Hypercoagulability in COVID-19: A review of the potential mechanisms underlying clotting disorders
| dc.contributor.author | Alam, Walid | |
| dc.contributor.department | Internal Medicine | |
| dc.contributor.faculty | Faculty of Medicine (FM) | |
| dc.contributor.institution | American University of Beirut | |
| dc.date.accessioned | 2025-01-24T12:01:06Z | |
| dc.date.available | 2025-01-24T12:01:06Z | |
| dc.date.issued | 2021 | |
| dc.description.abstract | Severe 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.doi | https://doi.org/10.1177/20503121211002996 | |
| dc.identifier.eid | 2-s2.0-85105764531 | |
| dc.identifier.uri | http://hdl.handle.net/10938/31438 | |
| dc.language.iso | en | |
| dc.publisher | SAGE Publications Ltd | |
| dc.relation.ispartof | SAGE Open Medicine | |
| dc.source | Scopus | |
| dc.subject | Clec4m | |
| dc.subject | Coagulopathy | |
| dc.subject | Covid-19 | |
| dc.subject | Fibrinolytic shutdown | |
| dc.subject | Infectious diseases | |
| dc.subject | Mechanism | |
| dc.subject | Sars-cov-2 | |
| dc.subject | Angiotensin converting enzyme 2 | |
| dc.subject | Beta2 glycoprotein 1 | |
| dc.subject | Blood clotting factor 8 | |
| dc.subject | C type lectin domain family 4 member m | |
| dc.subject | Cd147 antigen | |
| dc.subject | Cd209 antigen | |
| dc.subject | Complement component c3b | |
| dc.subject | Complement component c4b | |
| dc.subject | Complement component c5b | |
| dc.subject | D dimer | |
| dc.subject | Fibrinogen | |
| dc.subject | Granulocyte macrophage colony stimulating factor | |
| dc.subject | Interleukin 1 | |
| dc.subject | Interleukin 6 | |
| dc.subject | Lectin | |
| dc.subject | Neuropilin 1 | |
| dc.subject | Phospholipid antibody | |
| dc.subject | Reactive oxygen metabolite | |
| dc.subject | Thromboplastin | |
| dc.subject | Tumor necrosis factor | |
| dc.subject | Unclassified drug | |
| dc.subject | Vasculotropin | |
| dc.subject | Virus spike protein | |
| dc.subject | Vitronectin | |
| dc.subject | Von willebrand factor | |
| dc.subject | Autoimmunity | |
| dc.subject | Bleeding | |
| dc.subject | Blood clotting disorder | |
| dc.subject | Coronavirus disease 2019 | |
| dc.subject | Cytokine storm | |
| dc.subject | Disseminated intravascular clotting | |
| dc.subject | Fibrinolysis | |
| dc.subject | Human | |
| dc.subject | Hypercoagulability | |
| dc.subject | Pandemic | |
| dc.subject | Protein expression | |
| dc.subject | Prothrombin time | |
| dc.subject | Receptor binding | |
| dc.subject | Renin angiotensin aldosterone system | |
| dc.subject | Respiratory failure | |
| dc.subject | Review | |
| dc.subject | Severe acute respiratory syndrome coronavirus 2 | |
| dc.subject | Systematic review | |
| dc.subject | Th1 cell | |
| dc.subject | Thrombocyte adhesion | |
| dc.subject | Thrombocyte aggregation | |
| dc.subject | Thrombosis | |
| dc.subject | Virus replication | |
| dc.title | Hypercoagulability in COVID-19: A review of the potential mechanisms underlying clotting disorders | |
| dc.type | Review |
Files
Original bundle
1 - 1 of 1