Abstract
It is widely accepted that autoimmune mechanisms are involved in the pathogenesis of type I (insulin-dependent, IDDM) diabetes mellitus. (1)Islet cell antibodies (ICA) reacting with antigens in the cytoplasma, or on the surface of islet-cells (ICSA), or against a 64 kD human islet-cell protein, as well as insulin autoantibodies (lAA) are present years before the onset of clinical diabetes. They probably serve as serologic markers of ongoing beta-cell destruction in predisposed individuals. In monozygotic twins initially discordant for type I diabetes, loss of beta-cell function has been shown to be temporarily associated with the presence of ICA (2). Several studies in discordant monozygotic twins or first-degree relatives of type I diabetics revealed that ICA-positive relatives are more likely to develop overt diabetes than are the ICA-negative (3). Moreover, the presence of both ICA and lAA in these individuals confers an even higher risk of progression to IDDM (1)
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© 1988 Plenum Press, New York
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Spinas, G.A., Matter, L., Wilkin, T., Staffelbach, O., Berger, W. (1988). Iselt-Cell and Insulin Autoantibodies in First-Degree Relatives of Type I Diabetics: A 5-Year Follow-Up Study in a Swiss Population. 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_25
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DOI: https://doi.org/10.1007/978-1-4684-5616-5_25
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