ESPE Abstracts

Background: Type 1 Diabetes (T1D) is a chronic disease resulting from autoimmune destruction of insulin-secreting pancreatic β cells. Viruses are known to play a role in the pathogenesis of T1D. There is no consistent evidence that SARS-CoV-2 induces T1D in children or adults. Nevertheless, evidence suggests that the SARS-CoV-2 affects β cell function, suggesting a role for the virus in the pathogenesis of the disease. It is thus plausible that the effects of the SARS-CoV-2 on β cells and the environmental alterations caused by the COVID-19 pandemic affected the clinical and immunological characteristics of new-onset T1D.

Objective: To find the clinical and immunological signatures of the COVID-19 pandemic on children diagnosed with T1D.

Methods: A single-center, retrospective observational study comparing the clinical and immunological characteristics of children diagnosed with T1D at our clinic the year before and during the first two years of the COVID-19 pandemic. Data were extracted from the medical records of the children at the time of diabetes diagnosis, including clinical and demographic parameters, COVID-19 PCR results, and the presence of anti-islet, thyroid, and celiac-related autoantibodies. Also obtained from the medical records were a family history of T1D, celiac disease, and autoimmune thyroid disease in a first-degree family member.

Results: 376 children were diagnosed with T1D at our diabetes clinic during the study period. 132, 121, and 123 children were diagnosed during the pre-COVID-19 era, the first and second pandemic years, respectively. The rate of diabetic ketoacidosis at presentation was slightly higher during the COVID-19 era than in the pre-COVID-19 era (not reaching statistical significance) and comparable between the first and second pandemic years. Multiple antibodies were significantly higher among patients diagnosed in the pre-COVID-19 era than those diagnosed in the first two years of the pandemic (72% vs.61%, P=0.03). Islet-cell autoantibodies (ICA) levels were higher among children diagnosed during the COVID-19 era compared to pre-COVID-19 era (1341.34+1786.36U/ml vs.968.02+1495.66U/ml, P=0.042). GAD-antibodies levels were higher in children diagnosed with COVID-19 before the diagnosis of T1D than in children without COVID-19 (614.86+793.90U/ml vs.317.08+611.45U/ml, P=0.027). Tissue Transglutaminase antibodies were more common among children diagnosed during the COVID-19 era compared to the pre-COVID-19 era (17% vs. 8%, P=0.024).

Conclusions: Our findings suggest that SARS-CoV-2 and the environmental alterations caused by the pandemic affected the immunological profile of children diagnosed with T1D. Thus, it appears that the virus plays a role in the autoimmune process causing T1D.