[The pathogenesis of type 1 diabetes mellitus].

It is now widely accepted, that the development of type 1 diabetes is based on an autoimmune destruction of the insulin-producing betacells of the pancreas; however, a genetic predisposition is required. 90 to 95% of patients with type 1 diabetes are HLA-DR3 positive and/or HLA-DR4 positive. In addition, recent results from molecular-genetic research suggest an aspartate on position 57 of the HLA-DQ-beta protein, which seems to protect against the autoimmune destruction of the betacell, since it is not found in patients with type 1 diabetes in contrast to control persons. Trigger substances inducing the initial betacell destruction are not known, but might not be necessary according to an actual hypothesis. Finally, all insulin-producing cells are destroyed, and lifelong insulin replacement therapy cannot be circumvented. Prevention of the autoimmune destruction is not possible today; especially, not using immunosuppressive drugs because of side effects.