Assessment of systemic inflammatory reactions and coagulopathy against the background of hormonal therapy in covid-associated lung damage

Abstract

The mechanisms of COVID-19-associated coagulopathy (CAC) are complex and differ in many ways from the standard mechanisms of thrombosis in critically ill patients. This review presents the pathogenesis, diagnosis, and comparison of various types of coagu-lopathy with SAS. During COVID-19 infection, the number of sudden deaths outside the hospital increased. One possible reason is the high incidence of serious thrombotic events in patients with COVID-19. However, the pathogenesis of these life-threatening events is multifactorial and requires independent discussion. Deviations in laboratory studies of the hemostatic system in patients infected with SARS-CoV-2 with a severe course indicate the activation of the blood coagulation system corresponding to sepsis-induced coagulopathy (SIC) or DIC. However, hemostasis dis-orders in COVID-19 have characteristics that distinguish them from DIC in sepsis. The clinical and laboratory features of CAC overlap with hemophagocytic syndrome, antiphospholipid syndrome, and thrombotic microangiopathy. The review presents data on their similarities and differences. Inadequate diagnosis or inadequate treatment of hypercoagulability may explain the high incidence of unexplained deaths from COVID-19. They can be associated with potentially preventable microvascular and macrovascular thrombosis and subsequent cardiovascular complications, including myocardial injury and infarction, as well as insufficient information content of biomarkers for their assessment. Research to identify the most informative biomarkers for decision-making to intensify anticoagulant prophylaxis in patients with severe COVID-19 is progressing rapidly, with increasing focus on TEG and ROTEM. The review presents changes in CAC during hormone therapy for COVID-19-associated lung damage. Pulse therapy with high doses of GCS has a rapid anti-inflammatory effect, but at the same time increases the level of D-dimer, which increases the risk of venous thrombosis and thromboembolism.