ABSTRACT
Type 1 diabetes mellitus (T1D) accounts for 5-10% of all diabetic disorders. It is caused by cell-mediated autoimmune destruction of pancreatic islet beta cells, characterized by a silent phase of progressive beta cell destruction, followed by a symptomatic phase of hyperglycemia, when a greater amount of beta cell mass and function has been compromised. Beta cell abnormalities may have a causative role in the pathogenesis of T1D, leading to the hypothesis of beta cell suicide. Tight glycemic control associates with better outcomes in the long-term, and intensive insulin therapy is the recommended choice for T1D. Pancreas and islet transplantation at least transiently normalize glucose levels, mitigate microvascular complications of T1D, and improve quality of life. Pharmacological immunomodulation with monoclonal or polyclonal antibodies have failed to significantly affect insulin requirements. Ketoacidosis indicates extremely low production of insulin and thus may reflect a subset of patients with more advanced beta cell destruction.
