唑治疗Graves病(GD)之前,期间和之后甲状腺过氧化物酶抗体(TPOAb)和甲状腺刺激抗体(TSAb)活性的演变。在18个月的阻断治疗期间和停药后(12、24和36个月),对75例GD患者的血清中的TPOAb和TSAb进行了测定。在诊断时,TPOAb存在于85%的患者中,而TSAb则为99%。在治疗期间,与TSAb相比,TPOAb值和患病率显着降低。停药后,TPOAb水平再次升高,达到治疗前值,而TSAb保持不变。甲状腺功能正常的患者和甲状腺功能亢进复发的患者中,TPOAb值和停药率无显着差异。相反,复发患者停药时TSAb值和患病率较高。总之,在用卡咪唑进行GD治疗期间,TPOAb和TSAb的变化相似,但在停药后差异较大。 TPOAb可能独立于临床状态和甲状腺刺激活性而反映出自身免疫干扰。

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