Evidence map›Paper›PMID 32559419›Full record

ReviewThe Lancet. Respiratory medicine2020

Therapeutic blockade of granulocyte macrophage colony-stimulating factor in COVID-19-associated hyperinflammation: challenges and opportunities.

Puja Mehta, Joanna C Porter, Jessica J Manson, John D Isaacs, Peter J M Openshaw, Iain B McInnes, Charlotte Summers, Rachel C Chambers

Open access · bronzeAbstract readReview
In one paragraph

Review in The Lancet. Respiratory medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed, 3 pooled it
3.0field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

88 citing papers in PubMed, 3 syntheses or guidelines pooled it, 135 citations in OpenAlex.

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28 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 6 institutions in 1 country.

Puja MehtaCentre for Inflammation and Tissue Repair, Division of Medicine, University College London, London, UK; Department of Rheumatology, University College London Hospital, London, UK.
Joanna C PorterCentre for Inflammation and Tissue Repair, Division of Medicine, University College London, London, UK.
Jessica J MansonDepartment of Rheumatology, University College London Hospital, London, UK.
John D IsaacsInstitute of Cellular Medicine, Newcastle University, Newcastle, UK.
Peter J M OpenshawNational Heart and Lung Institute, Faculty of Medicine, Imperial College London, London, UK.
Iain B McInnesInstitute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, UK.
Charlotte SummersDepartment of Medicine, University of Cambridge, Cambridge, UK.
Rachel C ChambersCentre for Inflammation and Tissue Repair, Division of Medicine, University College London, London, UK. Electronic address: r.chambers@ucl.ac.uk.
Centre for Inflammation Research · GBUniversity College Hospital · GBImperial College London · GBNewcastle University · GBUniversity of Cambridge · GBUniversity of Glasgow · GB

Funding

Medical Research Council G1001518Medical Research Council MR/P502078/1Medical Research Council MR/P502091/1Medical Research Council MR/R502121/1Medical Research Council MR/T50256X/1
6 · The paper itself

Abstract

The COVID-19 pandemic is a global public health crisis, with considerable mortality and morbidity exerting pressure on health-care resources, including critical care. An excessive host inflammatory response in a subgroup of patients with severe COVID-19 might contribute to the development of acute respiratory distress syndrome (ARDS) and multiorgan failure. Timely therapeutic intervention with immunomodulation in patients with hyperinflammation could prevent disease progression to ARDS and obviate the need for invasive ventilation. Granulocyte macrophage colony-stimulating factor (GM-CSF) is an immunoregulatory cytokine with a pivotal role in initiation and perpetuation of inflammatory diseases. GM-CSF could link T-cell-driven acute pulmonary inflammation with an autocrine, self-amplifying cytokine loop leading to monocyte and macrophage activation. This axis has been targeted in cytokine storm syndromes and chronic inflammatory disorders. Here, we consider the scientific rationale for therapeutic targeting of GM-CSF in COVID-19-associated hyperinflammation. Since GM-CSF also has a key role in homoeostasis and host defence, we discuss potential risks associated with inhibition of GM-CSF in the context of viral infection and the challenges of doing clinical trials in this setting, highlighting in particular the need for a patient risk-stratification algorithm.

Indexed as

BetacoronavirusCoronavirus InfectionsCOVID-19COVID-19 Drug TreatmentDisease ProgressionGranulocyte-Macrophage Colony-Stimulating FactorHumansImmunologic FactorsImmunomodulationPandemicsPneumonia, ViralRespiratory Distress SyndromeSARS-CoV-2Granulocyte-Macrophage Colony-Stimulating FactorImmunologic Factors

Identifiers

PMID32559419
PMCPMC7834476
OpenAlexW3034437525

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.