Abstract
Diabetes always has been a defensive specialty for the physician. The treatment of insulin-dependent diabetes mellitus (IDDM) aims to mimic normal physiology, minimize hazards, palliate late complications, and offer guidance and support. It is essentially an exercise in damage limitation. Much can be achieved with current therapy, and microvascular complications can be prevented— or at least delayed—by improved glycemic control. Even so, current means of achieving safe near normoglycemia remain limited at best. Many of us hope and believe that, as the next millenium approaches, it will for the first time prove possible to assume the offensive, whether by restoring insulin secretion or halting the incipient disease process before clinical onset of IDDM. New and safer means of restoring normoglycemia are high on the research agenda for the established diabetic patient, but progress remains frustratingly slow. In contrast, work into the pathogenesis of IDDM continues to gather momentum 20 years after its human leukocyte antigen associations (1,2) and islet cell antibodies (ICAs) (3) were discovered.
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