Type 1 diabetes is due to an autoimmune destruction of the insulin producing b-cells in the Langerhans islets in the pancreas. The destruction is probably triggered by one or more unknown environmental factors which in genetically predisposed individuals starts a slowly progressive process. Only when the number of viable b-cells is below a critical threshold, does hyperglycaemia with the accompanying symptoms arise. Islet cell antibodies are detected with IIF on monkey pancreas and the analysis is positive in 70-90% of T1D patients at the time of the diagnosis.
The antibodies react with glutamic acid decarboxylase (GAD), insulinom-associated protein 2 (IA-2), insulin, zinc transporter 8 (ZnT8) antibodies and probably other unknown antigens. Specific antibodies against the different known antigens can be detected with immunoprecipitation or ELISA. So far all prospective studies of relatives of T1D patients have shown that the combination of two or more antibodies give a higher positive predictive value than only one antibody. Up to 90% of the asymptomatic antibody carriers will be insulin-dependent within 6 years.
Analysis: Islet cell antibodies, anti GAD-65, anti IA-2, anti-insulin.