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Abstract

Type 1 diabetes (T1D) [MIM 222100] is the third most prevalent chronic disease of childhood, affecting up to 0.4% of individuals in some populations by age 30 years, with an overall lifetime risk of nearly 1%.1,2 T1D is caused by absolute insulin deficiency due to destruction of the pancreatic β-cells. The majority of T1D cases are believed to develop as a result of immune-mediated destruction of the β-cells, leaving a small proportion of idiopathic cases in which immune markers cannot be detected, which are caused by other pathogenetic mechanisms such as rare genetic syndromes, β-cell lytic virus infections, or environmental factors.3 T1D is associated with an increased risk of premature death due to acute complications and chronic disabling and life-threatening manifestations, including eye disease and blindness, renal failure, neuropathy and cardiovascular disease.4

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