首页> 外文期刊>Journal of Hepatology: The Journal of the European Association for the Study of the Liver >Insulin-dependent diabetes mellitus during alpha-interferon therapy for chronic viral hepatitis.
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Insulin-dependent diabetes mellitus during alpha-interferon therapy for chronic viral hepatitis.

机译:α-干扰素治疗慢性病毒性肝炎期间的胰岛素依赖型糖尿病。

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A 29-year-old man was observed to develop insulin-dependent diabetes mellitus following a 5-month treatment with recombinant alpha-2b-interferon for chronic hepatitis C. After the onset of the disease, serum samples that had, respectively, been collected before therapy commencement, at month 3, and at the onset of insulin-dependent diabetes mellitus were tested for islet-cell (ICA-IgG), glutamic acid decarboxylase (GAD-Abs), IA2 (IA2-Abs) and insulin (IA-Abs) autoantibodies. The following results were obtained: ICA-IgG, 5, >80, and >80 JDF-U, respectively; GAD-Abs: >100 U/ml in all three measurements; IA2-Abs and IA-Abs: negative. During treatment, thyroid microsomal autoantibodies increased markedly (from 1:100 to 25,600 titer); thyroid-stimulating hormone was persistently normal. HLA class II typing revealed a genetic predisposition to insulin-dependent diabetes mellitus as demonstrated by the presence of DRB1* 04/08, DQ A1 52 Arg+/Arg+, and DQB1 57 N-Asp/Asp alleles. One year after the onset of insulin-dependent diabetes mellitus, the patient is still receiving 30 IU insulin daily; the liver function tests are normal and HCV-RNA is negative. These data support the hypothesis that, in predisposed patients, alpha-interferon therapy can enhance an ongoing autoimmune process against pancreatic beta-cells and induce overt insulin-dependent diabetes mellitus. We therefore suggest that, in patients with a documented predisposition to insulin-dependent diabetes mellitus, alpha-IFN therapy should be administered with caution.
机译:在重组α-2b-干扰素治疗慢性丙型肝炎5个月后,观察到一名29岁男子出现胰岛素依赖型糖尿病。该病发作后,分别收集了血清样本在开始治疗前,第3个月和胰岛素依赖型糖尿病发作之前,对胰岛细胞(ICA-IgG),谷氨酸脱羧酶(GAD-Abs),IA2(IA2-Abs)和胰岛素(IA- Abs)自身抗体。获得了以下结果:ICA-IgG,分别为5,> 80和> 80 JDF-U; GAD-Abs:所有三个测量值均大于100 U / ml; IA2-Abs和IA-Abs:阴性。在治疗过程中,甲状腺微粒体自身抗体显着增加(滴度从1:100增加到25,600)。甲状腺刺激激素持续正常。 HLA II类分型揭示了胰岛素依赖性糖尿病的遗传易感性,如DRB1 * 04/08,DQ A1 52 Arg + / Arg +和DQB1 57 N-Asp / Asp等位基因的存在所证明。胰岛素依赖型糖尿病发作一年后,患者仍每天接受30 IU胰岛素;肝功能检查正常,HCV-RNA阴性。这些数据支持以下假设:在易感患者中,α-干扰素治疗可增强正在进行的针对胰岛β细胞的自身免疫过程,并诱导明显的胰岛素依赖型糖尿病。因此,我们建议在有胰岛素依赖型糖尿病易感性的患者中,应谨慎使用α-IFN治疗。

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