Objective: Interferon therapy can trigger induction of several autoimmune diseases, including type 1 diabetes. To assess the clinical, immunologic, and genetic characteristics of type 1 diabetes induced by interferon therapy, we conducted a nationwide cross-sectional survey.
Research design and methods: Clinical characteristics, anti-islet autoantibodies, and HLA-DR typing were examined in 91 patients for whom type 1 diabetes developed during or shortly after interferon therapy.
Results: Median age at the onset of type 1 diabetes was 56 (interquartile range 48-63) years and mean ± SD BMI was 20.8 ± 2.7 kg/m(2). The time period from the initiation of interferon therapy to type 1 diabetes onset in patients receiving pegylated interferon and ribavirin was significantly shorter than that in patients with nonpegylated interferon single therapy (P < 0.05). Anti-islet autoantibodies were detected in 94.5% of patients at diabetes onset. Type 1 diabetes susceptibility HLA-DRs in the Japanese population, DR4 and DR9, were also associated with interferon treatment-related type 1 diabetes. Furthermore, the prevalence of HLA-DR13 was significantly higher in interferon treatment-related type 1 diabetes than in healthy control subjects (odds ratio 3.80 [95% CI 2.20-7.55]; P < 0.0001) and classical type 1 diabetes (2.15 [1.17-3.93]; P < 0.05).
Conclusions: Anti-islet autoantibodies should be investigated before and during interferon therapy to identify subjects at high risk of type 1 diabetes. Stronger antiviral treatment may induce earlier development of type 1 diabetes. Furthermore, patients who develop interferon-induced type 1 diabetes are genetically susceptible.