The Relationship between Inflammatory Cytokines and Coagulopathy in Patients with COVID-19

Abstract

Coronavirus disease 2019 (COVID-19), with a broad range of clinical and laboratory findings, is currently the most prevalent medical challenge worldwide. In this disease, hypercoagulability and hyperinflammation, two common features, are accompanied by a higher rate of morbidity and mortality. We assessed the association between baseline inflammatory cytokine levels and coagulopathy and disease outcome in COVID-19. One hundred and thirty-seven consecutive patients hospitalized with COVID-19 were selected for the study. Baseline interleukin-1 (IL-1), IL-6, and tumor necrosis factor alpha (TNF-α) level were measured at time of admission. At the same time, baseline coagulation parameters were also assessed during the patient’s hospitalization. Clinical findings, including development of thrombosis and clinical outcome, were recorded prospectively. Out of 136 patients, 87 (~64%) had increased cytokine levels (one or more cytokines) or abnormal coagulation parameters. Among them, 58 (~67%) had only increased inflammatory cytokines, 12 (~14%) had only coagulation abnormalities, and 17 (19.5%) had concomitant abnormalities in both systems. It seems that a high level of inflammatory cytokines at admission points to an increased risk of developing coagulopathy, thrombotic events, even death, over the course of COVID-19. Early measurement of these cytokines, and timely co-administration of anti-inflammatories with anticoagulants could decrease thrombotic events and related fatal consequences.

Mortality of Patients Infected by COVID-19 with and without Deep-Vein Thrombosis

“…This theory is supported by reports of high inflammatory markers and clotting as well as a correlation between high interleukin-6 (IL-6) levels and fibrinogen. The anti-inflammatories with anticoagulants could decrease thrombotic events and related fatal consequences [1][2][3][4].…”

Effects of vaccination, new SARS-CoV-2 variants and reinfections on post-COVID-19 complications

“…Based on this notion, it is possible that vaccination status may somehow prevent COVID-19-related exaggerated or otherwise maladaptive immune responses to SARS-CoV-2 infection. This proposal might be at least partially supported by a positive association between vaccination status and significantly reduced occurrence of post-COVID hypercoagulopathy condition (26), as hypercoagulopathy can be associated with maladaptive immune processes in COVID-19 (44,45). Another supportive argument for the possible link between decreased probability of COVID-related exaggerated immune processes and post-COVID complications stemming from COVID-related exaggerated immune processes might be found in significantly reduced odds of developing Multi-System Inflammatory Syndrome after COVID-19 in the vaccinated population (16).…”

A Real Pandora’s Box in Pandemic Times: A Narrative Review on the Acute Cardiac Injury Due to COVID-19

“…Pathogenesis of COVID-19 cardiomyopathy is intimately related to inflammatory cytokines, referring here to diastolic dysfunction and increased myocardial stiffness mediated by interleukin-6 (IL-6), negative inotropic effects exerted by interleukin-1β (IL-1β), or myocardial fibrosis induced by IL-1β and tumor necrosis factor alfa (TNF-α). Even higher levels of those biomarkers are detected during cytokine storms in the severe forms of SARS-CoV-2 infection [ 67 , 68 , 69 ]. A significantly increased incidence of acute HF was reported in patients deceased due to severe COVID-19, as compared to their survivor counterparts [ 70 ].…”