Type 1 diabetes mellitus (T1DM) is a chronic disease of insulin deficiency and hyperglycemia. In the vast majority of cases, insulin deficiency follows immune-mediated destruction of pancreatic beta cells. It most commonly presents in childhood or adolescence, but a significant number of cases are diagnosed in adults. Diabetes manifests only after the destruction of a majority of pancreatic beta cells.

Patients may present with symptoms of hyperglycemia such as weight loss, polyuria, polydipsia, fatigue, nocturnal enuresis, and blurry vision. T1DM patients may present with diabetic ketoacidosis (DKA), a state of severe dehydration and acidemia due to insulin deficiency. Symptoms include abdominal pain, nausea, emesis, inattention, confusion, and even coma in the setting of hyperglycemia and elevated anion gap. DKA is often associated with compensatory hyperventilation (Kussmaul respiration) in the setting of primary metabolic acidosis and a fruity breath odor.

The pathogenesis appears to be rooted in a genetic component that interacts with an environmental insult in most cases. The incidence of T1DM has been increasing in the United States over the last several decades, with 2-3 new cases per 10 000 person years. There have been several reports about increased incidence of T1DM following acute COVID-19 infections.

Genetic risks (HLA haplotype and other identified genes) for T1DM account for almost 40%-50% of cases. The anti-CD3 monoclonal antibody teplizumab-mzwv is approved by the US Food and Drug Administration (FDA) to delay the onset of clinical T1DM for genetic high-risk patients aged 8 years and older.

Related topics: bullosis diabeticorum, diabetes mellitus type 2, diabetic dermopathy, diabetic hyperosmolar syndrome, diabetic nephropathy, diabetic neuropathy, diabetic retinopathy, diabetic vulvitis, maturity-onset diabetes of the young (MODY), neurogenic ulcer