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Islet cell surface antibodies by an ELISA method in diabetic and nondiabetic patients

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Abstract

Islet cell surface antibodies (ICSA) were investigated by an ELISA method using a commercial kit in 146 subjects with and without islet cell antibodies (ICA): 28 with insulin-dependent diabetes mellitus (IDDM), 24 with noninsulin-dependent diabetes mellitus (NIDDM), 22 first-degree relatives (FDR) of IDDM patients, 31 organ-specific autoimmune patients (OSAP), 21 nonautoimmune hospitalized patients (NAP), and 20 ICA-negative normal controls. Furthermore, insulin autoantibodies (IAA) were evaluated in 87 of these subjects. ICSA were found in 11% of IDDM patients and in 14% of their FDR, in 4% of NIDDM patients, in 10% of OSAP, in 10% of NAP, and in 5% of normal controls. After absorption with rat liver powder, ICSA were detected in 7% of IDDM patients, in 5% of their FDR, in 4% of NIDDM, in 6% of OSAP, in 5% of NAP and in none of normal controls. ICSA were also detected in 4% of IAA-positive compared to 3% of IAA-negative sera. Neither correlation was found between ICSA and ICA in each group of subjects, nor between ICSA and IAA, suggesting that these autoantibodies recognize different pancreatic targets. Moreover, no significant difference was observed for ICSA prevalence in the various groups of patients studied when compared with normal controls. The prevalence of ICSA assessed by this ELISA method has been compared to that reported by other workers, who employed different techniques. We also discuss here the pathogenetic role and the clinical relevance of the most common markers of pancreatic autoimmunity. We conclude that the role of ICSA as possible indicators of β cell damage still remains to be evaluated in humans, and that the standardization of such antibodies is an essential prerequisite for understanding their actual prevalence and planning useful prospective investigations.

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Betterle, C., Presotto, F., Magrin, L. et al. Islet cell surface antibodies by an ELISA method in diabetic and nondiabetic patients. J Endocrinol Invest 14, 293–297 (1991). https://doi.org/10.1007/BF03346816

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  • DOI: https://doi.org/10.1007/BF03346816

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