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胰岛素受体自身抗体作为系统性红斑狼疮自身免疫性低血糖症的一个病因

Autoantibodies to the insulin receptor as a cause of autoimmune hypoglycemia in systemic lupus erythematosus.

作者信息

Moller D E, Ratner R E, Borenstein D G, Taylor S I

机构信息

Department of Medicine, George Washington University Medical Center, Washington, D.C. 20037.

出版信息

Am J Med. 1988 Feb;84(2):334-8. doi: 10.1016/0002-9343(88)90436-6.

Abstract

A 52-year-old black woman presented with clinical features of systemic lupus erythematosus (SLE) and severe fasting hypoglycemia. Hypoglycemia was secondary to autoantibodies to the insulin receptor that were detected in the patient's serum. There were no anti-insulin antibodies, and other causes of hypoglycemia were excluded. Treatment with high-dose glucocorticoids resulted in restoration of euglycemia associated with resolution of circulating anti-receptor antibodies and parallel improvement in clinical and laboratory features of SLE. This case is compared with other cases of autoimmune hypoglycemia due to anti-receptor antibodies.

摘要

一名52岁的黑人女性出现了系统性红斑狼疮(SLE)的临床特征以及严重的空腹低血糖症。低血糖是由患者血清中检测到的胰岛素受体自身抗体所致。不存在抗胰岛素抗体,且排除了低血糖的其他病因。高剂量糖皮质激素治疗使血糖恢复正常,同时循环抗受体抗体消失,SLE的临床和实验室特征也随之得到改善。将该病例与其他因抗受体抗体导致的自身免疫性低血糖病例进行了比较。

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