Ann Pediatr Endocrinol Metab.  2022 Sep;27(3):157-168. 10.6065/apem.2244150.075.

COVID-19 and diabetes in children

Affiliations
  • 1Department of Pediatrics, University of Chieti, Chieti, Italy

Abstract

This review describes the impact of coronavirus disease 2019 (COVID-19) in children and adolescents, investigating changes in diabetes presentation during the COVID-19 pandemic, possible links between severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection and diabetes, and mechanisms of pancreatic β-cell destruction. Although glycemic control in individuals with already known diabetes mellitus did not worsen during the pandemic, there was a worrying increase in diabetic ketoacidosis in children with new-onset diabetes, probably due to containment measures and delayed access to emergency departments. Moreover, new evidence suggests that SARS-CoV-2 has the capacity to directly and indirectly induce pancreatic β-cell destruction, and the risk of newly diagnosed diabetes after COVID-19 increased in both children and adults. While long-term studies continue to follow children with SARS-CoV-2 infection, this review discusses available findings on the relationship between COVID-19 and diabetes. It is important to emphasize the need to maintain close links between families of children with chronic conditions and their pediatricians, as well as to promote early access to healthcare services, in order to reduce dangerous delays in diabetes diagnosis and prevent diabetic ketoacidosis.

Keyword

SARS-CoV-2; COVID-19; Type 1 diabetes; Type 2 diabetes; DKA diabetic ketoacidosis; Obesity; Child; Adolescent

Figure

  • Fig. 1. RS-CoV-2 enters the pancreatic β cell and activates β-cell intracellular signaling, inducing processes that end in apoptosis, insulitis, and transdifferentiation into α cells and acinar cells. SARS-CoV-2, severe acute respiratory syndrome-coronavirus-2; ACE2, angiotensin converting enzyme 2; NRP-1, neuropilin-1; PAK, p21-activated kinase; JNK, c-Jun N-terminal kinases; PKR, protein kinase R; ELF2α, eukaryotic translation initiation factor 2 subunit 1; ISR, integrated stress response.


Reference

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