Evidence map›Paper›PMID 33640328›Full record

ArticleEBioMedicine2021

Increased apolipoprotein-B:A1 ratio predicts cardiometabolic risk in patients with juvenile onset SLE.

George A Robinson, Kirsty E Waddington, Leda Coelewij, Junjie Peng, Meena Naja, Chris Wincup, Anna Radziszewska, Hannah Peckham, David A Isenberg, Yiannis Ioannou and 3 more

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

Article in EBioMedicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
5.1field-weighted citation impact, top 4% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

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  19. CD8International journal of molecular sciences · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 2 institutions in 1 country.

George A RobinsonCentre for Rheumatology Research, Department of Medicine, University College London, Rayne Building, London W1CE 6JF, UK; Centre for Adolescent Rheumatology Versus Arthritis, Department of Medicine, University College London, Rayne Building, London W1CE 6JF, UK. Electronic address: george.robinson.15@ucl.ac.uk.
Kirsty E WaddingtonCentre for Rheumatology Research, Department of Medicine, University College London, Rayne Building, London W1CE 6JF, UK; Centre for Cardiometabolic and Vascular Science, Department of Medicine, University College London, London W1CE 6JF, UK.
Leda CoelewijCentre for Rheumatology Research, Department of Medicine, University College London, Rayne Building, London W1CE 6JF, UK; Centre for Cardiometabolic and Vascular Science, Department of Medicine, University College London, London W1CE 6JF, UK.
Junjie PengCentre for Rheumatology Research, Department of Medicine, University College London, Rayne Building, London W1CE 6JF, UK; Centre for Adolescent Rheumatology Versus Arthritis, Department of Medicine, University College London, Rayne Building, London W1CE 6JF, UK.
Meena NajaCentre for Adolescent Rheumatology Versus Arthritis, Department of Medicine, University College London, Rayne Building, London W1CE 6JF, UK.
Chris WincupCentre for Rheumatology Research, Department of Medicine, University College London, Rayne Building, London W1CE 6JF, UK.
Anna RadziszewskaCentre for Adolescent Rheumatology Versus Arthritis, Department of Medicine, University College London, Rayne Building, London W1CE 6JF, UK.
Hannah PeckhamCentre for Adolescent Rheumatology Versus Arthritis, Department of Medicine, University College London, Rayne Building, London W1CE 6JF, UK.
David A IsenbergCentre for Rheumatology Research, Department of Medicine, University College London, Rayne Building, London W1CE 6JF, UK; Centre for Adolescent Rheumatology Versus Arthritis, Department of Medicine, University College London, Rayne Building, London W1CE 6JF, UK.
Yiannis IoannouCentre for Adolescent Rheumatology Versus Arthritis, Department of Medicine, University College London, Rayne Building, London W1CE 6JF, UK.
Coziana CiurtinCentre for Rheumatology Research, Department of Medicine, University College London, Rayne Building, London W1CE 6JF, UK; Centre for Adolescent Rheumatology Versus Arthritis, Department of Medicine, University College London, Rayne Building, London W1CE 6JF, UK. Electronic address: c.ciurtin@ucl.ac.uk.
Ines Pineda-TorraCentre for Cardiometabolic and Vascular Science, Department of Medicine, University College London, London W1CE 6JF, UK. Electronic address: i.torra@ucl.ac.uk.
Elizabeth C JuryCentre for Rheumatology Research, Department of Medicine, University College London, Rayne Building, London W1CE 6JF, UK. Electronic address: e.jury@ucl.ac.uk.
Arthritis UK · GBUniversity College London · GB

Funding

Versus Arthritis 21992
6 · The paper itself

Abstract

backgroundCardiovascular disease is a leading cause of mortality in patients with juvenile-onset systemic lupus erythematosus (JSLE). Traditional factors for cardiovascular risk (CVR) prediction are less robust in younger patients. More reliable CVR biomarkers are needed for JSLE patient stratification and to identify therapeutic approaches to reduce cardiovascular morbidity and mortality in JSLE.

methodsSerum metabolomic analysis (including >200 lipoprotein measures) was performed on a discovery (n=31, median age 19) and validation (n=31, median age 19) cohort of JSLE patients. Data was analysed using cluster, receiver operating characteristic analysis and logistic regression. RNA-sequencing assessed gene expression in matched patient samples.

findingsHierarchical clustering of lipoprotein measures identified and validated two unique JSLE groups. Group-1 had an atherogenic and Group-2 had an atheroprotective lipoprotien profile. Apolipoprotein(Apo)B:ApoA1 distinguished the two groups with high specificity (96.2%) and sensitivity (96.7%). JSLE patients with high ApoB:ApoA1 ratio had increased CD8+ T-cell frequencies and a CD8+ T-cell transcriptomic profile enriched in genes associated with atherogenic processes including interferon signaling. These metabolic and immune signatures overlapped statistically significantly with lipid biomarkers associated with sub-clinical atherosclerosis in adult SLE patients and with genes overexpressed in T-cells from human atherosclerotic plaque respectively. Finally, baseline ApoB:ApoA1 ratio correlated positively with SLE disease activity index (r=0.43, p=0.0009) and negatively with Lupus Low Disease Activity State (r=-0.43, p=0.0009) over 5-year follow-up.

interpretationMulti-omic analysis identified high ApoB:ApoA1 as a potential biomarker of increased cardiometabolic risk and worse clinical outcomes in JSLE. ApoB:ApoA1 could help identify patients that require increased disease monitoring, lipid modification or lifestyle changes.

fundingLupus UK, The Rosetrees Trust, British Heart Foundation, UCL & Birkbeck MRC Doctoral Training Programme and Versus Arthritis.

Indexed as

AdolescentAdultAge of OnsetApolipoprotein A-IApolipoproteins BAtherosclerosisBiomarkersCD8-Positive T-LymphocytesCluster AnalysisCohort StudiesFemaleHumansLipidsLogistic ModelsLupus Erythematosus, SystemicMaleApolipoprotein A-IApolipoproteins BBiomarkersLipidsCardiovascular diseaseCD8+ T cellsInterferonJuvenile-onset systemic lupus erythematosusLipids

Identifiers

PMID33640328
PMCPMC7992074
OpenAlexW3132690282

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.