Prevalence of phenotypes of acute respiratory distress syndrome in critically ill patients with COVID-19: a prospective observational study.

APACHE COVID-19 / blood Case-Control Studies Cytokine Release Syndrome / blood Female Humans Male Middle Aged Phenotype Prospective Studies Receptors, Tumor Necrosis Factor, Type I Respiratory Distress Syndrome / classification

Journal

The Lancet. Respiratory medicine
ISSN: 2213-2619
Titre abrégé: Lancet Respir Med
Pays: England
ID NLM: 101605555

Informations de publication

Date de publication:
12 2020
Historique:
received: 02 06 2020
revised: 04 07 2020
accepted: 27 07 2020
pubmed: 31 8 2020
medline: 22 12 2020
entrez: 31 8 2020
Statut: ppublish

Résumé

In acute respiratory distress syndrome (ARDS) unrelated to COVID-19, two phenotypes, based on the severity of systemic inflammation (hyperinflammatory and hypoinflammatory), have been described. The hyperinflammatory phenotype is known to be associated with increased multiorgan failure and mortality. In this study, we aimed to identify these phenotypes in COVID-19-related ARDS. In this prospective observational study done at two UK intensive care units, we recruited patients with ARDS due to COVID-19. Demographic, clinical, and laboratory data were collected at baseline. Plasma samples were analysed for interleukin-6 (IL-6) and soluble tumour necrosis factor receptor superfamily member 1A (TNFR1) using a novel point-of-care assay. A parsimonious regression classifier model was used to calculate the probability for the hyperinflammatory phenotype in COVID-19 using IL-6, soluble TNFR1, and bicarbonate levels. Data from this cohort was compared with patients with ARDS due to causes other than COVID-19 recruited to a previous UK multicentre, randomised controlled trial of simvastatin (HARP-2). Between March 17 and April 25, 2020, 39 patients were recruited to the study. Median ratio of partial pressure of arterial oxygen to fractional concentration of oxygen in inspired air (PaO In this exploratory analysis of 39 patients, ARDS due to COVID-19 was not associated with higher systemic inflammation and was associated with a lower prevalence of the hyperinflammatory phenotype than that observed in historical ARDS data. This finding suggests that the excess mortality observed in COVID-19-related ARDS is unlikely to be due to the upregulation of inflammatory pathways described by the parsimonious model. US National Institutes of Health, Innovate UK, and Randox.

Sections du résumé

BACKGROUND
In acute respiratory distress syndrome (ARDS) unrelated to COVID-19, two phenotypes, based on the severity of systemic inflammation (hyperinflammatory and hypoinflammatory), have been described. The hyperinflammatory phenotype is known to be associated with increased multiorgan failure and mortality. In this study, we aimed to identify these phenotypes in COVID-19-related ARDS.
METHODS
In this prospective observational study done at two UK intensive care units, we recruited patients with ARDS due to COVID-19. Demographic, clinical, and laboratory data were collected at baseline. Plasma samples were analysed for interleukin-6 (IL-6) and soluble tumour necrosis factor receptor superfamily member 1A (TNFR1) using a novel point-of-care assay. A parsimonious regression classifier model was used to calculate the probability for the hyperinflammatory phenotype in COVID-19 using IL-6, soluble TNFR1, and bicarbonate levels. Data from this cohort was compared with patients with ARDS due to causes other than COVID-19 recruited to a previous UK multicentre, randomised controlled trial of simvastatin (HARP-2).
FINDINGS
Between March 17 and April 25, 2020, 39 patients were recruited to the study. Median ratio of partial pressure of arterial oxygen to fractional concentration of oxygen in inspired air (PaO
INTERPRETATION
In this exploratory analysis of 39 patients, ARDS due to COVID-19 was not associated with higher systemic inflammation and was associated with a lower prevalence of the hyperinflammatory phenotype than that observed in historical ARDS data. This finding suggests that the excess mortality observed in COVID-19-related ARDS is unlikely to be due to the upregulation of inflammatory pathways described by the parsimonious model.
FUNDING
US National Institutes of Health, Innovate UK, and Randox.

Identifiants

DOI: 10.1016/S2213-2600(20)30366-0 PMID: 32861275 PMC: PMC7718296
pubmed: 32861275
pii: S2213-2600(20)30366-0
doi: 10.1016/S2213-2600(20)30366-0
pmc: PMC7718296
mid: NIHMS1626794
pii:
doi:

Substances chimiques

Receptors, Tumor Necrosis Factor, Type I 0

Types de publication

Journal Article Multicenter Study Observational Study Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1209-1218

Subventions

Organisme : Wellcome Trust
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_G1002460
Pays : United Kingdom
Organisme : NHLBI NIH HHS
ID : R35 HL140026
Pays : United States
Organisme : NIGMS NIH HHS
ID : T32 GM008440
Pays : United States

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2020 Elsevier Ltd. All rights reserved.

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Auteurs

Pratik Sinha (P)

Division of Pulmonary, Critical Care, Allergy, and Sleep Medicine, Department of Medicine, University of California San Francisco, San Francisco, CA, USA; Department of Anesthesia, University of California San Francisco, San Francisco, CA, USA. Electronic address: pratik.sinha@ucsf.edu.

