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Original Contributions

Glutamic Acid Decarboxylase (GAD65) Autoantibodies in Prediction of β-Cell Function and Remission in Recent-Onset IDDM After Cyclosporin Treatment

  1. Jacob Sten Petersen,
  2. Thomas Dyrberg,
  3. Allan E Karlsen,
  4. Jens Mølvig,
  5. Birgitte Michelsen,
  6. Jørn Nerup,
  7. Thomas Mandrup-Poulsen and
  8. Canadian-European Randomized Control Trial Group
  1. Hagedorn Research Institute Gentofte, Denmark
  2. Novo Nordisk A/S Bagsvaerd, Denmark
  3. Steno Diabetes Centre Gentofte, Denmark
  1. Address correspondence and reprint requests to Jacob Sten Petersen, Hagedorn Research Institute, Niels Steensens Vej 6, DK-2820 Gentofte, Denmark.
Diabetes 1994 Nov; 43(11): 1291-1296. https://doi.org/10.2337/diab.43.11.1291
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Abstract

We have investigated whether glutamic acid decarboxylase (GAD) autoantibodies (GAD65 Ab) were affected by cyclosporin therapy and were related to subsequent noninsulin-requiring remission and loss of glucagon-stimulated C-peptide response in 132 recent-onset insulindependent diabetes mellitus (IDDM) patients treated with cyclosporin or placebo for 12 months. GAD65 Ab were detected in a quantitative radioligand assay using as tracer recombinant, in vitro translated, human islet [35S]methionine-labeled GAD65. GAD65 Ab were found at onset in 66% (87 of 132) of IDDM patients and in 1% (1 of 100) of healthy control subjects. The prevalence of GAD65 Ab and median GAD65 Ab levels did not change in serum samples taken 3, 6, 9, and 12 months after study entry in either the cyclosporin- or the placebo-treated groups. The presence or absence of GAD65 Ab at study entry did not predict non-insulin-requiring remission in either cyclosporin- or placebo-treated patients. However, the relative (compared with 0 months) glucagon-stimulated C-peptide response was more than 30% lower in GAD65 Ab+ patients receiving placebo at 9 and 12 months compared with the GAD65 Ab− placebo patients (P < 0.035). Islet cell cytoplasmic antibody (ICA) and GAD65 Ab+ placebotreated patients showed no significant differences in stimulated C-peptide levels compared with those who were ICA− and GAD65 Ab+, suggesting that ICA was not independently associated with loss of (β-cell function. We conclude that GAD65 Ab at diagnosis may predict a more rapid loss of β-cell function, a finding of importance when selecting individuals at risk of developing IDDM or recent-onset IDDM patients for intervention therapy.

  • Received April 22, 1994.
  • Revision received July 6, 1994.
  • Accepted July 6, 1994.
  • Copyright © 1994 by the American Diabetes Association

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November 1994, 43(11)
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Glutamic Acid Decarboxylase (GAD65) Autoantibodies in Prediction of β-Cell Function and Remission in Recent-Onset IDDM After Cyclosporin Treatment
Jacob Sten Petersen, Thomas Dyrberg, Allan E Karlsen, Jens Mølvig, Birgitte Michelsen, Jørn Nerup, Thomas Mandrup-Poulsen, Canadian-European Randomized Control Trial Group
Diabetes Nov 1994, 43 (11) 1291-1296; DOI: 10.2337/diab.43.11.1291

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Glutamic Acid Decarboxylase (GAD65) Autoantibodies in Prediction of β-Cell Function and Remission in Recent-Onset IDDM After Cyclosporin Treatment
Jacob Sten Petersen, Thomas Dyrberg, Allan E Karlsen, Jens Mølvig, Birgitte Michelsen, Jørn Nerup, Thomas Mandrup-Poulsen, Canadian-European Randomized Control Trial Group
Diabetes Nov 1994, 43 (11) 1291-1296; DOI: 10.2337/diab.43.11.1291
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