Trajectories of anti-islet autoantibodies before development of type 1 diabetes in interferon-treated hepatitis C patients. Case reports and a literature review

Endocrine Journal

Kan Nakamura²  Masakazu Kobayashi³  Ozora Jo³  Genpei Kuriya³  Tsuyoshi Satoh³  Hironaga Kuwahara³  Hironori Yamasaki⁴  Eiji Kawasaki²  Katsumi Eguchi²  Keiko Fukushima³  Tatsuya Ide¹  Norio Abiru³ 

[1] Division of Gastroenterology, Department of Medicine, Kurume University School of Medicine, Fukuoka, Japan;Department of Metabolism/Diabetes and Clinical Nutrition, Nagasaki University Hospital, Nagasaki, Japan;First Department of Internal Medicine, Graduate School of Biomedical Science, Nagasaki University, Nagasaki, Japan;Center for Health and Community Medicine, Nagasaki University, Nagasaki, Japan

关键词: Type 1 diabetes;    Interferon;    Glutamic acid decarboxylase 65 autoantibody;    HLA;   

DOI  :  10.1507/endocrj.K10E-207

学科分类：内分泌与代谢学

来源: Japan Endocrine Society

【 摘 要 】

References(17)Cited-By(5)Interferon-alpha (IFN-α) is widely used in the treatment of viral hepatitis, however, it is known that IFN-α 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-IFN-α 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-α+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 1A 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-α+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 1A 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-α therapy provoked acute islet autoimmunity and onset of type 1 diabetes. Therefore, during IFN-α therapy, patients should be closely monitored for the occurrence of type 1 diabetes.

【 授权许可】

Unknown