02 Dec 2022
30 Nov 2022
SARS-CoV-2 was first isolated in bronchoalveloar lavage (BAL) fluid from three patients with COVID-19 at Jinyintan Hospital in Wuhan, Hubei Province, China. The cases are increasing quickly with global mortality rate of 2.12%. The main cause of COVID-19 death is hypoxic respiratory failure due to acute respiratory distress syndrome (ARDS). Endothelial cell damage has a central role in ARDS pathogenesis and multi-organ failure in COVID-19. The endothelium, under homeostasis condition, is surrounded by mural cells (pericytes), which maintain vascular integrity and barrier function. These cells prevent inflammation by limiting the interaction of endothelial cells with immune cells and platelets and inhibit coagulation by expressing coagulation inhibitors and blood-clotting enzymes and producing glycocalyx. Vascular endothelial glycocalyx has a crucial role in endothelial function and is degraded systemically in elderly conditions and various comorbidities, which can be a potential mechanism for the development of lethal complications from COVID-19. Glycocalyx degradation due to endotheliopathy in SARS-CoV-2 infection causes increased levels of its fragments such as syndecan-1 and hyaluronan in the blood. Data from previous studies showed that the levels of these two biomarkers increased significantly in septic patient and several viral infections such as Kawasaki and dengue. These biomarkers are also markers of organ damage. Therefore, it can be indicated that hyaluronan and syndecan-1 are significant prognostic markers for morbidity and survival in COVID-19 patient.