Multinational study in children and adolescents with newly diagnosed type 1 diabetes: association of age,ketoacidosis, HLA status,and autoantibodies on residual beta‐cell function and glycemic control 12 months after diagnosis |
| |
Authors: | Henrik B Mortensen Peter GF Swift Reinhard W Holl P Hougaard Lars Hansen Hilde Bjoerndalen Carine E De Beaufort Michael Knip and Hvidoere Study Group on Childhood Diabetes |
| |
Affiliation: | 1. Department of Pediatrics, Glostrup University Hospital, Glostrup, Denmark;2. Leicester Royal Infirmary Children's Hospital, Leicester, UK;3. University of Ulm, Ulm, Germany;4. Department of Statistics, University of Southern Denmark, Odense, Denmark;5. Department of Pediatrics, Ulleval University Hospital, Oslo, Norway;6. Clinique Pediatrique, Centre Hospitalier de Luxembourg, Luxembourg;7. Hospital for Children and Adolescents, University of Helsinki, Helsinki, Finland |
| |
Abstract: | HB Mortensen, PGF Swift, RW Holl, P Hougaard, L Hansen, H Bjoerndalen, CE de Beaufort, M Knip. Multinational study in children and adolescents with newly diagnosed type 1 diabetes: association of age, ketoacidosis, HLA status, and autoantibodies on residual beta‐cell function and glycemic control 12 months after diagnosis. Objective: To identify predictors of residual beta‐cell function and glycemic control during the first 12 months after the diagnosis of type 1 diabetes (T1D). Subjects and Methods: Clinical information and blood samples were collected from 275 children. HbA1c, antibodies, HLA typing and mixed meal‐stimulated C‐peptide levels 1, 6, and 12 months after diagnosis were analyzed centrally. Results: Mean age at diagnosis was 9.1 yr. DKA with standard bicarbonate <15 mmol/L was associated with significantly poorer residual beta‐cell function 1 (p = 0.004) and 12 months (p = 0.0003) after diagnosis. At 12 months, the decline in stimulated C‐peptide levels compared with the levels at 1 month was 69% in the youngest age group and 50% in patients 10 yr and above (p < 0.001). Stimulated C‐peptide at 12 months was predicted by younger age (p < 0.02) and bicarbonate levels at diagnosis (p = 0.005), and by stimulated C‐peptide (p < 0.0001), postmeal blood glucose (p = 0.0004), insulin antibodies (IA; p = 0.02) and glutamic acid decarboxylase antibodies (GADA; p = 0.0004) at 1 month. HbA1c at 12 months was predicted by HbA1c at diagnosis (p < 0.0001), GADA at 1 month (p = 0.01), and non‐white Caucasian ethnicity (p = 0.002). Conclusions: Younger age, ketoacidosis at diagnosis, and IA and GADA 1 month after diagnosis were the strongest explanatory factors for residual beta‐cell function at 12 months. Glycemic control at 12 months was influenced predominantly by ethnicity, HbA1c at diagnosis, and GADA at 1 month. |
| |
Keywords: | C‐peptide pancreatic autoantibodies partial remission phase residual beta‐cell function |
|
|