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引用次数: 0
摘要
胰岛素自身免疫综合征(IAS)是一种罕见的内分泌疾病,以反复发作的严重低血糖、血清胰岛素明显升高和胰岛素自身抗体阳性为特征。近年来,各国相继有相关报道。可见,我们必须重视这种疾病。IAS 的诊断具有挑战性,需要进行仔细的检查,以排除导致高胰岛素血症性低血糖的其他原因。患者体内存在高水平的胰岛素自身抗体,而 C 肽与胰岛素不平行,这可能是诊断的依据。IAS 是一种预后良好的自限性疾病。其治疗主要包括对症支持治疗,如调整饮食、使用阿卡波糖等药物延缓葡萄糖的吸收以预防低血糖。对于症状严重的患者,可用的治疗方法包括减少胰岛素分泌的药物(如体生长抑素和地亚佐醇)、免疫抑制剂(糖皮质激素、扎普林和利妥昔单抗),甚至是血浆置换以清除体内的自身抗体。本综述全面分析了 IAS 的流行病学、发病机制、临床表现、诊断和鉴别以及监测和治疗管理。
Insulin autoimmune syndrome (IAS) is a rare endocrine disorder characterized by recurrent episodes of severe hypoglycemia, markedly elevated serum insulin, and positive insulin autoantibodies. In recent years, various countries have reported it one after another. It can be seen that we must pay attention to this disease. The diagnosis of IAS is challenging, requiring a careful workup aimed at excluding other causes of hyperinsulinemic hypoglycemia. High levels of insulin autoantibodies are found in patients, and C-peptide is not parallel to insulin, which could be diagnostic. IAS is a self-limiting disease with a good prognosis. Its treatment mainly includes symptomatic supportive treatment, such as adjusting the diet and using acarbose and other drugs to delay the absorption of glucose to prevent hypoglycemia. For patients with severe symptoms, available treatments may include drugs that reduce pancreatic insulin secretion (such as somatostatin and diazoxide), immunosuppressants (glucocorticoids, zaprin, and rituximab), and even plasma exchange to remove autoantibodies from the body. This review provides a comprehensive analysis of the epidemiology, pathogenesis, clinical manifestations, diagnosis and identification, and monitoring and treatment management of IAS.
期刊介绍:
International Journal of Endocrinology is a peer-reviewed, Open Access journal that provides a forum for scientists and clinicians working in basic and translational research. The journal publishes original research articles, review articles, and clinical studies that provide insights into the endocrine system and its associated diseases at a genomic, molecular, biochemical and cellular level.