(Santiago et al., 1992, p. 1029). Lastly, undiagnosed IDDM may also result in ketoacidosis or coma.
Through the measurement of C peptide levels, it can be shown these patients lack endogenous insulin (Hernandez, 1989, p. 162). Prior to the 1980s, it was thought that IDDM resulted from some viral infection. More recently, however, immune abnormalities have been associated with the disease. Researchers currently believe that autoimmune processes in susceptible children lead to destruction of their pancreatic B cells. Evidence for this hypothesis includes the common occurrence of insulitis or round cell infiltration of the pancreatic islets in recently diagnosed IDDM patients. Furthermore, in about 80% to 90% of patients, researchers have observed antibodies against either islet cells, insulin, or both. IDDM has also been closely associated with class II antigen genes located on the short arm of chromosome 6. These genes are thought to control the immune response. It could be that their alteration leads to IDDM susceptibility.
Finally, further evidence with regard to IDDM's autoimmune etiology involves immunosuppressive treatment strategies. In the initial stages of the disease, the formation of islet cell antibody may activate autoreactive T lymphocytes. Researchers have observed, however, that in newly diagnosed juveniles cyclosporine serum trough levels of 250 ng/mL will often induce remission. Following induction, this remission can then be maintained with cyclosporine serum levels of around 200 ng/mL. In general, immunosuppressive therapy must be continued for at least 2 years if IDDM relapse is to be avoided. While such therapy may be of benefit to juvenile IDDM patients, more research is needed to establish the long term effects of immunosuppressive agents (Hernandez, 1989, pp. 163 164).
More traditional therapy for IDDM generally involves blood glucose self monitoring (BGSM) and the use of exogeno...