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10.1007/s10067-020-05275-1 http://scihub22266oqcxt.onion/10.1007/s10067-020-05275-1 32654082!7353835!32654082     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Clin+Rheumatol 2020 ; 39 (9): 2529-2543 Nephropedia Template TP {{tp|p=32654082|t=2020. Thrombosis in Coronavirus disease 2019 (COVID-19) through the prism of Virchow s triad |pdf=|usr=}}{{32654082}} gab.com Text Thrombosis in Coronavirus disease 2019 (COVID-19) through the prism of Virchow s triad JO: Clin Rheumatol http://www.kidney.de/pget.php?&tw=1&pmid=32654082 #FOAvip The pathogenesis of Coronavirus disease 2019 (COVID-19) is gradually being comprehended. A high number of thrombotic episodes are reported, along with the mortality benefits of heparin. COVID-19 can be viewed as a prothrombotic disease. We overviewed the available evidence to explore this possibility. We identified various histopathology reports and clinical case series reporting thromboses in COVID-19. Also, multiple coagulation markers support this. COVID-19 can be regarded as a risk factor for thrombosis. Applying the principles of Virchow's triad, we described abnormalities in the vascular endothelium, altered blood flow, and platelet function abnormalities that lead to venous and arterial thromboses in COVID-19. Endothelial dysfunction, activation of the renin-angiotensin-aldosterone system (RAAS) with the release of procoagulant plasminogen activator inhibitor (PAI-1), and hyperimmune response with activated platelets seem to be significant contributors to thrombogenesis in COVID-19. Stratifying risk of COVID-19 thromboses should be based on age, presence of comorbidities, D-dimer, CT scoring, and various blood cell ratios. Isolated heparin therapy may not be sufficient to combat thrombosis in this disease. There is an urgent need to explore newer avenues like activated protein C, PAI-1 antagonists, and tissue plasminogen activators (tPA). These should be augmented with therapies targeting RAAS, antiplatelet drugs, repurposed antiinflammatory, and antirheumatic drugs. Key Points * Venous and arterial thromboses in COVID-19 can be viewed through the prism of Virchow's triad. * Endothelial dysfunction, platelet activation, hyperviscosity, and blood flow abnormalities due to hypoxia, immune reactions, and hypercoagulability lead to thrombogenesis in COVID-19. * There is an urgent need to stratify COVID-19 patients at risk for thrombosis using age, comorbidities, D-dimer, and CT scoring. * Patients with COVID-19 at high risk for thrombosis should be put on high dose heparin therapy. Twit Text FOAVip Thrombosis in Coronavirus disease 2019 (COVID-19) through the prism of Virchow s triad ????Clin Rheumatol http://www.kidney.de/pget.php?&tw=1&pmid=32654082 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32654082 #FOAvip English Wikipedia <ref>{{Cite pmid|32654082}}</ref> Thrombosis in Coronavirus disease 2019 (COVID-19) through the prism of Virchow s triad #MMPMID32654082 Ahmed S; Zimba O; Gasparyan AY Clin Rheumatol 2020[Sep]; 39 (9): 2529-2543 PMID32654082show ga The pathogenesis of Coronavirus disease 2019 (COVID-19) is gradually being comprehended. A high number of thrombotic episodes are reported, along with the mortality benefits of heparin. COVID-19 can be viewed as a prothrombotic disease. We overviewed the available evidence to explore this possibility. We identified various histopathology reports and clinical case series reporting thromboses in COVID-19. Also, multiple coagulation markers support this. COVID-19 can be regarded as a risk factor for thrombosis. Applying the principles of Virchow's triad, we described abnormalities in the vascular endothelium, altered blood flow, and platelet function abnormalities that lead to venous and arterial thromboses in COVID-19. Endothelial dysfunction, activation of the renin-angiotensin-aldosterone system (RAAS) with the release of procoagulant plasminogen activator inhibitor (PAI-1), and hyperimmune response with activated platelets seem to be significant contributors to thrombogenesis in COVID-19. Stratifying risk of COVID-19 thromboses should be based on age, presence of comorbidities, D-dimer, CT scoring, and various blood cell ratios. Isolated heparin therapy may not be sufficient to combat thrombosis in this disease. There is an urgent need to explore newer avenues like activated protein C, PAI-1 antagonists, and tissue plasminogen activators (tPA). These should be augmented with therapies targeting RAAS, antiplatelet drugs, repurposed antiinflammatory, and antirheumatic drugs. Key Points * Venous and arterial thromboses in COVID-19 can be viewed through the prism of Virchow's triad. * Endothelial dysfunction, platelet activation, hyperviscosity, and blood flow abnormalities due to hypoxia, immune reactions, and hypercoagulability lead to thrombogenesis in COVID-19. * There is an urgent need to stratify COVID-19 patients at risk for thrombosis using age, comorbidities, D-dimer, and CT scoring. * Patients with COVID-19 at high risk for thrombosis should be put on high dose heparin therapy. |Angiotensin Receptor Antagonists/therapeutic use[MESH] |Angiotensin-Converting Enzyme 2[MESH] |Angiotensin-Converting Enzyme Inhibitors/therapeutic use[MESH] |Anticoagulants/therapeutic use[MESH] |Betacoronavirus/metabolism[MESH] |Blood Platelets[MESH] |Blood Viscosity[MESH] |COVID-19[MESH] |Coronavirus Infections/*blood/complications/drug therapy/metabolism[MESH] |Endothelium, Vascular/*metabolism/physiopathology[MESH] |Fibrin Fibrinogen Degradation Products[MESH] |Fibrinogen/metabolism[MESH] |Fibrinolytic Agents/therapeutic use[MESH] |Heparin/therapeutic use[MESH] |Humans[MESH] |Pandemics[MESH] |Peptidyl-Dipeptidase A/*metabolism[MESH] |Plasminogen Activator Inhibitor 1/blood[MESH] |Platelet Activation[MESH] |Platelet Aggregation Inhibitors/therapeutic use[MESH] |Pneumonia, Viral/*blood/complications/drug therapy/metabolism[MESH] |SARS-CoV-2[MESH] |Severity of Illness Index[MESH] |Thrombophilia/*blood/etiology/metabolism[MESH] |Thrombosis/*blood/drug therapy/etiology[MESH]Thrombosis in Coronavirus disease 2019 (COVID-19) through the prism of(epmc).pdf DeepDyve Pubget Overpricing