Evidence map›Paper›PMID 36889041›Full record

ArticleMolecular genetics and metabolism2023

Phenotypic changes in low-density lipoprotein particles as markers of adverse clinical outcomes in COVID-19.

Helison Rafael P Carmo, Marcos Y Yoshinaga, Alejandro Rosell Castillo, Adriano Britto Chaves-Filho, Isabella Bonilha, Joaquim Barreto, Stéfanie Primon Muraro, Gabriela Fabiano de Souza, Gustavo Gastão Davanzo, Maurício W Perroud and 15 more

Open access · greenAbstract read
In one paragraph

Article in Molecular genetics and metabolism, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

7 citing papers in PubMed, 9 citations in OpenAlex.

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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

25 authors at 6 institutions in 4 countries.

Helison Rafael P CarmoCardiology Division, Unicamp Medical School, SP, Brazil.
Marcos Y YoshinagaDepartment of Biochemistry, Institute of Chemistry, University of São Paulo, SP, Brazil. Electronic address: marcosyukio@gmail.com.
Alejandro Rosell CastilloCardiology Division, Unicamp Medical School, SP, Brazil.
Adriano Britto Chaves-FilhoDepartment of Biochemistry, Institute of Chemistry, University of São Paulo, SP, Brazil.
Isabella BonilhaCardiology Division, Unicamp Medical School, SP, Brazil.
Joaquim BarretoCardiology Division, Unicamp Medical School, SP, Brazil.
Stéfanie Primon MuraroLaboratory of Emerging Viruses, Department of Genetics, Microbiology and Immunology, Institute of Biology, University of Campinas, Campinas, SP, Brazil.
Gabriela Fabiano de SouzaLaboratory of Emerging Viruses, Department of Genetics, Microbiology and Immunology, Institute of Biology, University of Campinas, Campinas, SP, Brazil.
Gustavo Gastão DavanzoLaboratory of Immunometabolism, Department of Genetics, Evolution, Microbiology and Immunology, Institute of Biology, University of Campinas, Campinas, SP, Brazil.
Maurício W PerroudPneumology Division, Unicamp, SP, Brazil.
Kishal LukhnaDivision of Cardiology, University of Cape Town, Cape Town, South Africa.
Mpiko NtsekheDivision of Cardiology, University of Cape Town, Cape Town, South Africa.
Sean DavidsonHatter Cardiovascular Institute, University College London, London, UK.
Licio A VellosoInternal Medicine Department, Unicamp Medical School, SP, Brazil.
Wilson NadruzCardiology Division, Unicamp Medical School, SP, Brazil.
Luiz Sérgio F CarvalhoCardiology Division, Unicamp Medical School, SP, Brazil.
Miguel Sáinz-JaspeadoMercodia AB, Uppsala, Sweden.
Alessandro S FariasLaboratory of Neuroimmunomodulation, Department of Genetics, Evolution, Microbiology and Immunology, Institute of Biology, University of Campinas, Campinas, SP, Brazil; Hub of Global Health (HGH), University of Campinas, Campinas, SP, Brazil.
José Luiz Proença-MódenaLaboratory of Emerging Viruses, Department of Genetics, Microbiology and Immunology, Institute of Biology, University of Campinas, Campinas, SP, Brazil; Hub of Global Health (HGH), University of Campinas, Campinas, SP, Brazil.
Pedro M Moraes-VieiraLaboratory of Immunometabolism, Department of Genetics, Evolution, Microbiology and Immunology, Institute of Biology, University of Campinas, Campinas, SP, Brazil; Hub of Global Health (HGH), University of Campinas, Campinas, SP, Brazil.
Sotirios K KarathanasisLipoprotein Metabolism Laboratory Translational Vascular Medicine Branch National Heart, Lung and Blood Institute National Institutes of Health, Bethesda, MD, USA.
Derek YellonHatter Cardiovascular Institute, University College London, London, UK.
Sayuri MiyamotoDepartment of Biochemistry, Institute of Chemistry, University of São Paulo, SP, Brazil.
Alan T RemaleyLipoprotein Metabolism Laboratory Translational Vascular Medicine Branch National Heart, Lung and Blood Institute National Institutes of Health, Bethesda, MD, USA.
Andrei C SpositoCardiology Division, Unicamp Medical School, SP, Brazil. Electronic address: sposito@unicamp.com.
Hospital de Clínicas da Unicamp · BRUniversidade Estadual de Campinas (UNICAMP) · BRUniversidade de São Paulo · BRNational Heart Lung and Blood Institute · USUniversity College London · GBUniversity of Cape Town · ZA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimsLow-density lipoprotein (LDL) plasma concentration decline is a biomarker for acute inflammatory diseases, including coronavirus disease-2019 (COVID-19). Phenotypic changes in LDL during COVID-19 may be equally related to adverse clinical outcomes.

methodsIndividuals hospitalized due to COVID-19 (n = 40) were enrolled. Blood samples were collected on days 0, 2, 4, 6, and 30 (D0, D2, D4, D6, and D30). Oxidized LDL (ox-LDL), and lipoprotein-associated phospholipase A2 (Lp-PLA2) activity were measured. In a consecutive series of cases (n = 13), LDL was isolated by gradient ultracentrifugation from D0 and D6 and was quantified by lipidomic analysis. Association between clinical outcomes and LDL phenotypic changes was investigated.

resultsIn the first 30 days, 42.5% of participants died due to Covid-19. The serum ox-LDL increased from D0 to D6 (p < 0.005) and decreased at D30. Moreover, individuals who had an ox-LDL increase from D0 to D6 to over the 90th percentile died. The plasma Lp-PLA2 activity also increased progressively from D0 to D30 (p < 0.005), and the change from D0 to D6 in Lp-PLA2 and ox-LDL were positively correlated (r = 0.65, p < 0.0001). An exploratory untargeted lipidomic analysis uncovered 308 individual lipids in isolated LDL particles. Paired-test analysis from D0 and D6 revealed higher concentrations of 32 lipid species during disease progression, mainly represented by lysophosphatidyl choline and phosphatidylinositol. In addition, 69 lipid species were exclusively modulated in the LDL particles from non-survivors as compared to survivors.

conclusionsPhenotypic changes in LDL particles are associated with disease progression and adverse clinical outcomes in COVID-19 patients and could serve as a potential prognostic biomarker.

Indexed as

1-Alkyl-2-acetylglycerophosphocholine EsteraseCOVID-19BiomarkersHumansLipoproteins, LDLLysophosphatidylcholines1-Alkyl-2-acetylglycerophosphocholine EsteraseBiomarkersLipoproteins, LDLLysophosphatidylcholinesCOVID-19Lipoprotein-associated phospholipase A2Oxidized low-density lipoproteinQuantitative lipidomics

Identifiers

PMID36889041
PMCPMC9969752
OpenAlexW4322505870

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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.