Endothelial Dysfunction as a Component of Severe Acute Respiratory Syndrome Coronavirus 2-Related Multisystem Inflammatory Syndrome in Children With Shock.


Journal

Critical care medicine
ISSN: 1530-0293
Titre abrégé: Crit Care Med
Pays: United States
ID NLM: 0355501

Informations de publication

Date de publication:
01 11 2021
Historique:
pubmed: 29 5 2021
medline: 27 10 2021
entrez: 28 5 2021
Statut: ppublish

Résumé

NCT04420468. Severe acute respiratory syndrome coronavirus 2-related multisystem inflammatory syndrome in children is frequently associated with shock; endothelial involvement may be one of the underlying mechanisms. We sought to describe endothelial dysfunction during multisystem inflammatory syndrome in children with shock and then assess the relationship between the degree of endothelial involvement and the severity of shock. Observational study. A PICU in a tertiary hospital. Patients aged under 18 (n = 28) with severe acute respiratory syndrome coronavirus 2-related multisystem inflammatory syndrome in children and shock, according to the Centers for Disease Control and Prevention criteria. None. Correlations between endothelial marker levels and shock severity were assessed using Spearman coefficient. The median (interquartile range) age was 9 years (7.5-11.2 yr). Sixteen children presented with cardiogenic and distributive shock, 10 presented with cardiogenic shock only, and two presented with distributive shock only. The median left ventricular ejection fraction, troponin level, and lactate level were, respectively, 40% (35-45%), 261 ng/mL (131-390 ng/mL), and 3.2 mmol/L (2-4.2 mmol/L). Twenty-five children received inotropes and/or vasopressors; the median Vasoactive and Inotropic Score was 8 (5-28). Plasma levels of angiopoietin-2 (6,426 pg/mL [2,814-11,836 pg/mL]), sE-selectin (130,405 pg/mL [92,987-192,499 pg/mL]), von Willebrand factor antigen (344% [288-378%]), and the angiopoietin-2/angiopoietin-1 ratio (1.111 [0.472-1.524]) were elevated and significantly correlated with the Vasoactive and Inotropic Score (r = 0.45, p = 0.016; r = 0.53, p = 0.04; r = 0.46, p = 0.013; and r = 0.46, p = 0.012, respectively). Endothelial dysfunction is associated with severe acute respiratory syndrome coronavirus 2-related multisystem inflammatory syndrome in children with shock and may constitute one of the underlying mechanisms.

Identifiants

pubmed: 34049308
doi: 10.1097/CCM.0000000000005093
pii: 00003246-202111000-00023
pmc: PMC8507588
doi:

Substances chimiques

Adrenal Cortex Hormones 0
Angiopoietin-2 0
Biomarkers 0
Cardiotonic Agents 0
Immunoglobulins 0
Interleukin-6 0
Troponin 0
Vasoconstrictor Agents 0
Lactic Acid 33X04XA5AT
C-Reactive Protein 9007-41-4

Banques de données

ClinicalTrials.gov
['NCT04420468']

Types de publication

Journal Article Observational Study

Langues

eng

Sous-ensembles de citation

IM

Pagination

e1151-e1156

Informations de copyright

Copyright © 2021 by the Society of Critical Care Medicine and Wolters Kluwer Health, Inc. All Rights Reserved.

Déclaration de conflit d'intérêts

Dr. Borgel’s institution received funding from Leo PHARMA and ROCHE Financial. The remaining authors have disclosed that they do not have any potential conflicts of interest.

Références

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Auteurs

Delphine Borgel (D)

Department of Biological Hematology, Necker Hospital, AP-HP Centre-Université de Paris, Paris, France.
HITh, UMR_S 1176, INSERM, Univ. Paris-Saclay, Le Kremlin-Bicêtre, France.

Richard Chocron (R)

Emergency Department, Georges Pompidou European Hospital, AP-HP Centre Université de Paris, Paris, France.
Université de Paris, PARCC, INSERM, Paris, France.

Marion Grimaud (M)

Pediatric Intensive Care Unit, Necker Hospital, AP-HP Centre Université de Paris, Paris, France.

Aurélien Philippe (A)

Hematology Department and Biosurgical Research Lab (Carpentier Foundation), Georges Pompidou European Hospital, AP-HP Centre Université de Paris, Paris, France.
Université de Paris, Innovative Therapies in Hemostasis, INSERM, Paris, France.

Judith Chareyre (J)

Pediatric Intensive Care Unit, Necker Hospital, AP-HP Centre Université de Paris, Paris, France.
Université de Paris, EA7323, Paris, France.

Charlyne Brakta (C)

Department of Biological Hematology, Necker Hospital, AP-HP Centre-Université de Paris, Paris, France.

Dominique Lasne (D)

Department of Biological Hematology, Necker Hospital, AP-HP Centre-Université de Paris, Paris, France.
HITh, UMR_S 1176, INSERM, Univ. Paris-Saclay, Le Kremlin-Bicêtre, France.

Damien Bonnet (D)

M3C-Necker, Congenital and Pediatric Cardiology, Necker Hospital, AP-HP Centre-Université de Paris, Paris, France.

Julie Toubiana (J)

Department of General Pediatrics and Pediatric Infectious Diseases, Necker Hospital, AP-HP Centre-Université de Paris, Paris, France.

François Angoulvant (F)

Pediatric Emergency Department, Necker Hospital, AP-HP Centre Université de Paris, Paris, France.
INSERM, Centre de Recherche des Cordeliers, UMRS 1138, Sorbonne Université, Université de Paris, Paris, France.

Maximilien Desvages (M)

Department of Biological Hematology, Necker Hospital, AP-HP Centre-Université de Paris, Paris, France.
HITh, UMR_S 1176, INSERM, Univ. Paris-Saclay, Le Kremlin-Bicêtre, France.

Sylvain Renolleau (S)

Pediatric Intensive Care Unit, Necker Hospital, AP-HP Centre Université de Paris, Paris, France.
Université de Paris, EA7323, Paris, France.

David M Smadja (DM)

Hematology Department and Biosurgical Research Lab (Carpentier Foundation), Georges Pompidou European Hospital, AP-HP Centre Université de Paris, Paris, France.
Université de Paris, Innovative Therapies in Hemostasis, INSERM, Paris, France.

Mehdi Oualha (M)

Pediatric Intensive Care Unit, Necker Hospital, AP-HP Centre Université de Paris, Paris, France.
Université de Paris, EA7323, Paris, France.

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