Coagulation and anticoagulation in COVID-19

Hadid, Tarik; Kafri, Zyad; Al-Katib, Ayad

doi:10.1016/j.blre.2020.100761

Cited by 166 publications

(210 citation statements)

References 88 publications

(203 reference statements)

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“…Elevated fibrinogen levels associated with COVID-19, partic-ularly in patients with a severe manifestation of the disease, are mainly associated with increased inflammation, thus reflecting the degree of immune response, rather than high thrombotic risk. 61 According to Thachil, fibrinogen fulfills a protective role during COVID-19 disease manifestation, 62 via one or both of two possible mechanisms: (1) the regulation of the immune response, independent of the hemostatic functions of fibrinogen, and (2) the formation of a fibrin network, thus constituting a specific barrier for the pathogen. 62 The enhanced procoagulant potential associated with COVID-19 is the result of several pathological processes, including a hyperimmune response and endothelial dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Hemostasis in Coronavirus Disease 2019—Lesson from Viscoelastic Methods: A Systematic Review

2021

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Haemostatic unbalance is often observed in patients with coronavirus disease 2019 (COVID-19), and patients with severe disease are at high risk of developing thromboembolic complications. Viscoelastic methods (VEMs), including thrombelastography (TEG) and thromboelastometry (TEM), provide data on the nature of haemostatic disturbance. In this systematic review, we assessed the performance of TEG and TEM in the assessment of blood coagulation and fibrinolysis in patients with COVID-19. PubMed, Scopus, Web of Science Core Collection, medRxiv and bioRxiv were systematically searched for clinical studies evaluating TEG and/or TEM variables in COVID-19 individuals. Ten studies, with a total of 389 COVID-19 patients, were included, and VEMs were performed in 292 of these patients. Most patients (90%) presented severe COVID-19 and required mechanical ventilation. TEG and TEM variables showed that these patients displayed hypercoagulability and fibrinolysis shutdown, despite the use of appropriate thromboprophylaxis. However, the mechanism underlying these phenomena and their clinical significance in COVID-19 patients who developed thrombosis, is still not clear. Further studies are warranted if VEMs might help to identify those at highest risk of thrombotic events and who therefore may derive the greatest benefit from antithrombotic therapy.

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Section: Discussionmentioning

confidence: 99%

Hemostasis in Coronavirus Disease 2019—Lesson from Viscoelastic Methods: A Systematic Review

2021

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“…IL-6, a cytokine that is significantly elevated in severe COVID-19 infection, is a key activator of coagulopathy by inducing tissue factor expression and increasing fibrinogen production. Similarly, IL-6 can mainly enhance the proliferation, differentiation, and activation of megakaryocytes through increasing the production of thrombopoietin [ 84 ]. Megakaryocytes along with platelet-derived fibrin characterize multi-organ thrombosis in COVID-19 patients [ 85 ].…”

Section: How Does Sars-cov-2 Initiate Cytokine Release and What Are Tmentioning

confidence: 99%

“…The release of cytokines and chemokines like TNFα, IL-1, IL-6, and IL-8 induces macrophage activation syndrome which triggers the endothelial cells, macrophages, and neutrophils to express TF within the lungs which in turn initiates and further augments pulmonary coagulopathy and microvascular thrombosis [ 84 , 89 ]. These small fibrin thrombi were observed in small pulmonary arterioles, in 8 COVID-19 cases out of 10, in areas of both damaged and preserved lung parenchyma [ 90 ].…”

Section: How Does Sars-cov-2 Initiate Cytokine Release and What Are Tmentioning

confidence: 99%

The pro-inflammatory cytokines in COVID-19 pathogenesis: What goes wrong?

Darif

Hammi

Kihel

et al. 2021

Microbial Pathogenesis

222

195

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The outbreak of coronavirus disease 2019 (COVID-19), caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection, has emerged in China in December 2019 and rapidly spread to more than 196 countries worldwide. The physiopathology of human SARS-CoV-2 has not been completely understood, but its pathogenesis has been linked to a disproportionate response of the immune system. Just as described for SARS and MERS, an uncontrolled systemic inflammatory response, known as cytokine release syndrome (CRS) was observed in severe COVID-19 patients. It results from the release by immune and non-immune effector cells of substantial amounts of pro-inflammatory cytokines and appears to contribute to SARS-CoV-2 pulmonary inflammation and extensive lung damage. In addition, hyper-coagulation and thrombosis resulted from the important release of pro-inflammatory cytokines contribute to the lethality of subjects severely infected with SARS-CoV-2. It is therefore essential to have a deep understanding of the various cytokines involved in this exacerbated immune response, and that could be targeted by potential immunological treatments. The aim of this review was to gather the current knowledge about the role of pro-inflammatory cytokines, namely IL-1β, IL-6, IL-8, IL-17 and TNFα in SARS-CoV-2 CRS , the probable causes and clinical outcomes of this phenomenon in severe cases of COVID-19.

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“…Further COVID-19 therapeutics under investigations include anticoagulants that target COVID-19-induced systemic coagulation and thrombosis (coagulopathy) [Hadid et al, 2020].…”

Section: Introductionmentioning

confidence: 99%

CD47 as a potential biomarker for the early diagnosis of severe COVID-19

McLaughlin

Bojkova

Bechtel

et al. 2021

Preprint

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The coronavirus SARS-CoV-2 is the cause of the ongoing COVID-19 pandemic. Most SARS-CoV-2 infections are mild or even asymptomatic. However, a small fraction of infected individuals develops severe, life-threatening disease, which is caused by an uncontrolled immune response resulting in hyperinflammation. Antiviral interventions are only effective prior to the onset of hyperinflammation. Hence, biomarkers are needed for the early identification and treatment of high-risk patients. Here, we show in a range of model systems and data from post mortem samples that SARS-CoV-2 infection results in increased levels of CD47, which is known to mediate immune escape in cancer and virus-infected cells. Systematic literature searches also indicated that known risk factors such as older age and diabetes are associated with increased CD47 levels. High CD47 levels contribute to vascular disease, vasoconstriction, and hypertension, conditions which may predispose SARS-CoV-2-infected individuals to COVID-19-related complications such as pulmonary hypertension, lung fibrosis, myocardial injury, stroke, and acute kidney injury. Hence, CD47 is a candidate biomarker for severe COVID-19. Further research will have to show whether CD47 is a reliable diagnostic marker for the early identification of COVID-19 patients requiring antiviral therapy.

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Coagulation and anticoagulation in COVID-19

Cited by 166 publications

References 88 publications

Hemostasis in Coronavirus Disease 2019—Lesson from Viscoelastic Methods: A Systematic Review

Hemostasis in Coronavirus Disease 2019—Lesson from Viscoelastic Methods: A Systematic Review

The pro-inflammatory cytokines in COVID-19 pathogenesis: What goes wrong?

CD47 as a potential biomarker for the early diagnosis of severe COVID-19

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