English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

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.

endocrine journal

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