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格雷夫斯病后发生的桥本甲状腺炎。

Hashimoto's thyroiditis following Graves' disease.

作者信息

Umar Husaini, Muallima Nur, Adam John M F, Sanusi Harsinen

机构信息

Department of Internal Medicine, Faculty of Medicine, University of Hasanuddin-Wahidin Sudirohusodo Hospital, Makassar 90245, Sulawesi Selatan, Indonesia.

出版信息

Acta Med Indones. 2010 Jan;42(1):31-5.

Abstract

Both Graves' disease and chronic thyroiditis (Hashimoto's thyroiditis) are autoimmune diseases of thyroid gland. Graves' disease is caused by stimulation of TSH receptor located on the thyroid gland by an antibody, which is known as TSH receptor antibody (TRAb). Furthermore, this may lead to hyperplasia and hyperfunction of the thyroid gland. On the contrary, the cause of Hashimoto's thyroiditis is thought due to a TSH stimulation-blocking antibody (TSBAb) which blocks the action of TSH hormone and subsequently brings damage and atrophy to thyroid gland. Approximately 15-20% of patients with Graves' disease had been reported to have spontaneous hypothyroidism resulting from the chronic thyroiditis (Hashimoto's disease). Pathogenesis for chronic thyroiditis following anti-thyroid drug treatment in patients with Graves' disease remains unclear. It has been estimated that chronic thyroiditis or Hashimoto's disease, which occurs following the Graves' disease episode is due to extended immune response in Graves' disease. It includes the immune response to endogenous thyroid antigens, i.e. thyroid peroxidase and thyroglobulin, which may enhance lymphocyte infiltration and finally causes Hashimoto's thyroiditis. We report four cases of chronic thyroiditis (Hashimoto's disease) in patients who have been previously diagnosed with Graves' hyperthyroidism. In three cases, Hashimoto's thyroiditis occurs in 7 to 25 years after the treatment of Grave's disease; while the other case has it only after few months of Grave's disease treatment. The diagnosis of Hashimoto's disease (chronic thyroiditis) was based on clinical manifestation, high TSHs level, positive thyroid peroxidase antibody and thyroglobulin antibody, and supported by positive results of fine needle aspiration biopsy. Moreover, the result of histopathological test has also confirmed the diagnosis in two cases. All cases have been successfully treated by levothyroxine treatment.

摘要

格雷夫斯病和慢性甲状腺炎(桥本甲状腺炎)均为甲状腺的自身免疫性疾病。格雷夫斯病是由一种抗体刺激甲状腺上的促甲状腺激素(TSH)受体所致,该抗体被称为TSH受体抗体(TRAb)。此外,这可能导致甲状腺增生和功能亢进。相反,桥本甲状腺炎的病因被认为是由于一种TSH刺激阻断抗体(TSBAb),它阻断TSH激素的作用,随后导致甲状腺损伤和萎缩。据报道,约15% - 20%的格雷夫斯病患者会因慢性甲状腺炎(桥本氏病)而出现自发性甲状腺功能减退。格雷夫斯病患者接受抗甲状腺药物治疗后发生慢性甲状腺炎的发病机制仍不清楚。据估计,格雷夫斯病发作后发生的慢性甲状腺炎或桥本氏病是由于格雷夫斯病中延长的免疫反应。它包括对内源性甲状腺抗原,即甲状腺过氧化物酶和甲状腺球蛋白的免疫反应,这可能会增强淋巴细胞浸润并最终导致桥本甲状腺炎。我们报告了4例先前被诊断为格雷夫斯甲亢的患者发生慢性甲状腺炎(桥本氏病)的病例。其中3例在格雷夫斯病治疗后7至25年出现桥本甲状腺炎;而另一例在格雷夫斯病治疗仅几个月后就出现了。桥本氏病(慢性甲状腺炎)的诊断基于临床表现、高促甲状腺激素水平、甲状腺过氧化物酶抗体和甲状腺球蛋白抗体阳性,并得到细针穿刺活检阳性结果的支持。此外,组织病理学检查结果也在2例中证实了诊断。所有病例均通过左甲状腺素治疗成功治愈。

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