• Taeko Uonaga, Kenichi Yoshida, Takanari Harada, Makiko Shimodahira, and Yoshio Nakamura.
• Division of Diabetes and Endocrinology, Department of Internal Medicine, Hyogo Prefectural Amagasaki Hospital, Japan. diabetesandendocrinology@gmail.com
• Intern. Med. 2012 Jan 1; 51 (14): 187518771875-7.

AbstractA 57-year-old woman who had been treated with interferon β-1a (IFNβ-1a) for multiple sclerosis was diagnosed with diabetic ketosis. Her fasting serum C-peptide (F-CPR) was 1.9 ng/mL and her daily urinary C-peptide (U-CPR) was 24.1 µg/day. Her anti-glutamic acid decarboxylase (GAD) antibody was 3.5 U/mL. Seven months later, she was hospitalized with body weight loss and a high level of hemoglobin A1c [11.1% (JDS)]. Her F-CPR and U-CPR were very low (0.1 ng/mL and 8.35 µg/day, respectively), and anti-GAD antibody became distinctly positive (12.4 U/mL). She had HLA-DRB1*04:05, A24, and B54. For these reasons, IFNβ-1a administration was considered a possible cause of type 1 diabetes mellitus in this case.

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