ESPE Abstracts

Background: Anti-islet autoantibodies are predictive and diagnostic markers for type 1 diabetes (T1D). The most frequently determined pancreatic autoantibodies in T1D are anti-glutamic acid decarboxilase (GAD), anti-tyrosine phosphatase (IA-2) and anti-insulin (AAI).

Objective and hypotheses: To study whether the pancreatic autoimmunity profile influences the initial presentation of diabetes, its metabolic behaviour and the presence of other autoimmune disorders in T1D.

Method: Retrospective study of 210 paediatric patients with T1D. We analyzed age, sex, age at diagnosis, type of clinical presentation (hyperglycaemia/ketosis/ketoacidosis (KAD)), HbA1c (HPLC-Menarini, NV 5.31±0.31%), C-peptide levels and pancreatic autoimmunity (GAD, IA2, AAI). Additional autoimmune disorders were screened with an antibody array at diagnosis and at follow-up. The metabolic control (last year mean HbA1c and acute complications) were also analysed. Data are reported in percentages, median and interquartile ranges. Statistical analysis was performed with SPSS 22.0.

Results: At diagnosis, mean age was 7 years (3.3–10.5), 53% female, Hb1Ac 10.7% (9.6–12.2), C-peptide 0.5 ng/ml (0.3–0.7). Initial presentation: hyperglycemia 23%, ketosis 40%, ketoacidosis 37%. Associated autoimmunity at follow-up: anti-thyroid antibodies 9%, celiac disease 10%, parietal cells antibodies 2%. Celiac disease was diagnosed in five patients before T1D. GAD+ patients showed more rapid progression to celiac disease. Other autoimmunity markers: one patient had adrenal antibodies (GAD+/IA2) with normal adrenal function, 4% of the patients presented positive ANA, one of them with olygoarthritis (IA2+) and another with associated autoimmune thyroiditis (GAD+/IA2+). Another patient was diagnosed with autoimmune hepatitis 3.7 years after T1D (GAD+). Within the last year follow-up no patient presented episodes of severe hypoglycaemia or ketoacidosis. No significant differences were found between patient-groups with isolated, combined or absence of pancreatic autoantibodies (table 1).

Conclusion: In our cohort 88% of patients have pancreatic autoimmunity markers, which did not influence the debut, the subsequent] metabolic outcome of T1D or the prevalence of other autoimmune diseases.