Evidence map›Paper›PMID 32336276›Full record

ArticleMalaria journal2020

Depleted circulatory complement-lysis inhibitor (CLI) in childhood cerebral malaria returns to normal with convalescence.

Samuel Eneọjọ Abah, Florence Burté, Steven A Howell, Ikeoluwa Lagunju, Wuraola A Shokunbi, Mats Wahlgren, Olugbemiro Sodeinde, Biobele J Brown, Anthony A Holder, Delmiro Fernandez-Reyes

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Malaria journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.1field-weighted citation impact, top 57% 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

0 citing papers in PubMed, 2 citations in OpenAlex.

No citing paper in PubMed yet.

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

10 authors at 3 institutions in 3 countries.

Samuel Eneọjọ AbahFrancis Crick Institute, 1 Midland Road, London, NW1 1AT, UK.
Florence BurtéFrancis Crick Institute, 1 Midland Road, London, NW1 1AT, UK.
Steven A HowellFrancis Crick Institute, 1 Midland Road, London, NW1 1AT, UK.
Ikeoluwa LagunjuDepartment of Paediatrics, College of Medicine, University of Ibadan, University College Hospital, Ibadan, Nigeria.
Wuraola A ShokunbiChildhood Malaria Research Group, College of Medicine, University of Ibadan, University College Hospital, Ibadan, Nigeria.
Mats WahlgrenDepartment of Microbiology, Tumour and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
Olugbemiro SodeindeDepartment of Paediatrics, College of Medicine, University of Ibadan, University College Hospital, Ibadan, Nigeria.
Biobele J BrownDepartment of Paediatrics, College of Medicine, University of Ibadan, University College Hospital, Ibadan, Nigeria.
Anthony A HolderFrancis Crick Institute, 1 Midland Road, London, NW1 1AT, UK.
Delmiro Fernandez-ReyesDepartment of Paediatrics, College of Medicine, University of Ibadan, University College Hospital, Ibadan, Nigeria. Delmiro.Fernandez-Reyes@ucl.ac.uk.ORCID http://orcid.org/0000-0001-5070-9198
University of Ibadan · NGThe Francis Crick Institute · GBKarolinska Institutet · SE

Funding

Medical Research Council U117532067Medical Research Council U117585869Wellcome Trust FC001097
6 · The paper itself

Abstract

backgroundCerebral malaria (CM), is a life-threatening childhood malaria syndrome with high mortality. CM is associated with impaired consciousness and neurological damage. It is not fully understood, as yet, why some children develop CM. Presented here is an observation from longitudinal studies on CM in a paediatric cohort of children from a large, densely-populated and malaria holoendemic, sub-Saharan, West African metropolis.

methodsPlasma samples were collected from a cohort of children with CM, severe malarial anaemia (SMA), uncomplicated malaria (UM), non-malaria positive healthy community controls (CC), and coma and anemic patients without malaria, as disease controls (DC). Proteomic two-dimensional difference gel electrophoresis (2D-DIGE) and mass spectrometry were used in a discovery cohort to identify plasma proteins that might be discriminatory among these clinical groups. The circulatory levels of identified proteins of interest were quantified by ELISA in a prospective validation cohort.

resultsThe proteome analysis revealed differential abundance of circulatory complement-lysis inhibitor (CLI), also known as Clusterin (CLU). CLI circulatory level was low at hospital admission in all children presenting with CM and recovered to normal level during convalescence (p < 0.0001). At acute onset, circulatory level of CLI in the CM group significantly discriminates CM from the UM, SMA, DC and CC groups.

conclusionsThe CLI circulatory level is low in all patients in the CM group at admission, but recovers through convalescence. The level of CLI at acute onset may be a specific discriminatory marker of CM. This work suggests that CLI may play a role in the pathophysiology of CM and may be useful in the diagnosis and follow-up of children presenting with CM.

Indexed as

ConvalescenceAdolescentChildChild, PreschoolClusterinFemaleHumansInfantMalaria, CerebralMalaria, FalciparumMaleProspective StudiesCLU protein, humanClusterinBiomarkersCerebral malariaChildhood severe malariaPathogenesis

Identifiers

PMID32336276
PMCPMC7184698
OpenAlexW3020612678

What OpenQuestion holds

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Registered trials

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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.