Autoimmune diabetes is an organ-specific autoimmune disease that caused by an autoimmune process in the body that mistakenly destroys the insulin-producing cells, or pancreatic β-cells and after an inflammatory process leads to a chronic deficiency of insulin in genetically susceptible individuals. Cytokines such as interleukin-1, released by activated immune cells, have been shown to inhibit insulin secretion from pancreatic β-cells and cause islet destruction.
There may be some β-cells re-formation (by cell division or by new cell formation) that replaces the destroyed cells. But over the years, the net destruction is greater than the replacement.
When the number of β-cells is reduced by approximately 80%, the body is unable to secrete enough insulin, the blood sugar rises and clinical diabetes is diagnosed.
People with Severe autoimmune diabetes are typically diagnosed early, at a young age. They usually have a low body mass index (BMI), insulin deficiency, poor control of blood sugar, and presence of glutamate decarboxylase antibodies (GADA).
The clinical manifestation (i.e., hyperglycemia) represents the final stage of insulitis (i.e., inflammation in pancreatic islets). The exact cause is unknown, but it is believed to be the result of an interaction of genetic and environmental factors. A patient needs insulin replacement to survive and, except in cases where a pancreatic or islet cell transplant occurs, insulin will be required every day for the rest of their life.
Cluster 1: Severe autoimmune diabetes
