About: Endotheliopathy in COVID-19-associated coagulopathy: evidence from a single-centre, cross-sectional study

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An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Endotheliopathy in COVID-19-associated coagulopathy: evidence from a single-centre, cross-sectional study
Creator	Phd, Zhang Cruz, Dela Bahel, Parveen Bona, Robert Chun, Hyung Goshua, George Halene, Stephanie Hwa, John Lee, Alfred Pine, Alexander Price, Christina Siner, Jonathan Tormey, Christopher Rinder, Henry Baluha, Audrey Bar, Noffar Burns, Adrienne Chang, C-H Chang, C-Hong Chun, H Dumont, Anne Hwa, J Koff, Jonathan Meizlish, Matthew Menninger, Hope Neparidze, Natalia Zhang, Hanming
Source	Elsevier; Medline; PMC
abstract	BACKGROUND: An important feature of severe acute respiratory syndrome coronavirus 2 pathogenesis is COVID-19-associated coagulopathy, characterised by increased thrombotic and microvascular complications. Previous studies have suggested a role for endothelial cell injury in COVID-19-associated coagulopathy. To determine whether endotheliopathy is involved in COVID-19-associated coagulopathy pathogenesis, we assessed markers of endothelial cell and platelet activation in critically and non-critically ill patients admitted to the hospital with COVID-19. METHODS: In this single-centre cross-sectional study, hospitalised adult (≥18 years) patients with laboratory-confirmed COVID-19 were identified in the medical intensive care unit (ICU) or a specialised non-ICU COVID-19 floor in our hospital. Asymptomatic, non-hospitalised controls were recruited as a comparator group for biomarkers that did not have a reference range. We assessed markers of endothelial cell and platelet activation, including von Willebrand Factor (VWF) antigen, soluble thrombomodulin, soluble P-selectin, and soluble CD40 ligand, as well as coagulation factors, endogenous anticoagulants, and fibrinolytic enzymes. We compared the level of each marker in ICU patients, non-ICU patients, and controls, where applicable. We assessed correlations between these laboratory results with clinical outcomes, including hospital discharge and mortality. Kaplan–Meier analysis was used to further explore the association between biochemical markers and survival. FINDINGS: 68 patients with COVID-19 were included in the study from April 13 to April 24, 2020, including 48 ICU and 20 non-ICU patients, as well as 13 non-hospitalised, asymptomatic controls. Markers of endothelial cell and platelet activation were significantly elevated in ICU patients compared with non-ICU patients, including VWF antigen (mean 565% [SD 199] in ICU patients vs 278% [133] in non-ICU patients; p<0·0001) and soluble P-selectin (15·9 ng/mL [4·8] vs 11·2 ng/mL [3·1]; p=0·0014). VWF antigen concentrations were also elevated above the normal range in 16 (80%) of 20 non-ICU patients. We found mortality to be significantly correlated with VWF antigen (r = 0·38; p=0·0022) and soluble thrombomodulin (r = 0·38; p=0·0078) among all patients. In all patients, soluble thrombomodulin concentrations greater than 3·26 ng/mL were associated with lower rates of hospital discharge (22 [88%] of 25 patients with low concentrations vs 13 [52%] of 25 patients with high concentrations; p=0·0050) and lower likelihood of survival on Kaplan–Meier analysis (hazard ratio 5·9, 95% CI 1·9–18·4; p=0·0087). INTERPRETATION: Our findings show that endotheliopathy is present in COVID-19 and is likely to be associated with critical illness and death. Early identification of endotheliopathy and strategies to mitigate its progression might improve outcomes in COVID-19. FUNDING: This work was supported by a gift donation from Jack Levin to the Benign Hematology programme at Yale, and the National Institutes of Health.
has issue date	2020-06-30(xsd:dateTime)
bibo:doi	10.1016/s2352-3026(20)30216-7
bibo:pmid	32619411
has license	no-cc
sha1sum (hex)	0171d6e4bc9f17ab939f6660c0a5d1a2b9ec58be
schema:url	https://doi.org/10.1016/s2352-3026%2820%2930216-7
resource representing a document's title	Endotheliopathy in COVID-19-associated coagulopathy: evidence from a single-centre, cross-sectional study
has PubMed Central identifier	PMC7326446
has PubMed identifier	32619411
schema:publication	Lancet Haematol
resource representing a document's body	covid:0171d6e4bc9f17ab939f6660c0a5d1a2b9ec58be#body_text
is schema:about of	named entity 'assessed' named entity 'patients' named entity 'cross-sectional study' named entity 'HOSPITAL' named entity 'COVID-19-ASSOCIATED COAGULOPATHY' named entity 'CELL INJURY' named entity 'PLATELET ACTIVATION' covid:arg/0171d6e4bc9f17ab939f6660c0a5d1a2b9ec58be named entity 'COVID-19' named entity 'endothelial cell' named entity 'coagulopathy' named entity 'coagulopathy' named entity 'thrombotic' named entity 'pathogenesis' named entity 'COVID' named entity 'COVID-19' named entity 'comorbidities' named entity 'endothelial cells' named entity 'VWF' named entity 'ICU' named entity 'coagulopathy' named entity 'P-selectin' named entity 'platelet activation' named entity 'thrombomodulin' named entity 'VWF' named entity 'thrombomodulin' named entity 'ICU' named entity 'coagulopathy' named entity 'thrombomodulin' named entity 'thrombomodulin' named entity 'IL-6' named entity 'plasma' named entity 'COVID' named entity 'COVID' named entity 'ICU' named entity 'platelet' named entity 'plasminogen activator' named entity 'antigen' named entity 'endothelial cells' named entity 'COVID' named entity 'urokinase-type plasminogen activator' named entity 'critically ill' named entity 'IL-6' named entity 'VWF' named entity 'circadian' named entity 'normal distribution' named entity 'multiorgan dysfunction' named entity 'thromboprophylaxis' named entity 'hospital discharge' named entity 'sodium citrate' named entity 'PAI-1' named entity 'coronavirus' named entity 'VWF' named entity 'thrombomodulin' named entity 'centrifuged'

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