Hypercoagulability in COVID-19: A review of the potential mechanisms underlying clotting disorders

dc.contributor.authorAlam, Walid
dc.contributor.departmentInternal Medicine
dc.contributor.facultyFaculty of Medicine (FM)
dc.contributor.institutionAmerican University of Beirut
dc.date.accessioned2025-01-24T12:01:06Z
dc.date.available2025-01-24T12:01:06Z
dc.date.issued2021
dc.description.abstractSevere acute respiratory syndrome coronavirus-2 has emerged as a new viral pandemic, causing Coronavirus disease 2019 (COVID-19) leading to a wide array of symptoms ranging from asymptomatic to severe respiratory failure. However, coagulation disorders have been found in some patients infected with SARS-CoV-2, leading to either a clotting disorder or hemorrhage. Several mechanisms attempt to explain the mechanism behind the pro-coagulant state seen with COVID-19 patients, including different receptor binding, cytokine storm, and direct viral endothelial damage. SARS-CoV-2 has also been recently found to bind to CLEC4M receptor, a receptor that participates in the clearance of von Willebrand Factor and Factor VIII. The competitive binding of SARS-CoV-2 to CLEC4M could lead to decreased clearance, and therefore a promotion of a pro-coagulative state; however, an experimental study needs to be done to prove such an association. © The Author(s) 2021.
dc.identifier.doihttps://doi.org/10.1177/20503121211002996
dc.identifier.eid2-s2.0-85105764531
dc.identifier.urihttp://hdl.handle.net/10938/31438
dc.language.isoen
dc.publisherSAGE Publications Ltd
dc.relation.ispartofSAGE Open Medicine
dc.sourceScopus
dc.subjectClec4m
dc.subjectCoagulopathy
dc.subjectCovid-19
dc.subjectFibrinolytic shutdown
dc.subjectInfectious diseases
dc.subjectMechanism
dc.subjectSars-cov-2
dc.subjectAngiotensin converting enzyme 2
dc.subjectBeta2 glycoprotein 1
dc.subjectBlood clotting factor 8
dc.subjectC type lectin domain family 4 member m
dc.subjectCd147 antigen
dc.subjectCd209 antigen
dc.subjectComplement component c3b
dc.subjectComplement component c4b
dc.subjectComplement component c5b
dc.subjectD dimer
dc.subjectFibrinogen
dc.subjectGranulocyte macrophage colony stimulating factor
dc.subjectInterleukin 1
dc.subjectInterleukin 6
dc.subjectLectin
dc.subjectNeuropilin 1
dc.subjectPhospholipid antibody
dc.subjectReactive oxygen metabolite
dc.subjectThromboplastin
dc.subjectTumor necrosis factor
dc.subjectUnclassified drug
dc.subjectVasculotropin
dc.subjectVirus spike protein
dc.subjectVitronectin
dc.subjectVon willebrand factor
dc.subjectAutoimmunity
dc.subjectBleeding
dc.subjectBlood clotting disorder
dc.subjectCoronavirus disease 2019
dc.subjectCytokine storm
dc.subjectDisseminated intravascular clotting
dc.subjectFibrinolysis
dc.subjectHuman
dc.subjectHypercoagulability
dc.subjectPandemic
dc.subjectProtein expression
dc.subjectProthrombin time
dc.subjectReceptor binding
dc.subjectRenin angiotensin aldosterone system
dc.subjectRespiratory failure
dc.subjectReview
dc.subjectSevere acute respiratory syndrome coronavirus 2
dc.subjectSystematic review
dc.subjectTh1 cell
dc.subjectThrombocyte adhesion
dc.subjectThrombocyte aggregation
dc.subjectThrombosis
dc.subjectVirus replication
dc.titleHypercoagulability in COVID-19: A review of the potential mechanisms underlying clotting disorders
dc.typeReview

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