Presentation of type 1 diabetes (T1D) appears to differ among patients with different ancestries. In this study, medical record data were taken from type 1 diabetes patients, diagnosed from 2010 to 2017 at a single site, UCSF Benioff Children’s Hospital Oakland (BCHO). Patients were grouped into ancestry classes based on medical records. European (EUR; n = 81), Hispanic (HIS; n = 84), and African (AFR; n = 48) groups were compared for C-peptide levels at diagnosis and for levels of four autoantibodies (aAb); insulin (IAA), protein phosphatase-like IA-2 (IA-2A), glutamic acid decarboxylase (GADA), and zinc transporter (ZnT8A). All aAb measurements were performed at a single reference laboratory in Denver. The proportion of patients with no evidence of any aAb was similar in EUR and AFR groups (5% and 4%, respectively) but higher in HIS (14%). For up to three aAb, the number of aAb was correlated with the number of patients in the EUR (r = 0.96; p = 0.039) and AFR (r = 0.96; p = 0.038) groups but not in the HIS group (r = 0.58; p = 0.24). The pattern of autoantibody positivity differed among groups; most prevalent were IA-2A in EUR (75%), GADA in AFR (75%), and both IA-2A and GADA (both at 68%) in HIS. Differences in aAb patterns did not reach statistical significance but were consistent with published reports. As expected, C-peptide levels were below the normal range in the EUR group, regardless of aAb positivity. In contrast, in the HIS group, mean C-peptide levels were in the normal range for patients with up to three positive aAb; only HIS patients with all four aAb positive had C-peptide levels below the normal range. The AFR group was similar to the EUR group, with below normal C-peptide levels, except that the subset of AFR patients with a single positive aAb had C-peptide in the normal range. Observed differences in C-peptide mean and median values were significant between HIS and EUR groups (mean p = 0.013; median p = 0.046). Differences in biomarkers between HIS and EUR T1D patients may have implications for both differential diagnosis and management of T1D.
N. Keller: None. K.E. Fuller: None. B.J. Shum: None. J. Noble: Employee; Spouse/Partner; Roche Diagnostic USA.