2020
DOI: 10.1159/000512007
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The Impact of COVID-19 Disease on Platelets and Coagulation

Abstract: Coronavirus disease 2019 (COVID-19) causes a spectrum of disease; some patients develop a severe proinflammatory state which can be associated with a unique coagulopathy and procoagulant endothelial phenotype. Initially, COVID-19 infection produces a prominent elevation of fibrinogen and D-dimer/fibrin(ogen) degradation products. This is associated with systemic hypercoagulability and frequent venous thromboembolic events. The degree of D-dimer elevation positively correlates with mortality in COVID-19 patient… Show more

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Cited by 442 publications
(541 citation statements)
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References 102 publications
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“…Taken together, these and previous findings are suggestive of some degrees of coagulation exhaustion in COVID-19, at least at a stage of disease needing oxygen therapy and/or intensive care, which would hence confirm the existence of initial local and/or systemic activation of blood coagulation, followed by significant exhaustion, as earlier noted in other studies, even using different markers. [12][13][14][15] These findings are also in keeping with solid evidence of prolonged prothrombin times and decreased platelet counts in COVID-19 patients, especially those progressing to severe/critical illness, as underpinned in most recent meta-analyses. [16][17][18] It is also noteworthy that the almost unvaried evidence in thrombin generation values performed with or without TM would suggest that the protein C system may be a minor player on COVID-19 coagulopathy, while activation of platelets and the factor XII-dependent pathway may alternatively appear as major drivers.…”
Section: Issue Theme Maintaining Hemostasis and Preventing Thrombosissupporting
confidence: 77%
“…Taken together, these and previous findings are suggestive of some degrees of coagulation exhaustion in COVID-19, at least at a stage of disease needing oxygen therapy and/or intensive care, which would hence confirm the existence of initial local and/or systemic activation of blood coagulation, followed by significant exhaustion, as earlier noted in other studies, even using different markers. [12][13][14][15] These findings are also in keeping with solid evidence of prolonged prothrombin times and decreased platelet counts in COVID-19 patients, especially those progressing to severe/critical illness, as underpinned in most recent meta-analyses. [16][17][18] It is also noteworthy that the almost unvaried evidence in thrombin generation values performed with or without TM would suggest that the protein C system may be a minor player on COVID-19 coagulopathy, while activation of platelets and the factor XII-dependent pathway may alternatively appear as major drivers.…”
Section: Issue Theme Maintaining Hemostasis and Preventing Thrombosissupporting
confidence: 77%
“…The SPSS™ (IBM™ Statistical Package for the Social Science version 26.0) was used for statistical analyses, and GraphPad Prism version 8.0.0 (GraphPad Software, San Diego, California, USA) was used for graph plotting. (45)(46)(47)(48)(49)(50)(51)(52)(53)(54)(55)(56)(57)(58)(59)(60)(61)(62)(63)(64) years, p = 0.002], had a higher SOFA score at study inclusion [median (IQR), 8 (6-9) vs. 5 (3-6) points, p = 0.002], a higher number of coexisting conditions [median (IQR), 3 (2-3) vs. 1 (0-2), p<0.001], had diabetes mellitus more frequently [9/14 (64.3) vs. 2/16 (12.5), p = 0.007] and received renal replacement therapy more frequently [10/14 (71.4) vs. 0/16 (0.0), p<0.001] (Table 1).…”
Section: Resultsmentioning
confidence: 99%
“…Several mechanics can explain the relationship between viral infection and our findings, as endothelial cell disruption, tissue factor expression, and activation of the coagulation cascade by cytokines released during viral infections are other possible mechanisms of thrombosis. This pro-inflammatory state can promote microthrombosis in the vascular lung system and consequently promoting more hypoxia with local impact creating a deleterious positive thrombo-inflammatory feedback loop [39,47,48].…”
Section: Plos Onementioning
confidence: 99%
“…Increased thrombosis may lead to increased consumption of platelets and the onset of thrombocytopenia in 5–41.7% of the patients, percentage varying according to the severity of the disease, being more frequent in patients with more severe disease (58–95%) ( Wool and Miller, 2020 ). More severe thrombocytopenia is encountered in cases of disseminated intravascular coagulation (DIC), diagnosed in 2% of the patients in a study including 400 patients, of which 144 were critically ill ( Al-Samkari et al, 2020 ).…”
Section: Introductionmentioning
confidence: 99%