Racial and ethnic differences among children with new‐onset autoimmune Type 1 diabetes

Abstract

Abstract Aim To compare demographic and clinical characteristics among children from ethnic minorities and non‐Hispanic white children with new‐onset autoimmune Type 1 diabetes. Methods We analysed a single‐centre series of 712 children with new‐onset autoimmune Type 1 diabetes between January 2008 and March 2011. The median (range) age was 9.7 (0.3–18.1) years, the mean ( sd ) BMI percentile was 69.7 (25.4) and 48.3% of the cohort were girls. The cohort comprised 57.3% non‐Hispanic white, 20.5% Hispanic and 14.8% African‐American children, and 7.4% were of other, mixed or unknown race. Results The Hispanic subgroup, compared with non‐Hispanic white subgroup, had a higher mean ( sd ) C‐peptide level [0.82 (1.62) vs 0.55 (0.47) ng/ml; P =0.004), and a greater proportion of children with elevated BMI (overweight or obesity; 49.6% vs 32.5%; P <0.001) and diabetic ketoacidosis (51.8% vs 38.2%; P =0.006). The African‐American group had a higher mean ( sd ) glucose level [24.4 (12.8) vs 21.4 (10.7) mmol/l; P =0.017], a greater proportion of children with ketoacidosis (56.7% vs 38.2%; P =0.001), a greater proportion with elevated BMI (52.9% vs 32.5%; P <0.001), and a lower proportion of children at pre‐pubertal stage (49.0% vs 61.6%; P =0.01), and tended to have higher C‐peptide levels [0.65 (0.59) vs 0.55 [0.47] ng/ml; P =0.079) compared with the non‐Hispanic white children. The differences in C‐peptide levels compared with non‐Hispanic white children persisted for Hispanic ( P =0.01) but not African‐American children ( P =0.29) after adjustment for age, sex, BMI , ketoacidosis, glucose, Tanner stage and autoantibody number. Conclusion At the onset of paediatric autoimmune Type 1 diabetes, Hispanic, but not African‐American children had higher C‐peptide levels, after adjustment for potential confounders, compared with non‐Hispanic white children. These findings suggest that ethnicity may contribute to the heterogeneity of Type 1 diabetes pathogenesis, with possible implications for intervention.