Recent advances in type 1 diabetes
Type 1 diabetes (T1D) affects around 120 000 Australians, half of whom are diagnosed in adulthood.1 It is caused by the immune-mediated destruction of pancreatic beta cells, leading to insulin deficiency, hyperglycaemia and the risk of ketoacidosis. Antibodies directed against the beta-cell antigens insulin, glutamic acid decarboxylase 65 (GAD65), insulinoma-associated protein 2 (IA-2) and zinc transporter 8 (ZnT8) are markers of T1D autoimmunity used to confirm the diagnosis of T1D and to identify normoglycaemic people at high risk of progressing to T1D.2 The incidence of T1D has doubled in Australia during the past 20 years,3 leading to speculation that it is caused by environmental or epigenetic factors. Environmental changes that may play a pathogenic role include viral infections, a more hygienic environment, and increased caloric intake with associated weight gain.4
Some individuals with insulin deficiency presenting as T1D do not express the typical beta-cell autoantibodies, and alternative diagnoses, such as early-onset type 2 diabetes or idiopathic (type 1b) diabetes, should be considered. Another possibility is monogenic diabetes, particularly in children with a strong family history and unusual clinical features, such as renal impairment or exocrine pancreatic insufficiency.
General management principles