About: Prothrombotic antiphospholipid antibodies in COVID-19

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Prothrombotic antiphospholipid antibodies in COVID-19
Creator	Shi, Hui Gockman, Kelsey Kanthi, Yogendra Knight Are Co-Corresponding, Jason Knight, Jason Madison, Jacqueline Yalavarthi, Srilakshmi Zuo, Melanie Zuo, Yu Yogendra, ‡ Ali, Ramadan Estes, Shanea Gandhi, Alex Lezak, Sean Lugogo, Njira Sule, Gautam Woodward, Wrenn
Source	MedRxiv; Medline
abstract	Patients with coronavirus disease 19 (COVID-19) are at high risk for thrombotic arterial and venous occlusions. At the same time, lung histopathology often reveals fibrin-based occlusion of small vessels in patients who succumb to the disease. Antiphospholipid syndrome (APS) is an acquired and potentially life-threatening thrombophilia in which patients develop pathogenic autoantibodies (aPL) targeting phospholipids and phospholipid-binding proteins. Small case series have recently detected aPL in patients with COVID-19. Here, we measured eight types of aPL (anticardiolipin IgG/IgM/IgA, anti-beta-2 glycoprotein I IgG/IgM/IgA, and anti- phosphatidylserine/prothrombin (PS/PT) IgG/IgM) in the sera of 172 patients hospitalized with COVID-19. We detected anticardiolipin IgM antibodies in 23%, anti-PS/PT IgG in 24%, and anti-PS/PT IgM in 18%. Any aPL was present in 52% of patients using the manufacturer's threshold and in 30% using a more stringent cutoff (>40 units). Higher levels of aPL were associated with neutrophil hyperactivity (including the release of neutrophil extracellular traps/NETs), higher platelet count, more severe respiratory disease, and lower glomerular filtration rates. Similar to patients with known and longstanding APS, IgG fractions isolated from patients with COVID-19 promoted NET release from control neutrophils. Furthermore, injection of these COVID-19 IgG fractions into mice accelerated venous thrombosis. Taken together, these studies suggest that a significant percentage of patients with COVID-19 become at least transiently positive for aPL and that these aPL are potentially pathogenic.
has issue date	2020-06-17(xsd:dateTime)
bibo:doi	10.1101/2020.06.15.20131607
bibo:pmid	32587992
has license	medrxiv
sha1sum (hex)	f55fd8d630f9f86ef463589b4c1b29cf4f6ace8c
schema:url	https://doi.org/10.1101/2020.06.15.20131607
resource representing a document's title	Prothrombotic antiphospholipid antibodies in COVID-19
has PubMed identifier	32587992
schema:publication	medRxiv : the preprint server for health sciences
resource representing a document's body	covid:f55fd8d630f9f86ef463589b4c1b29cf4f6ace8c#body_text
is schema:about of	named entity 'antiphospholipid antibodies' named entity 'platelet count' named entity 'lupus anticoagulant' named entity 'RPMI' named entity 'prothrombotic' named entity 'IgG' named entity 'primary antibody' named entity 'EDTA' named entity 'coagulopathy' named entity 'medRxiv' named entity 'IVC' named entity 'MPO' named entity 'Prolene' named entity 'lungs' named entity 'Mice' named entity 'endothelial cells' named entity 'aPL' named entity 'mouse models' named entity 'antibodies' named entity 'activates the endothelium' named entity 'mice' named entity 'autoantibodies' named entity 'platelets' named entity 'SpO2' named entity 'lung' named entity 'aPL' named entity 'NETosis' named entity 'lupus anticoagulant' named entity 'IgG' named entity 'autoantibodies' named entity 'IgM' named entity 'thrombotic events' named entity 'subcutaneously' named entity 'positive correlation' named entity 'C-reactive protein' named entity 'RPMI' named entity 'thrombotic diseases' named entity 'platelets' named entity 'catastrophic antiphospholipid syndrome' named entity 'platelet counts' named entity 'ARDS' named entity 'synergistic' named entity 'viral infection' named entity 'statistical significance' named entity 'venous thrombosis' named entity 'anesthesia' named entity 'correction for multiple comparisons' named entity 'coagulopathy' named entity 'calprotectin' named entity 'dextran' named entity 'sodium chloride' named entity 'neutrophil elastase' named entity 'pathogenesis' named entity 'myeloperoxidase' named entity 'endothelial cells' named entity 'thrombomodulin' named entity 'degradation products' named entity 'aPL' named entity 'NETs' named entity 'neutrophils' named entity 'incubation' named entity 'eGFR' named entity 'estimated glomerular filtration rate' named entity 'prothrombin' named entity 'Mann-Whitney' named entity 'thrombosis'

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