ABSTRACT
Introduction
The COVID-19 pandemic represents an unprecedented challenge for public health worldwide, not only for the very high number of cases and deaths but also due to a wide variety of indirect consequences. Among these, the possible relationship between SARS-CoV-2 infection and type 1 diabetes (T1D) in pediatric age has aroused notable interest in the scientific community.
Areas covered
This perspective article aims to focus on the epidemiological trend of T1D during the pandemic, the diabetogenic role of SARS-CoV-2, and the influence of preexisting T1D on COVID-19 outcomes.
Expert opinion
The incidence of T1D has considerably changed during the COVID-19 pandemic, but any direct role of SARS-CoV-2 is uncertain. It is more likely that SARS-CoV-2 infection acts as an accelerator of pancreatic β-cell immunological destruction, which is activated by known viral triggers whose spread has been abnormal during these pandemic years. Another interesting aspect to consider is the role of immunization as a potential protective factor both for T1D development and the risk of severe outcomes in already diagnosed patients. Future studies are still required to address unmet needs, including the early use of antiviral drugs to reduce the risk of metabolic decompensation in children with T1D.
Article highlights
The mutual interaction between COVID-19 and type 1 diabetes in children and adolescents has been widely investigated and discussed during the pandemic years.
Since the first months of the COVID-19 pandemic, an unexpected change in the trend of type 1 diabetes incidence has been observed.
Despite several hypotheses being reported, the exact role of SARS-CoV-2 infection in the epidemiological changes of type 1 diabetes is still uncertain.
COVID-19 is strictly related to the risk of metabolic decompensation in children with already diagnosed type 1 diabetes, especially in those with high levels of glycated hemoglobin.
SARS-CoV-2 seems to interfere with glucose homeostasis through different mechanisms, including a direct effect related to tropism to pancreatic β-cells and an indirect effect sustained by hyperinflammation and peripheral insulin resistance.
Declaration of interest
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
Reviewer disclosures
Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.