Type 1 diabetes, commonly referred to as insulin-dependent diabetes (IDDM), is caused by pancreatic beta-cell destruction that leads to an absolute insulin deficiency. The clinical onset of diabetes does not occur until 80% to 90% of these cells have been destroyed. Prior to clinical onset, type 1 diabetes is often characterized by circulating autoantibodies against a variety of islet cell antigens, including glutamic acid decarboxylase (GAD), tyrosine phosphatase (IA2), and insulin. The autoimmune destruction of the insulin-producing pancreatic beta cells is thought to be the primary cause of type 1 diabetes. The presence of these autoantibodies provides early evidence of autoimmune disease activity, and their measurement can be useful in assisting the physician with the prediction, diagnosis, and management of patients with diabetes. Autoantibodies to IA2, a tyrosine phosphatase-like protein, are found in 50% to 75% of type 1 diabetics at and prior to disease onset. These autoantibodies are generally more prevalent in younger onset patients. Because the risk of diabetes is increased with the presence of each additional autoantibody, the positive predictive value of the IA2 antibody test is enhanced when measured in conjunction with antibodies to GAD and insulin.
References:
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IA-2 Autoantibodies
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