Insulin-independent diabetes mellitus. Current aspects of its morphology, etiology, and pathogenesis

Type I and type II diabetes are the most common types of diabetes. The ratio of type I to type II diabetes is about 1:9. Type I diabetes is caused by an absolute insulin deficiency and is therefore referred to as insulin-dependent diabetes. The disease becomes manifest clinically in childhood or adolescence (''juvenile diabetes''), although manifestation in adulthood is being increasingly observed. Morphologically, a subtotal (>80%) to total loss of beta cells in the pancreatic islets occurs. Lymphocytic insulitis, which disappears after the beta cells have been totally destroyed, is pathognomonic of type I diabetes. This insulitis is an expression of an autoimmune event that is triggered by a multitude of factors. An important factor appears to be a genetic predisposition (HLA DR3/DR4/DQ8) in connection with as yet unknown environmental factors (e. g., viruses). Autoantibodies, such as islet cell cytoplasmic antibodies (ICA), insulin autoantibodies (IAA), and/or autoantibodies to the GABA-synthesizing enzyme glutamic acid carboxylase (GAD), are already detectable in a prediabetic phase, although it is not possible to predict the time of clinical manifestion. The course of the disease is dependent on age. Young children require insulin therapy sooner than juveniles or adults.