ESPE Abstracts (2015) 84 P-3-731

Influence of Pancreatic Autoinmunity in the Onset and Progression of Diabetes in Paediatric Population

Yoko Oyakawa, María Martín-Frías, Rosa Yelmo, Milagros Alonso, Belén Roldán & Raquel Barrio

Hospital Universitario Ramón y Cajal, Madrid, Spain

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).

Table 1 (for abstract P3-731)
n (%)45 (21%)45 (21%)92 (44%)2 (1%)26 (12%)
Years at DM1 onset 5.0 (2.1–10.5)6.8 (3.6–9.8)8.3 (4.7–10.9)7.0 (3.8–10.3)4.1 (2.7–8.2)
Sex (F%)4462525054
DM1 debut (%) HG/Ketosis/KAD29/38/3320/32/4829/38/3350/0/5019/58/23
HbA1c at DM1 debut (%)10.6 (8.7–12.1)10.7 (9.6–12.6)10.7 (9.8–11.9)9.9 (6.8–13.0)11.0 (9.9–12.1)
Basal C-Peptide (ng/ml)0.4 (0.3–0.5)0.5 (0.3–0.6)0.5 (0.3–0.7)0.5 (0.4–0.7)0.3 (0.1–0.6)
Celiac antibodies (%)1197019
Anti-thyroid antib (%)99908
Anti-parietal cells antibodies (%)02200
Follow up (years)4.4 (2.6–8.3)4.5 (2.2–7.8)4.0 (2.1–6.6)3.6 (2.6–4.6)5.3 (3.0–9.2)
Mean HbA1c in the last year (%)6.5 (6.2–7.2)6.7 (6.2–7.1)6.6 (6.3–7.0)6.4 (6.3–6.5)6.7 (6.3–7.1)

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.

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