PMC:7652766 / 112492-113446 JSONTXT

{"project":"LitCovid-PD-HP","denotations":[{"id":"T159","span":{"begin":107,"end":145},"obj":"Phenotype"},{"id":"T160","span":{"begin":150,"end":162},"obj":"Phenotype"},{"id":"T161","span":{"begin":184,"end":190},"obj":"Phenotype"},{"id":"T162","span":{"begin":195,"end":233},"obj":"Phenotype"},{"id":"T163","span":{"begin":246,"end":260},"obj":"Phenotype"},{"id":"T164","span":{"begin":373,"end":382},"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"}],"text":"A 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)."}

{"project":"LitCovid-sentences","denotations":[{"id":"T554","span":{"begin":0,"end":169},"obj":"Sentence"},{"id":"T555","span":{"begin":170,"end":348},"obj":"Sentence"},{"id":"T556","span":{"begin":349,"end":631},"obj":"Sentence"},{"id":"T557","span":{"begin":632,"end":861},"obj":"Sentence"},{"id":"T558","span":{"begin":862,"end":954},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"A 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)."}

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