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糖尿病患者谷氨酸脱羧酶自身抗体滴度快速正常化及内源性胰岛素分泌保留:一例报告及文献综述

Rapid Normalization of High Glutamic Acid Decarboxylase Autoantibody Titers and Preserved Endogenous Insulin Secretion in a Patient with Diabetes Mellitus: A Case Report and Literature Review.

作者信息

Ohara Nobumasa, Kaneko Masanori, Furukawa Tatsuo, Koike Tadashi, Sone Hirohito, Tanaka Shoichiro, Kaneko Kenzo, Kamoi Kyuzi

机构信息

Department of Endocrinology and Metabolism, Nagaoka Red Cross Hospital, Japan.

出版信息

Intern Med. 2016;55(5):485-9. doi: 10.2169/internalmedicine.55.5398. Epub 2016 Mar 1.

Abstract

A 59-year-old Japanese woman developed diabetes mellitus without ketoacidosis in the presence of glutamic acid decarboxylase autoantibody (GADA) (24.7 U/mL). After the amelioration of her hyperglycemia, the patient had a relatively preserved serum C-peptide level. Her endogenous insulin secretion capacity remained almost unchanged during 5 years of insulin therapy. The patient's GADA titers normalized within 15 months. The islet-related autoantibodies, including GADA, are believed to be produced following the autoimmune destruction of pancreatic beta cells and are predictive markers of type 1 diabetes mellitus. Therefore, the transient appearance of GADA in our patient may have reflected pancreatic autoimmune processes that terminated without progression to insulin deficiency.

摘要

一名59岁的日本女性在存在谷氨酸脱羧酶自身抗体(GADA)(24.7 U/mL)的情况下发生了无酮症酸中毒的糖尿病。在她的高血糖得到改善后,患者的血清C肽水平相对保留。在胰岛素治疗的5年期间,她的内源性胰岛素分泌能力几乎保持不变。患者的GADA滴度在15个月内恢复正常。包括GADA在内的胰岛相关自身抗体被认为是在胰腺β细胞自身免疫性破坏后产生的,并且是1型糖尿病的预测标志物。因此,我们患者中GADA的短暂出现可能反映了胰腺自身免疫过程,该过程在未进展至胰岛素缺乏的情况下终止。

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