FeaturesType 2 diabetesType 1 diabetesLatent autoimmune diabetes in adults
KetoacidosisUsually absentWill develop rapidly unless patient receives insulin replacement therapyAbsent at diagnosis, but may be present when patient becomes severely insulinopenic
Cardiovascular complicationsRisk 2–4 times higher than individuals who are euglycemicIncreased risk of cardiovascular morbidity and mortality related to strokes, acute coronary events, and coronary revascularizations; high incidence rates compared with euglycemic individuals, especially in womenSame risk as patients with T2DM
Microvascular complications (retinopathy, nephropathy, neuropathy)IncreasedIncreasedIncreased
PathophysiologyPeripheral insulin resistance; reduced pancreatic beta-cell mass and function; reduced insulin secretionAutoimmune destruction of pancreatic beta-cellsLatent autoimmune destruction of pancreatic beta-cells
AutoantibodiesNegative

  • GAD-65 autoantibodies

  • Islet-cell antigen-2

  • Insulin autoantibodies

  • note: Unlike LADA, T1DM patients typically are positive for all three autoantibodies

  • GAD-65 autoantibody is typically the only one detected

  • Islet-cell antibodies

Insulin requirements for treatmentUsually late in the disease when the remaining beta-cell mass and function can no longer support acceptable glycemic control achieved by oral agents or incretin mimeticsInsulin is required from the time of diagnosisInsulin should be initiated as soon as the patient develops autoantibodies