Trajectories of anti-islet autoantibodies before development of type 1 diabetes in interferon-treated hepatitis C patients. Case reports and a literature review
Trajectories of anti-islet autoantibodies before development of type 1 diabetes in interferon-treated hepatitis C patients. Case reports and a literature review
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DOI：
10.1507/endocrj.k10e-207
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发表时间：
2010-11-01
影响因子：
2
通讯作者：
Eguchi, Katsumi
中科院分区：
文献类型：
--
作者：
Nakamura, Kan;Kawasaki, Eiji;Eguchi, Katsumi
干扰素-α（IFN-α）被广泛用于治疗病毒性肝炎，然而，已知IFN-α疗法可诱发1型糖尿病。我们在此报告两例慢性丙型病毒性肝炎患者，在聚乙二醇-ITN-α加利巴韦林（RBV）治疗期间发生自身免疫性1型糖尿病。病例1：48岁男性，慢性丙型肝炎伴慢性甲状腺炎。在Peg-IFN-α +RBV治疗前，患者的血糖水平正常，抗胰岛自身抗体试验阴性。治疗5个月后观察到谷氨酸脱羧酶65自身抗体（GAD 65 Ab）的出现。胰岛素和胰岛素瘤相关抗原-2（IA-2）的自身抗体也呈阳性。11个月后，出现口渴和烦渴，空腹血糖水平升高，患者被诊断为IA型糖尿病。锌转运蛋白-8自身抗体（ZnT 8Ab）在任何时间点均未检出。患者具有1型糖尿病易感HLA-DRB 1-DQB 1单倍型 *0405-*0401和 *0901-*0303。病例2：一名65岁男性慢性丙型肝炎伴2型糖尿病，正在接受胰岛素治疗。Peg-IFN-α +RBV治疗前GAD 65 Ab和IA-2 Ab均为阴性，但9个月后观察到GAD 65 Ab的单一出现。12个月后，他的血糖控制迅速恶化，并被诊断为IA型糖尿病。IA-2Ab和ZnT 8Ab在整个临床过程中均为阴性。HLA-DRB 1-DQB 1单倍型为 *0410-*0402和 *1407-*0503。两种情况均显示出独特的GAD 65 Ab表位（氨基酸360-442）。这些临床过程表明，IFN-α治疗引起急性胰岛自身免疫和1型糖尿病的发病。因此，在IFN-α治疗期间，应密切监测患者1型糖尿病的发生。
Interferon-alpha (IFN-alpha) is widely used in the treatment of viral hepatitis, however, it is known that IFN-alpha therapy may induce type 1 diabetes. We report here on two cases of chronic viral hepatitis C who developed autoimmune type 1 diabetes during Peg-ITN-alpha plus ribavirin (RBV) therapy. Case 1: a 48-year-old male with chronic hepatitis C with chronic thyroiditis. The patient's plasma glucose level was normal and anti-islet autoantibody tests were negative before Peg-IFN-alpha+RBV therapy. The emergence of glutamic acid decarboxylase 65 autoantibody (GAD65Ab) was observed after five months of treatment. Autoantibodies to insulin and insulinoma-associated antigen-2 (IA-2) also became positive. Eleven months later, thirst and polydipsia occurred with increased fasting plasma glucose level and the patient was diagnosed with type IA diabetes. Zinc transporter-8 autoantibody (ZnT8Ab) was not detectable at any point. The patient has type 1 diabetes-susceptible HLA-DRB1-DQB1 haplotypes *0405-*0401 and *0901-*0303. Case 2: a 65-year-old male with chronic hepatitis C with type 2 diabetes on insulin treatment. GAD65Ab and IA-2Ab were negative before Peg-IFN-alpha+RBV therapy, however, nine months later, a single appearance of GAD65Ab was observed. After twelve months, his plasma glucose control worsened rapidly, and he was diagnosed with type IA diabetes. IA-2Ab and ZnT8Ab were negative throughout the clinical course. His HLA-DRB1-DQB1 haplotypes were *0410-*0402 and *1407-*0503. Both cases showed a unique GAD65Ab epitope (amino acids 360-442). These clinical courses suggest that IFN-alpha therapy provoked acute islet autoimmunity and onset of type 1 diabetes. Therefore, during IFN-alpha therapy, patients should be closely monitored for the occurrence of type 1 diabetes.