PMC:7386875 / 9292-12966 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7386875","sourcedb":"PMC","sourceid":"7386875","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7386875","text":"SARS-CoV-2 and Its Impact on Coagulation\nAn emerging threat of the COVID-19 pandemic is the propensity of SARS-CoV-2 to cause microvascular, venous, and arterial thrombosis, and thereby exacerbating organ injury. Patients with severe COVID-19 appear to have a hyperinflammatory response, which is linked to the development of ARDS and multiorgan failure.6 However, it is now well appreciated that the innate immune response and thrombotic response are closely linked (Figure 2) and accordingly in patients with severe COVID-19 there is a correlation with elevated acute phase reactants, such as fibrinogen and CRP (C-reactive protein), which may contribute to COVID-associated hypercoagulability.7–9 Moreover, these biomarkers and acute phase reactants are associated with adverse clinical outcomes and increased severity of infection.7,9,10 In addition, abnormal coagulation parameters, including prolonged prothrombin time and activated partial thromboplastin time, are found to be associated with a higher mortality from COVID-19, demonstrating the significance of coagulation abnormalities in this population.3\nFigure 2. Mechanisms regulating immunothrombosis. In vascular homeostasis, the endothelium possesses anti-inflammatory and antithrombotic properties due to the expression of CD39, nitric oxide (NO), and prostacyclin in addition to the natural anticoagulants, TFPI (tissue factor pathway inhibitor), activated protein C, and thrombomodulin. In the setting of infection or inflammation, endothelial cells upregulate the expression of VWF (von Willebrand factor) and adhesion molecules such as ICAM (intercellular adhesion molecule)-1, αvβ3, P-selectin and E-selectin, promoting the adhesion of leukocytes and platelets. Activated platelets release chemokines CXCL1, PF (platelet factor)-4, CXCL5, CXCL7, CCL3, RANTES (regulated on activation, normal T-cell expressed and secreted), and CCL7 to enhance leukocyte recruitment. Leukocytes interact with platelets via several receptor/ligand pairs. These include platelet P-selectin binding to its cognate receptor PSGL (P-selectin glycoprotein)-1 on leukocytes, GP-Ib on platelets interacting with Mac-1 on monocytes and neutrophils, and GPIIb/IIIa binding to SLC44A2/CTL-2 on neutrophils. Activated platelets release polyphosphate (polyP), which activates the contact pathway, and HMGB (high mobility group box)-1, which enhances monocyte recruitment and monocyte tissue factor (TF) expression, thereby amplifying thrombin generation by way of the TF pathway of coagulation. Neutrophils release neutrophil extracellular traps (NETs) which promote thrombosis via activation of the contact pathway and the binding and activation of platelets. Finally, complement activation leads to the recruitment of leukocytes and upregulates TF expression, amplifies platelet activation and upregulates endothelial expression of proinflammatory cytokines, including IL (interleukin)-1, IL-6, IL-8, and MCP (monocyte chemoattractant protein)-1. These mechanisms result in excess thrombin generation, which potentiates the activation of platelets, leukocytes, and endothelium via PARs (protease-activated receptors) and culminates in a fibrin clot. Plasma D-dimer measurement is emerging as a direct prognostic marker in COVID-19. In this regard, D-dimer, a fibrin degradation product released when plasmin cleaves cross-linked fibrin, appears to be higher in patients with severe COVID-19 when compared with nonsevere disease.11–15 Subsequently, further studies have highlighted that patients who do not survive COVID-19 have an elevated D-dimer level, and D-dimer continues to increase during admission before 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