Pathogenesis of COVID-19. Role of heparins in the therapy of severe conditions in patients with COVID-19

ABSTRACT

The novel viral disease and its associated severe acute respiratory syndrome are currently the world's most significant public health crisis. The main stages of alveolar injury are mediated by endothelial damage, which leads to the release of cytokines and chemokines, the recruitment of immune cells, and the activation of the coagulation system and thrombosis. Numerous studies, including autopsy and histological data, confirm endothelial dysfunction in coronavirus infection and note an increased risk of venous thromboembolic events in patients with a severe course. Increases in D-dimer and fibrinogen degradation products remain to be the main prognostically important laboratory criteria, correlating with a higher risk of severe disease and mortality. Taking into account the presence of coagulopathy, heparins may be effective and affordable drugs for reducing the risk of severe acute respiratory syndrome. Low-molecular-weight heparins reduce the release and activity of IL-6 that is responsible for the development of cytokine storm, which is associated with better outcomes in patients with severe COVID-19. In addition, the antiviral and anti-inflammatory activity of heparins should be taken into consideration, which is very important for leveling the release of pro-inflammatory cytokines and mitigating the damaging effect of the virus on the endothelium. Conclusion. At this stage of understanding the pathophysiology of coronavirus infection, it is worth considering the use of low-molecular-weight heparins in patients with severe COVID-19, including those with sepsis-induced coagulopathy. The use of heparins in a therapeutic dosage has shown a significantly greater efficacy than that in prophylactic doses.