Carolyn S Calfee (CS)

Division of Pulmonary, Critical Care, Allergy, and Sleep Medicine, Department of Medicine, University of California San Francisco, San Francisco, CA, USA; Department of Anesthesia, University of California San Francisco, San Francisco, CA, USA.

Shiney Cherian (S)

Critical Care Directorate, Royal Gwent Hospital, Newport, UK.

David Brealey (D)

Division of Critical Care, National Institute for Health Research University College London Hospitals Biomedical Research Centre, London, UK.

Sean Cutler (S)

Critical Care Directorate, Royal Gwent Hospital, Newport, UK.

Charles King (C)

Critical Care Directorate, Royal Gwent Hospital, Newport, UK; Department of Anaesthesia, Intensive Care and Pain Medicine, Division of Population Medicine, Cardiff University, Cardiff, UK.

Charlotte Killick (C)

Critical Care Directorate, Royal Gwent Hospital, Newport, UK; Department of Anaesthesia, Intensive Care and Pain Medicine, Division of Population Medicine, Cardiff University, Cardiff, UK.

Owen Richards (O)

Critical Care Directorate, Royal Gwent Hospital, Newport, UK; Department of Anaesthesia, Intensive Care and Pain Medicine, Division of Population Medicine, Cardiff University, Cardiff, UK.

Yusuf Cheema (Y)

Critical Care Directorate, Royal Gwent Hospital, Newport, UK; Department of Anaesthesia, Intensive Care and Pain Medicine, Division of Population Medicine, Cardiff University, Cardiff, UK.

Catherine Bailey (C)

Critical Care Directorate, Royal Gwent Hospital, Newport, UK.

Kiran Reddy (K)

Department of Anaesthesiology and Critical Care, Beaumont Hospital, Dublin, Ireland.

Kevin L Delucchi (KL)

Department of Psychiatry, University of California San Francisco, San Francisco, CA, USA.

Manu Shankar-Hari (M)

ICU support offices, St Thomas' Hospital, Guy's and St Thomas' NHS Foundation Trust, London, UK; School of Immunology and Microbial Sciences, Kings College London, London, UK.

Anthony C Gordon (AC)

Division of Anaesthetics, Pain Medicine and Intensive Care, Imperial College London, London, UK.

Murali Shyamsundar (M)

Wellcome-Wolfson Institute for Experimental Medicine, Queen's University Belfast, Belfast, UK; Regional Intensive Care Unit, Royal Victoria Hospital, Belfast, UK.

Cecilia M O'Kane (CM)

Wellcome-Wolfson Institute for Experimental Medicine, Queen's University Belfast, Belfast, UK.

Daniel F McAuley (DF)

Wellcome-Wolfson Institute for Experimental Medicine, Queen's University Belfast, Belfast, UK; Regional Intensive Care Unit, Royal Victoria Hospital, Belfast, UK.

Tamas Szakmany (T)

Critical Care Directorate, Royal Gwent Hospital, Newport, UK; Department of Anaesthesia, Intensive Care and Pain Medicine, Division of Population Medicine, Cardiff University, Cardiff, UK.

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questionsmedicales.fr › Environnement et santé publique › Santé publique › Méthodes épidémiologiques › Collecte de données › Enquêtes et questionnaires › Enquêtes de santé › Indicateurs d'état de santé › Acuité des besoins du patient › Indice de gravité de la maladie › Indice APACHE › Prevalence of phenotypes of acute respiratory...
questionsmedicales.fr › Maladies de l'appareil respiratoire › Infections de l'appareil respiratoire › Pneumopathie infectieuse › Pneumopathie virale › COVID-19 › Prevalence of phenotypes of acute respiratory...
questionsmedicales.fr › Environnement et santé publique › Santé publique › Méthodes épidémiologiques › Caractéristiques des études épidémiologiques › Études épidémiologiques › Études cas-témoins › Prevalence of phenotypes of acute respiratory...
questionsmedicales.fr › États, signes et symptômes pathologiques › Processus pathologiques › Choc › Syndrome de réponse inflammatoire généralisée › Syndrome de libération de cytokines › Prevalence of phenotypes of acute respiratory...
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questionsmedicales.fr › Phénomènes génétiques › Phénotype › Prevalence of phenotypes of acute respiratory...
questionsmedicales.fr › Environnement et santé publique › Santé publique › Méthodes épidémiologiques › Caractéristiques des études épidémiologiques › Études épidémiologiques › Études de cohortes › Études prospectives › Prevalence of phenotypes of acute respiratory...
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Protéines membranaires › Récepteurs de surface cellulaire › Récepteurs immunologiques › Récepteurs aux cytokines › Récepteurs aux facteurs de nécrose tumorale › Récepteur au facteur de nécrose tumorale de type I › Prevalence of phenotypes of acute respiratory...
questionsmedicales.fr › Maladies de l'appareil respiratoire › Troubles respiratoires › Syndrome de détresse respiratoire de l'adulte › Prevalence of phenotypes of acute respiratory...