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{"project":"LitCovid-PD-HP","denotations":[{"id":"T96","span":{"begin":65,"end":84},"obj":"Phenotype"},{"id":"T97","span":{"begin":181,"end":200},"obj":"Phenotype"},{"id":"T98","span":{"begin":1029,"end":1044},"obj":"Phenotype"}],"attributes":[{"id":"A96","pred":"hp_id","subj":"T96","obj":"http://purl.obolibrary.org/obo/HP_0002960"},{"id":"A97","pred":"hp_id","subj":"T97","obj":"http://purl.obolibrary.org/obo/HP_0002960"},{"id":"A98","pred":"hp_id","subj":"T98","obj":"http://purl.obolibrary.org/obo/HP_0001907"}],"text":"2.3.3. Antiphospholipid Syndrome\nAntiphospholipid syndrome is an autoimmune disorder characterized by antiphospholipid autoantibodies production. If it is not associated with other autoimmune diseases, it is called primary [97]. The incidence of the pathology is greater in young women of reproductive age and it often has a negative impact on pregnancy, with unfortunate outcomes due to the development of placental ischemic pathologies. Resonance spectroscopy, indeed, revealed that the fetal brain and placenta are the main targets of autoantibodies localization [95]. As complement activation plays a central role in the occurrence of the disease, many studies have evaluated the role of HCQ in inhibiting complement activation. In a mouse model of obstetric antiphospholipid syndrome, HCQ, administered in a daily dose of 200 μg per mouse limited placental abnormalities, with an increase of fetal survival, by inhibiting complement activation [95]. A case report on the use of HCQ on a pregnant woman with recurrent venous thromboembolism confirmed the efficacy of HCQ also in clinical practice. The addition of 400 mg daily of HCQ to a common therapeutic regimen of aspirin and heparin dramatically reduced the episodes of vascular thrombosis [96], showing great antithrombotic properties. Given these results, the mechanisms underlying the use of HCQ in thromboprophylaxis were assessed. Two similar preclinical studies, using one-week treatment with 12 μg/g/day of HCQ and three-weeks treatment with 20 mg/kg/day of HCQ, respectively, were in accordance to assess that the overall amelioration of thrombotic status in mice models of antiphospholipid syndrome was linked to endothelial function improvement by modulating the expression of nitric oxide synthase [97,98]. Moreover, the efficacy of HCQ in antithrombotic therapy may lie in the interference in the coagulation cascade. HCQ, indeed, was revealed to decrease the levels of soluble tissue factor, a key initiator of the process, in patients with antiphospholipid syndrome after three months of therapy with a daily dose of HCQ of 200 mg [99]."}

LitCovid-sentences

{"project":"LitCovid-sentences","denotations":[{"id":"T352","span":{"begin":0,"end":6},"obj":"Sentence"},{"id":"T353","span":{"begin":7,"end":32},"obj":"Sentence"},{"id":"T354","span":{"begin":33,"end":145},"obj":"Sentence"},{"id":"T355","span":{"begin":146,"end":228},"obj":"Sentence"},{"id":"T356","span":{"begin":229,"end":438},"obj":"Sentence"},{"id":"T357","span":{"begin":439,"end":571},"obj":"Sentence"},{"id":"T358","span":{"begin":572,"end":732},"obj":"Sentence"},{"id":"T359","span":{"begin":733,"end":954},"obj":"Sentence"},{"id":"T360","span":{"begin":955,"end":1101},"obj":"Sentence"},{"id":"T361","span":{"begin":1102,"end":1296},"obj":"Sentence"},{"id":"T362","span":{"begin":1297,"end":1395},"obj":"Sentence"},{"id":"T363","span":{"begin":1396,"end":1777},"obj":"Sentence"},{"id":"T364","span":{"begin":1778,"end":1889},"obj":"Sentence"},{"id":"T365","span":{"begin":1890,"end":2110},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"2.3.3. Antiphospholipid Syndrome\nAntiphospholipid syndrome is an autoimmune disorder characterized by antiphospholipid autoantibodies production. If it is not associated with other autoimmune diseases, it is called primary [97]. The incidence of the pathology is greater in young women of reproductive age and it often has a negative impact on pregnancy, with unfortunate outcomes due to the development of placental ischemic pathologies. Resonance spectroscopy, indeed, revealed that the fetal brain and placenta are the main targets of autoantibodies localization [95]. As complement activation plays a central role in the occurrence of the disease, many studies have evaluated the role of HCQ in inhibiting complement activation. In a mouse model of obstetric antiphospholipid syndrome, HCQ, administered in a daily dose of 200 μg per mouse limited placental abnormalities, with an increase of fetal survival, by inhibiting complement activation [95]. A case report on the use of HCQ on a pregnant woman with recurrent venous thromboembolism confirmed the efficacy of HCQ also in clinical practice. The addition of 400 mg daily of HCQ to a common therapeutic regimen of aspirin and heparin dramatically reduced the episodes of vascular thrombosis [96], showing great antithrombotic properties. Given these results, the mechanisms underlying the use of HCQ in thromboprophylaxis were assessed. Two similar preclinical studies, using one-week treatment with 12 μg/g/day of HCQ and three-weeks treatment with 20 mg/kg/day of HCQ, respectively, were in accordance to assess that the overall amelioration of thrombotic status in mice models of antiphospholipid syndrome was linked to endothelial function improvement by modulating the expression of nitric oxide synthase [97,98]. Moreover, the efficacy of HCQ in antithrombotic therapy may lie in the interference in the coagulation cascade. HCQ, indeed, was revealed to decrease the levels of soluble tissue factor, a key initiator of the process, in patients with antiphospholipid syndrome after three months of therapy with a daily dose of HCQ of 200 mg [99]."}

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PMC:7696151 / 55001-57111 JSON TXT