Type 1 Diabetes Mellitus

Type 1 diabetes mellitus (T1DM) is the most common chronic endocrine disorder of childhood and is increasing worldwide. It is defined by immune-mediated destruction of pancreatic β-cells in genetically susceptible individuals – principally those carrying HLA-DR3/DR4-DQ2/DQ8 haplotypes – with additional contributions from non-HLA loci (e.g., INS, PTPN22, CTLA4, IL2RA) and environmental triggers such as viral infections, early-life nutritional exposures, vitamin D deficiency, microbiome dysbiosis, and obesity-related insulin resistance. The disease often presents abruptly after ~80%–90% β-cell loss with polyuria, polydipsia, weight loss, and, in 20%–40% of cases, diabetic ketoacidosis. Diagnosis relies on ADA/ISPAD glucose or HbA1c thresholds, supported by islet autoantibodies and preserved C-peptide patterns in differential diagnoses. Management centers on lifelong insulin replacement delivered as multiple daily injections or continuous subcutaneous insulin infusion, increasingly optimized by continuous glucose monitoring and hybrid closed-loop systems. Individualized glycemic targets (HbA1c < 7.0% for most; CGM time-in-range > 70%) balance safety and efficacy across developmental stages. Acute complications include hypoglycemia and DKA; chronic complications warrant structured screening for retinopathy, nephropathy, neuropathy, dyslipidemia, and hypertension, alongside surveillance for associated autoimmune diseases. Preventive strategies now include risk stratification by autoantibodies and emerging immunotherapies; notably, teplizumab delays progression from stage 2 to clinical T1DM. Comprehensive, multidisciplinary care remains essential to optimize outcomes.