Clinical Information

Type 1 diabetes, commonly referred to as insulin-dependent diabetes mellitus (IDDM), is caused by pancreatic beta-cell destruction that leads to an absolute insulin deficiency.(1) 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.(2-5) 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. Insulin is the only beta-cell specific autoantigen thus far identified.(4-6) Antibodies to insulin are found predominantly, though not exclusively, in young children developing type 1 diabetes. In insulin-naive (untreated) patients, the prevalence of antibodies to insulin is almost 100% in very young individuals and almost absent in adult onset of type 1 diabetes. Because the risk of diabetes is increased with the presence of each additional autoantibody marker, the positive predictive value of insulin antibody measurement is increased when measured in conjunction with antibodies to GAD and IA2.(2-4)