1425-P: C-Peptide and Islet Autoantibodies at Diagnosis Predict Long-Term ß-Cell Function and Insulin Dependence in Pediatric Diabetes

We asked if assessment of islet autoimmunity and β cell function in children at diabetes diagnosis is useful for prognosis, using the “Aβ” system, [“A” representing autoimmunity (A+ = ≥1 autoantibody; A- = no antibodies), “β” representing β cell function (β+ = random serum C-peptide ≥0.6 ng/mL; β- = C-peptide <0.6 ng/mL)]. We followed β cell function longitudinally with 2h post-prandial urinary C-peptide-creatinine ratio (UCPCR) at 3-12 wk (V1) and 6-12 m (V2). We compared clinical characteristics, glycemia and β cell function at baseline and clinical outcomes at V2 between the groups. The cohort (n=74) was 50% female, 76% White, 22% non-Hispanic Black, 2% Other, 47% Hispanic. Median age (25p-75p) was 12.6 (8.5-14.6) years, median BMI 70.7 (16.7-96.1) %ile. Phenotypic frequencies were A+β- (36.5%), A-β+ (29.7%), A+β+ (31.1%) and A-β- (2.7%). Baseline serum C-peptide correlated with UCPCR at V1 (r=0.37, p=0.03). Adjusting for age, sex, race/ethnicity, and BMI, UCPCR at V2 was higher in A-β+ than A+β- (β=1.18, 95% CI:0.31-2.07, p=0.009). Fully 36% of A-β+ but none of A+β+ and A+β- were insulin-independent at V2 (p<0.001). The remaining results are shown in Table 1. The A-β+ phenotype at diagnosis predicts sustained β cell function and potential insulin-independence after 6-12 months. Random serum C-peptide at diagnosis correlates with 2h post-prandial UCPCR at 3-12 weeks. Disclosure M.Tosur: Advisory Panel; Provention Bio, Inc. A.Balasubramanyam: None. X.C.Huang: None. S.Deen: None. S.Uysal: None. M.Astudillo: None. W.Hagopian: Research Support; Janssen Research & Development, LLC, Provention Bio, Inc., Randox R & D. R.A.Oram: Consultant; Janssen Research & Development, LLC, Research Support; Randox R & D. F.Jahoor: None. M.J.Redondo: None. Funding Texas Children's Hospital (to M.T.); Rutherford Fund (to A.B.); National Institutes of Health (K23DK129821 to M.T.)