PMC:7652766 / 112477-114778 JSONTXT

{"project":"LitCovid-PD-HP","denotations":[{"id":"T159","span":{"begin":122,"end":160},"obj":"Phenotype"},{"id":"T160","span":{"begin":165,"end":177},"obj":"Phenotype"},{"id":"T161","span":{"begin":199,"end":205},"obj":"Phenotype"},{"id":"T162","span":{"begin":210,"end":248},"obj":"Phenotype"},{"id":"T163","span":{"begin":261,"end":275},"obj":"Phenotype"},{"id":"T164","span":{"begin":388,"end":397},"obj":"Phenotype"},{"id":"T165","span":{"begin":1150,"end":1162},"obj":"Phenotype"},{"id":"T166","span":{"begin":1389,"end":1395},"obj":"Phenotype"},{"id":"T167","span":{"begin":1404,"end":1416},"obj":"Phenotype"}],"attributes":[{"id":"A159","pred":"hp_id","subj":"T159","obj":"http://purl.obolibrary.org/obo/HP_0005521"},{"id":"A160","pred":"hp_id","subj":"T160","obj":"http://purl.obolibrary.org/obo/HP_0003256"},{"id":"A161","pred":"hp_id","subj":"T161","obj":"http://purl.obolibrary.org/obo/HP_0100806"},{"id":"A162","pred":"hp_id","subj":"T162","obj":"http://purl.obolibrary.org/obo/HP_0005521"},{"id":"A163","pred":"hp_id","subj":"T163","obj":"http://purl.obolibrary.org/obo/HP_0001907"},{"id":"A164","pred":"hp_id","subj":"T164","obj":"http://purl.obolibrary.org/obo/HP_0002090"},{"id":"A165","pred":"hp_id","subj":"T165","obj":"http://purl.obolibrary.org/obo/HP_0003256"},{"id":"A166","pred":"hp_id","subj":"T166","obj":"http://purl.obolibrary.org/obo/HP_0100806"},{"id":"A167","pred":"hp_id","subj":"T167","obj":"http://purl.obolibrary.org/obo/HP_0003256"}],"text":"Anticoagulants\nA high mortality risk in severe COVID-19 patients has been described, especially due to the development of disseminated intravascular coagulation and coagulopathy (395). Patients with sepsis and disseminated intravascular coagulation may develop thromboembolic complications or microvascular clot deposition, contributing to multiple organ failure. In patients with severe pneumonia, the activation of vascular endothelium, platelets, and leukocytes results in the unregulated generation of thrombin, both locally, in the lungs, and systemically, leading to fibrin deposition and subsequent tissue damage and microangiopathy (396). In COVID-19 patients, severe pulmonary inflammation is believed to be associated with the regulation of pro-inflammatory cytokines, which can cause the dysfunction of endothelial cells and consequently higher thrombin production. Therefore, the use of anticoagulant therapy could be beneficial for COVID-19 patients (397).\nIn a retrospective study with 449 patients with severe COVID-19, Tang et al. (395) observed a lower mortality rate in individuals treated with prophylactic heparin associated with coagulopathy compared with those who had not been treated with an anticoagulant. The study associated the use of thrombosis prophylaxis with lower 28-day mortality in COVID-19 patients, but only for those presenting a high value of either sepsis-induced coagulopathy score (≥4) or D-dimer (≥3.0 mg/L).\nParanjpe et al. (398) carried out a large cohort analysis with 2773 COVID-19 patients in the United States, among which 28% received anticoagulant therapy, and also found an association of anticoagulant-based treatment with lower mortality risk. The mortality rate in patients who required mechanical ventilation and received anticoagulant therapy was lower than those who had not been treated with an anticoagulant.\nIt is important to highlight that heparin has an anti-inflammatory effect that can bind to inflammatory cytokines, chemokines, and proinflammatory proteins, inhibiting neutrophil chemotaxis and leukocyte migration (399–401). In the current COVID-19 context, there are over 60 ongoing clinical trials covering the use of thromboprophylaxis, which will certainly clarify the potential role of anticoagulants in patients with COVID-19."}

