The objective was to assess changes in diabetes autoantibodies (DA) in children and adolescents with diabetes and explore whether observed changes were associated with participants’ characteristics, clinical parameters and diabetes complications. Participants with diabetes had DA (GAD, IA2 and ZnT8) measured at baseline (within 10.3± 7.1 months of diagnosis) and at 1, 2 and/or ≥ 5 years after baseline. At the > 5 year follow-up, the following measures were obtained: HbA1c, insulin dose, c-peptide, frequency of diabetes ketoacidosis (DKA) and severe hypoglycemia in the past 6 months, presence of microalbuminuria, hypertension, arterial stiffness, retinopathy and neuropathy. In those with positive baseline DAs, we examined the association between the change in the number of positive DA and change in each DA status with participants’ characteristics and clinical parameters. At baseline, 3,183 participants had positive DAs. At a mean diabetes duration of 7.3±2.3 years, 1,749 participants had longitudinal DA data, with 83.4% remaining positive (35.0% had 1 DA, 48.4% had 2 or more DAs). There was less DA persistence associated with longer diabetes duration (p=0.003 for those with baseline 1 DA and p<0.001 for baseline 2 DA) and younger age at diagnosis for baseline 2 DA (p<0.001). For the 1,391 individuals with clinical and complication data at diabetes duration of 7.7±1.9 years, we found no association between HbA1c, insulin dose, acute or chronic complications with change in number of positive DA. HLA risk category was not associated with the change in DA status or titers over time.

Conclusions: DA status remained relatively stable at 7 years after diabetes diagnosis in those with baseline positive DA. Younger age at diagnosis and longer duration were associated with less DA persistence. Measuring DAs after initial presentation may aid in diabetes classification but not in prediction of clinical course.


L. Merjaneh: None. D. Dabelea: None. C. Pihoker: None. L. M. Dolan: None. C. Suerken: None. R. Dagostino: Consultant; Self; AstraZeneca, Biogen, Daiichi Sankyo. G. Imperatore: None. S. Saydah: None. A. J. Roberts: None. S. M. Marcovina: None. E. J. Mayer-davis: None.


Centers for Disease Control and Prevention (00097, DP-05-069, DP-10-001); National Institute of Diabetes and Digestive and Kidney Diseases (1UC4DK108173, 1U18DP006131, U18DP006133, U18DP006134, U18DP006136, U18DP006138, U18DP006139); Kaiser Permanente Southern California (U18DP006133, U48/CCU919219, U01DP000246, U18DP002714); University of Colorado Denver (U18DP006139, U48/CCU819241-3, U01DP000247, U18DP000247-06A1); Cincinnati’s Children’s Hospital Medical Center (U18DP006134, U48/CCU519239, U01DP000248, 1U18DP002709); University of North Carolina at Chapel Hill (U18DP006138, U48/CCU419249, U01DP000254, U18DP002708); Seattle Children’s Hospital (U18DP006136, U58/CCU019235-4, U01DP000244, U18DP002710-01); Wake Forest University School of Medicine (U18DP006131, U48/CCU919219, U01DP000250, 200-2010-35171)

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