Using continuous glucose monitoring to detect early dysglycaemia in children participating in the Environmental Determinants of Islet Autoimmunity (ENDIA) study (Sub Protocol)

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Type 1 diabetes (T1D) is classically regarded as a metabolic disorder diagnosed when the symptoms of persistently high blood glucose levels appear. The clinical presentation, however, follows an extended period of months to years when the immune system attacks the insulin producing cells in the pancreas. Prospective longitudinal studies of older children at genetic risk of T1D have shown that impaired glucose homeostasis starts much earlier than symptomatic diabetes. A gradual decline in insulin secretion and beta cell sensitivity can be detected at least 2 years before the onset of clinical symptoms, and these changes become more rapid in the last few months prior to diagnosis. Higher glucose levels and increased glycaemic variability are also detectable prior to the onset of clinical T1D. This recent recognition that T1D progresses in these three distinct stages has led to a paradigm shift that re-defines T1D as an autoimmune beta cell disorder with clear characteristics associated with Stage 1, Stage 2, and Stage 3 (symptomatic) disease. The purpose of this sub-study is to undertake serial measurements of continuous glucose monitoring data in the ENDIA protocol that will provide the longitudinal data required to define the transition in islet autoantibody-positive children from normoglycaemia (Stage 1 T1D) to dysglycaemia (Stage 2 T1D). Moreover, it will enable characterisation of asymptomatic hyper- or hypo-glycaemia and inform clinical care for such children prior to onset of symptomatic clinical T1D (State 3 T1D).

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