{"project":"LitCovid-sentences","denotations":[{"id":"T553","span":{"begin":0,"end":14},"obj":"Sentence"},{"id":"T554","span":{"begin":15,"end":184},"obj":"Sentence"},{"id":"T555","span":{"begin":185,"end":363},"obj":"Sentence"},{"id":"T556","span":{"begin":364,"end":646},"obj":"Sentence"},{"id":"T557","span":{"begin":647,"end":876},"obj":"Sentence"},{"id":"T558","span":{"begin":877,"end":969},"obj":"Sentence"},{"id":"T559","span":{"begin":970,"end":1230},"obj":"Sentence"},{"id":"T560","span":{"begin":1231,"end":1451},"obj":"Sentence"},{"id":"T561","span":{"begin":1452,"end":1697},"obj":"Sentence"},{"id":"T562","span":{"begin":1698,"end":1868},"obj":"Sentence"},{"id":"T563","span":{"begin":1869,"end":2093},"obj":"Sentence"},{"id":"T564","span":{"begin":2094,"end":2301},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Anticoagulants\nA high mortality risk in severe COVID-19 patients has been described, especially due to the development of disseminated intravascular coagulation and coagulopathy (395). Patients with sepsis and disseminated intravascular coagulation may develop thromboembolic complications or microvascular clot deposition, contributing to multiple organ failure. In patients with severe pneumonia, the activation of vascular endothelium, platelets, and leukocytes results in the unregulated generation of thrombin, both locally, in the lungs, and systemically, leading to fibrin deposition and subsequent tissue damage and microangiopathy (396). In COVID-19 patients, severe pulmonary inflammation is believed to be associated with the regulation of pro-inflammatory cytokines, which can cause the dysfunction of endothelial cells and consequently higher thrombin production. Therefore, the use of anticoagulant therapy could be beneficial for COVID-19 patients (397).\nIn a retrospective study with 449 patients with severe COVID-19, Tang et al. (395) observed a lower mortality rate in individuals treated with prophylactic heparin associated with coagulopathy compared with those who had not been treated with an anticoagulant. The study associated the use of thrombosis prophylaxis with lower 28-day mortality in COVID-19 patients, but only for those presenting a high value of either sepsis-induced coagulopathy score (≥4) or D-dimer (≥3.0 mg/L).\nParanjpe et al. (398) carried out a large cohort analysis with 2773 COVID-19 patients in the United States, among which 28% received anticoagulant therapy, and also found an association of anticoagulant-based treatment with lower mortality risk. The mortality rate in patients who required mechanical ventilation and received anticoagulant therapy was lower than those who had not been treated with an anticoagulant.\nIt is important to highlight that heparin has an anti-inflammatory effect that can bind to inflammatory cytokines, chemokines, and proinflammatory proteins, inhibiting neutrophil chemotaxis and leukocyte migration (399–401). In the current COVID-19 context, there are over 60 ongoing clinical trials covering the use of thromboprophylaxis, which will certainly clarify the potential role of anticoagulants in patients with COVID-19."}

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high mortality risk in severe COVID-19 patients has been described, especially due to the development of disseminated intravascular coagulation and coagulopathy (395). Patients with sepsis and disseminated intravascular coagulation may develop thromboembolic complications or microvascular clot deposition, contributing to multiple organ failure. In patients with severe pneumonia, the activation of vascular endothelium, platelets, and leukocytes results in the unregulated generation of thrombin, both locally, in the lungs, and systemically, leading to fibrin deposition and subsequent tissue damage and microangiopathy (396). In COVID-19 patients, severe pulmonary inflammation is believed to be associated with the regulation of pro-inflammatory cytokines, which can cause the dysfunction of endothelial cells and consequently higher thrombin production. Therefore, the use of anticoagulant therapy could be beneficial for COVID-19 patients (397).\nIn a retrospective study with 449 patients with severe COVID-19, Tang et al. (395) observed a lower mortality rate in individuals treated with prophylactic heparin associated with coagulopathy compared with those who had not been treated with an anticoagulant. The study associated the use of thrombosis prophylaxis with lower 28-day mortality in COVID-19 patients, but only for those presenting a high value of either sepsis-induced coagulopathy score (≥4) or D-dimer (≥3.0 mg/L).\nParanjpe et al. (398) carried out a large cohort analysis with 2773 COVID-19 patients in the United States, among which 28% received anticoagulant therapy, and also found an association of anticoagulant-based treatment with lower mortality risk. The mortality rate in patients who required mechanical ventilation and received anticoagulant therapy was lower than those who had not been treated with an anticoagulant.\nIt is important to highlight that heparin has an anti-inflammatory effect that can bind to inflammatory cytokines, chemokines, and proinflammatory proteins, inhibiting neutrophil chemotaxis and leukocyte migration (399–401). In the current COVID-19 context, there are over 60 ongoing clinical trials covering the use of thromboprophylaxis, which will certainly clarify the potential role of anticoagulants in patients with COVID-19."}