Abstract:
One of the key pathogenetic mechanisms of COVID-19 is endothelial dysfunction, which enhances prothrombotic phenomena, endotheliitis, and multiorgan immunothrombosis. The mechanisms of endothelialdamage in children remain insufficiently studied.
Aim: to determine the levels ofendothelialdysfunction in children with SARS-CoV-2-associated pneumonia and to analyze its relationships with clinical and laboratory indicators ofthe activity of the infectious and inflammatory process.
Materials and methods. The Main group consisted of 160 children with SARS-CoV-2-associated pneumonia and 40 healthy children (Controlgroup). The Main group was divided depending on gender, age, disease severity, levels ofC-reactive protein (CRP), and procalcitonin. To assess endothe¬lial dysfunction, the levelof endothelin-1 and vascular endothelialgrowth factor (VEGF) in blood serum was determined.
Results. The values of VEGF and endothelin-1 were the highest in patients with severe pneumonia. The values of laboratory markers of endothelial dysfunction were significantly higher with higher levels of CRP in children ofthe Main group by 31.95% and 33.14% for endothelin-1 and VEGF, respec¬tively A positive medium-strength relationship was established between the values of fibrinogen and CRP with VEGF levels; a weak positive relation¬ship between the levels of VEGF and procalcitonin; fibrinogen and endothelin-1 levels. A probable medium-strength positive relationship was estab¬lished between the values of endothelin-1 and VEGF, with the levels of interleukins (IL) 1,6.
Conclusions Children ofthe Main group have endothelialdysfunction, as evidenced by increased levels of endothelin-1 and VEGF. These values were associated with disease severity, CRP levels, and gender. VEGF levels were highest in patients with severe pneumonia. There was a moderate positive association between laboratory markers of endothelialdysfunction, such as endothelin-1 and VEGF, and IL-1 and IL-6 levels
