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自身免疫性甲状腺疾病——最新进展

Autoimmune thyroid disorders-An update.

作者信息

Swain Manorama, Swain Truptirekha, Mohanty Binoy Kumar

机构信息

Department of Biochemistry, M.K.C.G. Medical College, 760 004 Berhampur.

出版信息

Indian J Clin Biochem. 2005 Jan;20(1):9-17. doi: 10.1007/BF02893034.

Abstract

Autoimmune thyroid disease (AITD), a common organ specific autoimmune disorder is seen mostly in women between 30-50 yrs of age. Thyroid autoimmunity can cause several forms of thyroiditis ranging from hypothyroidism (Hashimoto's thyroiditis) to hyperthyroidism (Graves'Disease). Prevalence rate of autoimmune mediated hypothyroidism is about 0.8 per 100 and 95% among them are women. Graves' disease is about one tenth as common as hypothyroidism and tends to occur more in younger individuals. Both these disorders share many immunologic features and the disease may progress from one state to other as the autoimmune process changes. Genetic, environmental and endogenous factors are responsible for initiation of thyroid autoimmunity. At present the only confirmed genetic factor lies in HLA complex (HLA DR-3) and the T cell regulatory gene (CTLA 4). A number of environmental factors like viral infection, smoking, stress & iodine intake are associated with the disease progression. The development of antibodies to thyroid peroxidase (TPO) thyroglobulin (TG) and Thyroid stimulating hormone receptor (TSH R) is the main hallmark of AITD. Circulating T Lymphocytes are increased in AITD and thyroid gland is infiltrated with CD4+ and CD8+ T Cells. Wide varieties of cytokines are produced by infiltrated immune cells, which mediate cytotoxicity leading to thyroid cell destruction. Circulating antibodies to TPO and TG are measured by immunofluorescense, hemagglutination, ELISA & RIA. TSHR antibodies of Graves' disease can be measured in bioassays or indirectly in assays that detect antibody binding to the receptor.

摘要

自身免疫性甲状腺疾病(AITD)是一种常见的器官特异性自身免疫性疾病,多见于30至50岁的女性。甲状腺自身免疫可导致多种形式的甲状腺炎,从甲状腺功能减退(桥本甲状腺炎)到甲状腺功能亢进(格雷夫斯病)。自身免疫介导的甲状腺功能减退的患病率约为每100人中有0.8人,其中95%为女性。格雷夫斯病的发病率约为甲状腺功能减退的十分之一,且更易发生于年轻人。这两种疾病具有许多免疫特征,并且随着自身免疫过程的变化,疾病可能从一种状态发展为另一种状态。遗传、环境和内源性因素是引发甲状腺自身免疫的原因。目前唯一确定的遗传因素存在于HLA复合体(HLA DR-3)和T细胞调节基因(CTLA 4)中。许多环境因素,如病毒感染、吸烟、压力和碘摄入,都与疾病进展有关。针对甲状腺过氧化物酶(TPO)、甲状腺球蛋白(TG)和促甲状腺激素受体(TSH R)的抗体的产生是AITD的主要标志。AITD患者循环T淋巴细胞增多,甲状腺内浸润有CD4+和CD8+ T细胞。浸润的免疫细胞产生多种细胞因子,介导细胞毒性,导致甲状腺细胞破坏。通过免疫荧光、血凝、ELISA和RIA检测循环中抗TPO和TG抗体。格雷夫斯病的TSHR抗体可通过生物测定法或间接检测抗体与受体结合的测定法进行检测。

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