Abstract
For many decades insulin-dependent diabetes mellitus (IDDM = Type I diabetes) has been regarded as a metabolic disorder with a typical acute clinical onset. In the past 15 years, however, there have been substantial changes in previously established concepts of the etiopathogenesis of Type I diabetes (1,2). Based on immunologic, genetic and epidemiologic studies it is apparent that the majority of patients with Type I diabetes have a long, clinically silent prediabetic period. This latency period, which can antedate clinically overt manifestation of insulin-deficiency for up to several years, is featured by the presence of various autoimmune phenomena (2,3). Currently chronic autoimmune reactions are widely believed to play a key role in the progressive destruction of the insulin-producing beta-cells of the Langerhans islets, although a direct autoimmune attack has still to be proved.
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© 1988 Plenum Press, New York
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Gleichmann, H., Bottazzo, G.F., Gries, F.A. (1988). Cytoplasmic Islet Cell Autoantibodies: Prevalence and Pathognomic Significance. In: Camerini-Davalos, R.A., Cole, H.S. (eds) Prediabetes. Advances in Experimental Medicine and Biology, vol 246. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5616-5_9
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DOI: https://doi.org/10.1007/978-1-4684-5616-5_9
Publisher Name: Springer, Boston, MA
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