Fulminant Autoantibody-Negative and Type 1A Diabetes Phenotypes in a Korean HLA Identical Dizygotic Twin
- Jung H. Jung, MD1,
- Jong R. Hahm, MD12,
- Me A. Kim, MD23,
- Myoung H. Park, MD4,
- Deok R. Kim, PHD25,
- Tae S. Jung, MD1 and
- Soon I. Chung, MD12
- 1Department of Internal Medicine, Gyeongsang National University Hospital, Jinju, Republic of Korea
- 2Gyeongsang Institute of Health Sciences, Jinju, Republic of Korea
- 3Department of Laboratory Medicine, Gyeongsang National University Hospital, Jinju, Republic of Korea
- 4Department of Laboratory Medicine, Seoul National University Hospital, Seoul, Republic of Korea
- 5College of Medicine, Biochemistry, Gyeongsang National University, Jinju, Republic of Korea
- Address correspondence to Jong Ryeal Hahm, Gyeongsang National University Hospital, #90 Chilamdong, Jinju, Republic of Korea. E-mail: jrhahm{at}gshp.gsnu.ac.kr
Type 1 diabetes is a complex, heterogenous autoimmune disease. Many genetic and environmental factors are thought to be involved in type 1 diabetes pathogenesis as shown in other autoimmune disorders. Although some immune-related genes such as HLA, AIRE, and CTLA-4 have been elucidated about their association in pathogenesis, the detailed genetic factors causing type 1 diabetes are unclear. In a study of twins with type 1 diabetes, significant subsets of monozygotic and dizygotic twins did not progress to clinical diabetes (1), suggesting that genetic heterogeneity and other random factors are crucial for type 1 diabetic pathogenesis, even in twins. Typically, type 1 diabetes is initiated by an autoimmune response against β-cells and followed by progressive defect of insulin secretion from β-cells. These results cause hyperglycemia and transient, usually partial remission, and finally lead to complete insulinopenia. Since Imagawa et al. …
