INSULIN-DEPENDENT DIABETES-MELLITUS - ISLET CHANGES IN RELATION TO 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 absolute insulin deficiency and is therefore referred to as insulin-dependent diabetes. The disease becomes manifest clinically in childhood or adolescence (''juvenile diabetes''), though onset in adu lthood is increasingly being observed. Morphologically a subtotal (>80 %) to total loss of beta-cells in the pancreatic islets occurs. Lympho cytic insulitis, which disappears after the beta-cells have been total ly destroyed, is pathogneumonic 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 (human leukocyte antigen [HLA] DR3/DR4/DQ8) in connection with as-yet -unknown environmental factors (e.g., viruses). Autoantibodies, such a s islet cell cytoplasmic antibodies (ICA), insulin autoantibodies (IAA ), and/or autoantibodies to the gamma-aminobutyric acid (GABA)-synthes izing enzyme glutamic acid carboxylase (CAD), are already detectable i n a prediabetic phase, though it is not possible to predict the time o f clinical onset. The course of the disease is dependent on age. Young children require insulin therapy sooner than juveniles or adults.