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1 型糖尿病患者甲状腺球蛋白和谷氨酸脱羧酶自身抗体的顺序升高。

Sequential elevation of autoantibodies to thyroglobulin and glutamic acid decarboxylase in type 1 diabetes.

机构信息

Eiji Kawasaki, Toshiyuki Ikeoka, Department of Metabolism/Diabetes and Clinical Nutrition, Nagasaki University Hospital, Nagasaki 852-8501, Japan.

出版信息

World J Diabetes. 2013 Oct 15;4(5):227-30. doi: 10.4239/wjd.v4.i5.227.

DOI:10.4239/wjd.v4.i5.227
PMID:24147207
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3797888/
Abstract

We have previously reported the high levels of glutamic acid decarboxylase 65 autoantibodies (GAD65A) in patients with type 1 diabetes and autoimmune thyroid disease. Here we describe a 32-year-old Japanese female with a thirteen-year history of type 1 diabetes whose levels of GAD65A were elevated just after the emergence of anti-thyroid autoimmunity. At 19 years of age, she developed diabetic ketoacidosis and was diagnosed with type 1 diabetes. She had GAD65A, insulinoma-associated antigen-2 autoantibodies (IA-2A), and zinc transporter-8 autoantibodies (ZnT8A), but was negative for antibodies to thyroid peroxidase (TPOAb) and thyroglobulin (TGAb) at disease onset. ZnT8A and IA-2A turned negative 2-3 years after the onset, whereas GAD65A were persistently positive at lower level (approximately 40 U/mL). However, just after the emergence of TGAb at disease duration of 12.5 years, GAD65A levels were reelevated up to 5717 U/mL in the absence of ZnT8A and IA-2A. Her thyroid function was normal and TPOAb were consistently negative. She has a HLA-DRB1*03:01/04:01-DQB102:01/*03:02 genotype. Persistent positivity for GAD65A might be associated with increased risk to develop anti-thyroid autoimmunity.

摘要

我们之前曾报道过 1 型糖尿病和自身免疫性甲状腺疾病患者谷氨酸脱羧酶 65 自身抗体(GAD65A)水平较高。在这里,我们描述了一位 32 岁的日本女性,她患有 13 年的 1 型糖尿病,在自身免疫性甲状腺疾病出现后不久,GAD65A 水平升高。19 岁时,她出现糖尿病酮症酸中毒,并被诊断为 1 型糖尿病。她有 GAD65A、胰岛素瘤相关抗原-2 自身抗体(IA-2A)和锌转运蛋白-8 自身抗体(ZnT8A),但在发病时对甲状腺过氧化物酶(TPOAb)和甲状腺球蛋白(TGAb)抗体呈阴性。ZnT8A 和 IA-2A 在发病后 2-3 年内转为阴性,而 GAD65A 则持续呈低水平阳性(约 40 U/mL)。然而,就在发病 12.5 年后 TGAb 出现后,GAD65A 水平再次升高至 5717 U/mL,此时没有 ZnT8A 和 IA-2A。她的甲状腺功能正常,TPOAb 持续阴性。她具有 HLA-DRB1*03:01/04:01-DQB102:01/*03:02 基因型。GAD65A 的持续阳性可能与发生抗甲状腺自身免疫的风险增加有关。

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本文引用的文献

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2
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PLoS One. 2012;7(9):e45216. doi: 10.1371/journal.pone.0045216. Epub 2012 Sep 21.
3
Immunogenetic mechanisms leading to thyroid autoimmunity: recent advances in identifying susceptibility genes and regions.导致甲状腺自身免疫的免疫遗传机制:鉴定易感性基因和区域的最新进展。
Curr Genomics. 2011 Dec;12(8):526-41. doi: 10.2174/138920211798120790.
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Clinical and genetic characteristics of autoimmune polyglandular syndrome type 3 variant in the Japanese population.在日本人群中,自身免疫性多腺体综合征 3 型变异的临床和遗传特征。
J Clin Endocrinol Metab. 2012 Jun;97(6):E1043-50. doi: 10.1210/jc.2011-3109. Epub 2012 Mar 30.
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GADA positivity at onset of type 1 diabetes is a risk factor for the development of autoimmune thyroiditis.1 型糖尿病发病时 GADA 阳性是发生自身免疫性甲状腺炎的危险因素。
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