THE CONDITION OF THE VASCULAR ENDOTHELIUM IN CHILDREN WITH COVID-19 AND BRONCHO-OBSTRUCTIVE SYNDROME

Abstract

Introduction: The impact of SARS-CoV-2 infection on the human organism has proven to be more diverse than that of previously known viral infections. However, the full spectrum of the long-term consequences of the disease, especially in children, has not been thoroughly studied. One key area of concern is the development of broncho-obstructive syndrome (BOS) as a post-COVID-19 complication, which involves airway inflammation and hyperreactivity. This study investigates the relationship between endothelial dysfunction and BOS in pediatric patients following SARS-CoV-2 infection. Objective: To explore the endothelial status in children with SARS-CoV-2 infection and its association with the development of BOS, and to assess the role of endothelial dysfunction markers—circulating endothelial cells (CECs), endothelin-1, and nitric oxide metabolites—in this context. Methods: A retrospective study was conducted between 2020 and 2022, involving 486 children. The study included two primary groups: (1) Control: Healthy children with no history of SARS-CoV-2 infection or BOS; children with SARS-CoV-2 infection but no BOS, and (2) Main: Children with BOS but no SARS-CoV-2 infection; children with SARS-CoV-2 infection followed by the development of BOS. Endothelial function was assessed by measuring levels of CECs, endothelin-1, and nitric oxide metabolites. Results: The study found significantly elevated CECs and endothelin-1 levels, along with decreased nitric oxide metabolites, in children who developed BOS following SARS-CoV-2 infection. The highest levels of endothelial dysfunction markers were observed in this group, suggesting a synergistic effect of SARS-CoV-2 infection and BOS on endothelial damage. Notably, 64.3% of children in this group exhibited elevated CEC levels, reflecting severe endothelial dysfunction. Endothelin-1 levels were also significantly higher in children with BOS after SARS-CoV-2 infection (0.46 ± 0.02 fmol/mL) compared to healthy controls and children with BOS without a history of SARS-CoV-2 infection. These findings highlight the critical role of endothelial dysfunction in the pathogenesis of post-COVID-19 respiratory complications. Conclusion: SARS-CoV-2 infection contributes to significant endothelial dysfunction in children, particularly in those who develop BOS. The combination of SARS-CoV-2 infection and BOS exacerbates endothelial damage, which likely plays a critical role in the pathogenesis of post-COVID-19 respiratory complications. These findings suggest the need for further research into therapeutic strategies aimed at correcting endothelial dysfunction, potentially improving outcomes for pediatric patients suffering from long-term respiratory sequelae following COVID-19.