Inflammatory Response and Activation of Coagulation after COVID-19 Infection

Abstract

SARS-CoV-2 (COVID-19) infection is responsible for causing a disease with a wide spectrum of clinical presentations. Predisposition to thromboembolic disease due to excessive inflammation is also attributed to the disease. The objective of this study was to characterize the clinical and laboratory aspects of hospitalized patients, in addition to studying the pattern of serum cytokines, and associate them with the occurrence of thromboembolic events. Methodology: A retrospective cohort study with 97 COVID-19 patients hospitalized from April to August 2020 in the Triângulo Mineiro macro-region was carried out. A review of medical records was conducted to evaluate the clinical and laboratory aspects and the frequency of thrombosis, as well as the measurement of cytokines, in the groups that presented or did not present a thrombotic event. Results: There were seven confirmed cases of thrombotic occurrence in the cohort. A reduction in the time of prothrombin activity was observed in the group with thrombosis. Further, 27.8% of all patients had thrombocytopenia. In the group that had thrombotic events, the levels of IL1b, IL-10, and IL2 were higher (p < 0.05). Conclusions: In the studied sample, there was an increase in the inflammatory response in patients with thrombotic events, confirmed by the increase in cytokines. Furthermore, in this cohort, a link was observed between the IL-10 percentage and an increased chance of a thrombotic event.

Comparative analysis of monocyte-derived dendritic cell phenotype and T cell stimulatory function in patients with acute-on-chronic liver failure with different clinical parameters

“…In patients with acute-on-chronic liver failure, there is a correlation between prothrombin activity, infection, and poor prognosis ( 41 – 43 ). While prothrombin activity is primarily used to assess clotting function, there is extensive interaction between the clotting system and the immune system ( 44 ). A study on HBV-ACLF revealed a correlation between white blood cell count, lymphocytes, and peripheral T lymphocytes with prothrombin activity (PTA) ( 45 ).…”

Inhibition of SARS-CoV-2-Induced NLRP3 Inflammasome-Mediated Lung Cell Inflammation by Triphala-Loaded Nanoparticle Targeting Spike Glycoprotein S1

“…Critical to the pathophysiology of COVID-19 is the pro-inflammatory milieu orchestrated by elevated levels of cytokines, including interleukin-6 (IL-6), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α), among others [ 3 ]. This cytokine storm contributes to systemic inflammation, vascular endothelial dysfunction, and tissue damage, culminating in acute respiratory distress syndrome (ARDS) and multiorgan dysfunction [ 4 , 5 ].…”

Editorial Comment on the Special Issue Discussing COVID-19 and Thrombosis, Second Edition

“…The prolonged state of inflammation present since the first phases of SARS-CoV-2 infection [ 5 ] induces dysfunctions after viral clearance, and it is responsible of several coagulation-based abnormalities in patients with long COVID [ 5 ], especially in the presence of thrombophilia [ 6 ].…”