التفاصيل البيبلوغرافية
| العنوان: |
Genetic risk factors for type 1 diabetes. |
| المؤلفون: |
Pociot, Flemming1, Lernmark, Åke2 ake.lernmark@med.lu.se |
| المصدر: |
Lancet. 6/4/2016, Vol. 387 Issue 10035, p2331-2339. 9p. 1 Color Photograph, 1 Chart, 4 Graphs. |
| مصطلحات موضوعية: |
TYPE 1 diabetes, AUTOIMMUNITY, AUTOANTIBODIES, GLUTAMATE decarboxylase, BIOMARKERS, HAPLOTYPES, DIABETES risk factors |
| مستخلص: |
Type 1 diabetes is diagnosed at the end of a prodrome of β-cell autoimmunity. The disease is most likely triggered at an early age by autoantibodies primarily directed against insulin or glutamic acid decarboxylase, or both, but rarely against islet antigen-2. After the initial appearance of one of these autoantibody biomarkers, a second, third, or fourth autoantibody against either islet antigen-2 or the ZnT8 transporter might also appear. The larger the number of β-cell autoantibody types, the greater the risk of rapid progression to clinical onset of diabetes. This association does not necessarily mean that the β-cell autoantibodies are pathogenic, but rather that they represent reproducible biomarkers of the pathogenesis. The primary risk factor for β-cell autoimmunity is genetic, mainly occurring in individuals with either HLA-DR3-DQ2 or HLA-DR4-DQ8 haplotypes, or both, but a trigger from the environment is generally needed. The pathogenesis can be divided into three stages: 1, appearance of β-cell autoimmunity, normoglycaemia, and no symptoms; 2, β-cell autoimmunity, dysglycaemia, and no symptoms; and 3, β-cell autoimmunity, dysglycaemia, and symptoms of diabetes. The genetic association with each one of the three stages can differ. Type 1 diabetes could serve as a disease model for organ-specific autoimmune disorders such as coeliac disease, thyroiditis, and Addison's disease, which show similar early markers of a prolonged disease process before clinical diagnosis. [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: |
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