Correlation between residual beta-cell function and islet cell antibodies in newly diagnosed type I diabetes. Follow-up study

Publisher Website
Google Scholar
Abstract
To establish whether there is a correlation between the autoimmune response to the islets and β-cell function during the initial stages of type I (insulin-dependent) diabetes, an islet cell antibody (ICA) titer and C-peptide levels (fasting and glucagon stimulated) were determined in 39 newly diagnosed patients at onset of diabetes and every 3–6 mo for 2 yr. ICAs were detected in 74% of the patients, and β-cell function was detected in 84% of the patients at onset. The ICA+ and ICA− groups had similar C-peptide values at diagnosis and at 3 mo, but from 6 mo on, the ICA+ group consistently showed a tendency to lose C-peptide secretory capacity more quickly when assessed by fasting and glucagon-stimulated C-peptide levels (ICA+ vs. ICA− fasting C-peptide levels at 18 and 24 mo, P = .013 and .017, respectively; ICA+ vs. ICA− glucagon-stimulated C-peptide levels at 6,18, and 24 mo, P = .023, .007, and .028, respectively). The initial ICA titer had the highest predictive value on the outcome of β-cell function ( P = .04), and patients with complement-fixing ICAs did not behave differently from the general ICA+ group. This correlation between β-cell function and ICA titer supports the role of autoimmunity in the pathogenesis of type I diabetes and has important implications for the design of immunotherapy trials.