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10.1182/blood.2020007252

http://scihub22266oqcxt.onion/10.1182/blood.2020007252
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32678428!7483437!32678428
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suck abstract from ncbi


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pmid32678428      Blood 2020 ; 136 (11): 1330-1341
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  • Platelet activation and platelet-monocyte aggregate formation trigger tissue factor expression in patients with severe COVID-19 #MMPMID32678428
  • Hottz ED; Azevedo-Quintanilha IG; Palhinha L; Teixeira L; Barreto EA; Pao CRR; Righy C; Franco S; Souza TML; Kurtz P; Bozza FA; Bozza PT
  • Blood 2020[Sep]; 136 (11): 1330-1341 PMID32678428show ga
  • Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is an emergent pathogen responsible for the coronavirus disease 2019 (COVID-19). Since its emergence, the novel coronavirus has rapidly achieved pandemic proportions causing remarkably increased morbidity and mortality around the world. A hypercoagulability state has been reported as a major pathologic event in COVID-19, and thromboembolic complications listed among life-threatening complications of the disease. Platelets are chief effector cells of hemostasis and pathological thrombosis. However, the participation of platelets in the pathogenesis of COVID-19 remains elusive. This report demonstrates that increased platelet activation and platelet-monocyte aggregate formation are observed in severe COVID-19 patients, but not in patients presenting mild COVID-19 syndrome. In addition, exposure to plasma from severe COVID-19 patients increased the activation of control platelets ex vivo. In our cohort of COVID-19 patients admitted to the intensive care unit, platelet-monocyte interaction was strongly associated with tissue factor (TF) expression by the monocytes. Platelet activation and monocyte TF expression were associated with markers of coagulation exacerbation as fibrinogen and D-dimers, and were increased in patients requiring invasive mechanical ventilation or patients who evolved with in-hospital mortality. Finally, platelets from severe COVID-19 patients were able to induce TF expression ex vivo in monocytes from healthy volunteers, a phenomenon that was inhibited by platelet P-selectin neutralization or integrin alphaIIb/beta3 blocking with the aggregation inhibitor abciximab. Altogether, these data shed light on new pathological mechanisms involving platelet activation and platelet-dependent monocyte TF expression, which were associated with COVID-19 severity and mortality.
  • |Adult[MESH]
  • |Betacoronavirus/*immunology[MESH]
  • |Biomarkers/metabolism[MESH]
  • |Blood Coagulation Disorders/immunology/metabolism/*pathology/virology[MESH]
  • |Blood Platelets/metabolism/*pathology/virology[MESH]
  • |COVID-19[MESH]
  • |Case-Control Studies[MESH]
  • |Coronavirus Infections/*complications/immunology/metabolism/virology[MESH]
  • |Female[MESH]
  • |Follow-Up Studies[MESH]
  • |Humans[MESH]
  • |Male[MESH]
  • |Middle Aged[MESH]
  • |Monocytes/metabolism/*pathology/virology[MESH]
  • |P-Selectin/metabolism[MESH]
  • |Pandemics[MESH]
  • |Platelet Activation[MESH]
  • |Pneumonia, Viral/*complications/immunology/metabolism/virology[MESH]
  • |Prognosis[MESH]
  • |Prospective Studies[MESH]
  • |SARS-CoV-2[MESH]
  • |Survival Rate[MESH]


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