کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2910414 | 1174625 | 2008 | 6 صفحه PDF | دانلود رایگان |

SummaryBackground and aimsAutoantibodies to islet cell antigens such as insulin (IAA), the 65-kDa isoform of glutamate decarboxylase (GAD65) and the protein tyrosine phosphatase (PTP) like antigen IA-2 are markers of the autoimmune process preceding type 1 diabetes (T1DM) and may help to predict the rapid decrease in residual β-cell function. The present investigation was undertaken to evaluate the relation between GAD65 and IA-2 in children with newly diagnosed T1DM and to compare the frequency and levels of autoantibodies with clinical characteristics.Method and resultsA total of 102 T1DM subjects (age at onset <30 years; mean duration of disease 6.7 ± 2.8 years) from north India were characterized by serological determination of the islet cell antibodies, GAD65 and IA-2. One hundred and two age and sex matched non-diabetic subjects of the non-diabetic parents served as control. Prevalence of autoantibodies in diabetic population was 47%, GAD65 antibodies was positive in 42 (41.2%) and IA-2 in 21 subjects (20.6%). A total of 14.7% (n = 15) TIDM subjects showed both GAD65 plus IA-2 autoantibody positivity. Comparison between GAD65 positive and GAD65 negative groups showed younger age of onset, low BMI and decreased C-peptide. GAD65 positivity alone was associated with 6.39 times risk, IA-2 autoantibodies positivity with 5.4 times risk of developing TIDM. Risk increased to 7.6 times of control population, when both autoantibodies were positive.ConclusionPrevalence of autoantibodies in TIDM and control group is much less than that of western population suggesting heterogeneous nature of a young diabetic population with substantial percentage of patients having non-immune type 1B diabetes. Despite low positivity, islets cell autoimmunity plays dominant role in young TIDM of north India.
Journal: Diabetes & Metabolic Syndrome: Clinical Research & Reviews - Volume 2, Issue 1, February 2008, Pages 59–64