Trajectories of anti-islet autoantibodies before development of type 1 diabetes in interferon-treated hepatitis C patients. Case reports and a literature review
| Autor: | Kan Nakamura, Keiko Fukushima, Ozora Jo, Masakazu Kobayashi, Eiji Kawasaki, Katsumi Eguchi, Tatsuya Ide, Norio Abiru, Hironori Yamasaki, Genpei Kuriya, Hironaga Kuwahara, Tsuyoshi Satoh |
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| Rok vydání: | 2010 |
| Předmět: |
Male
Endocrinology Diabetes and Metabolism Hepacivirus Zinc Transporter 8 Type 2 diabetes Islets of Langerhans Endocrinology Diabetes mellitus medicine Humans Chronic thyroiditis Cation Transport Proteins Aged Autoantibodies Type 1 diabetes Glutamate Decarboxylase business.industry Autoantibody Interferon-alpha Hepatitis C Hepatitis C Chronic Middle Aged medicine.disease Diabetes Mellitus Type 1 Immunology medicine.symptom business Viral hepatitis Polydipsia |
| Zdroj: | Endocrine Journal. 57:947-951 |
| ISSN: | 1348-4540 0918-8959 |
| DOI: | 10.1507/endocrj.k10e-207 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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