Graves' & Hashimoto's diseases and apoptosis

有两种自身免疫性甲状腺疾病；Graves病和桥本病。前者引起甲状腺毒症，后者引起甲状腺功能减退。有许多病人患有格雷夫斯病和桥本病。然而，这两种疾病的发病机制仍然知之甚少。细胞凋亡可能在Graves病和桥本病的发生发展中起一定作用。1)Graves病TRAb （TSH受体抗体）引起Graves病。该TRAb为促甲状腺抗体（TSAb）。这种TSAb刺激甲状腺，增加甲状腺激素的合成和分泌；因此TSAb引起甲状腺毒症。我们研究了277例未经治疗的Graves患者和686例正常对照者的TSAb和TBII （tsh结合抑制IgG）作为TRAb （Takasu N et al . J Endocrinol Invest 20: 452-461,1997）。ROC分析显示TSAb的临界值为150%，TBII的临界值为10%。几乎所有未经治疗的Graves患者TSAb和/或TBII阳性。抗甲状腺药物治疗后，TSAB和TBII降至正常水平。TSAb和TBII的变化预测Graves患者的临床病程。淋巴细胞异常在桥本甲状腺炎的发生发展中起重要作用。成人t细胞白血病（ATL）是一种t淋巴细胞疾病。免疫异常见于ATL患者。我们报道了ATL和HTLV-I携带者中桥本甲状腺炎的高发率（临床内分泌杂志45:461-466,1996）。我们还揭示了阻断抗体诱导的萎缩性甲状腺炎患者甲状腺功能减退的发生机制（临床内分泌杂志47:319-324,1997）。

There are two autoimmune thyroid diseases ; Graves' and Hashimoto's diseases. The former causes thyrotoxicosis and the latter hypothyroidism. There are many patients with Graves' and Hashimoto's diseases. However, the mechanisms for the development of both diseases are still poorly known. Apoptosis might play some roles in the development of Graves' and Hashimoto's diseases.1)Graves' disease TRAb (TSH receptor antibody) causes Graves' disease. This TRAb is thyroid stimulating antibody (TSAb). This TSAb stimulates thyroid glands and increases thyroid hormone synthesis and secretion ; thus TSAb causes thyrotoxicosis. We studied TSAb and TBII (TSH-binding inhibitory IgG) as TRAb in 277 untreated Graves' patients and 686 normal control subjects (Takasu N et al : J Endocrinol Invest 20 : 452-461,1997). ROC analysis revealed that cut-off value for TSAb is 150% and that for TBII is 10%. Almost all untreated Graves' patients have positive TSAb and/or TBII.TSAB and TBII decreased to normal levels with antithyroid drug treatment. The changes of TSAb and TBII predict the clinical courses of Graves' patients.Hashimoto's diseases Lymphocyte abnormality plays an essential role in the development of Hashimoto's thyroiditis. Adult T-cell leukemia (ATL) is a disease of T-lymphocyts. Immune abnormalities are seen in ATL patients. We reported that high prevalence of Hashimoto's thyroiditis in the patients with ATL and HTLV-I carriers (Clin Endocrinol 45 : 461-466,1996).We also revealed the mechanism of the development of blocking antibody-induced hypothyroidism in the patients with atrophic thryoiditis (Clin Endocrinol 47 : 319-324,1997).