Fluctuations in GAD65 Antibodies After Clinical Diagnosis of IDDM in Young Children
- Manou R Batstra, MSC,
- Mònica Pina, BSC,
- Joanne Quan, BSC,
- Paul Mulder, PHD,
- Carine E de Beaufort, MD,
- G Jan Bruining, MD and
- Henk-Jan Aanstoot, MD
- Department of Pediatrics and Clinical Genetics, Sophia Children's Hospital and Erasmus University Medical School Rotterdam, The Netherlands
- Department of Epidemiology and Biostatistics, Sophia Children's Hospital and Erasmus University Medical School Rotterdam, The Netherlands
- Address correspondence and reprint requests to Henk-Jan Aanstoot, MD, Department of Pediatrics, Erasmus University Medical School, Dr. Molewaterplein 60, sp-3435, 3015 GJ Rotterdam, The Netherlands. Email: aanstoot{at}alkg.azr.nl
Abstract
OBJECTIVE To investigate whether the presence of GAD antibodies at onset of IDDM correlates to a more aggressive rate of β-cell destruction after clinical onset.
RESEARCH DESIGN AND METHODS We studied GAD antibodies at onset of disease, after 1 year, and after 6 years in 33 consecutively referred children (mean age 8.08, range 1.7–16.3). In a subset of 11 patients, GAD antibodies were studied very frequently. The correlation between GAD antibodies and clinical parameters, including glycosylated hemoglobin, residual insulin secretion, and insulin dosage, was evaluated.
RESULTS GAD antibody titers were highly variable. Four patients became GAD antibody positive weeks to years after clinical onset. Other patients switched between testing positive and negative for GAD antibodies shortly after clinical onset. No correlation was found between the presence of GAD antibodies and the rate of β-cell destruction, but patients with high GAD antibody indexes at onset had significantly higher glycosylated hemoglobin levels.
CONCLUSIONS GAD antibodies at clinical onset do not predict the rate of β-cell destruction in young children with newly diagnosed IDDM. The highly variable GAD antibody levels suggest variation of the autoimmune process.
- Received April 29, 1996.
- Accepted November 1, 1996.
- Copyright © 1997 by the American Diabetes Association
