Evidence map›Paper›PMID 37137941›Full record

ArticleScientific reports2023

Role of paraoxonase 1 activity and PON1 gene polymorphisms in sickle cell disease.

Joelma Figueiredo Menezes, Magda Oliveira Seixas Carvalho, Larissa Carneiro Rocha, Felipe Miranda Dos Santos, Elisângela Vitória Adorno, Cyntia Cajado de Souza, Rayra Pereira Santiago, Caroline Conceição da Guarda, Rodrigo Mota de Oliveira, Camylla Vilas Boas Figueiredo and 9 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 35% 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

4 citing papers in PubMed, 1 synthesis or guideline pooled it, 3 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
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

19 authors at 5 institutions in 2 countries.

Joelma Figueiredo MenezesLaboratório de Investigação em Genética e Hematologia Translacional, Instituto Gonçalo Moniz, Fundação Oswaldo Cruz (FIOCRUZ), Salvador, Bahia, Brazil.
Magda Oliveira Seixas CarvalhoLaboratório de Investigação em Genética e Hematologia Translacional, Instituto Gonçalo Moniz, Fundação Oswaldo Cruz (FIOCRUZ), Salvador, Bahia, Brazil.
Larissa Carneiro RochaFundação de Hematologia e Hemoterapia do Estado da Bahia (HEMOBA), Salvador, Bahia, Brazil.
Felipe Miranda Dos SantosFaculdade de Medicina, Universidade Federal da Bahia, Salvador, Bahia, Brazil.
Elisângela Vitória AdornoDepartamento de Toxicologias e Análises Clínicas, Faculdade de Farmácia, Universidade Federal da Bahia, Salvador, Bahia, Brazil.
Cyntia Cajado de SouzaLaboratório de Investigação em Genética e Hematologia Translacional, Instituto Gonçalo Moniz, Fundação Oswaldo Cruz (FIOCRUZ), Salvador, Bahia, Brazil.
Rayra Pereira SantiagoLaboratório de Investigação em Genética e Hematologia Translacional, Instituto Gonçalo Moniz, Fundação Oswaldo Cruz (FIOCRUZ), Salvador, Bahia, Brazil.
Caroline Conceição da GuardaLaboratório de Investigação em Genética e Hematologia Translacional, Instituto Gonçalo Moniz, Fundação Oswaldo Cruz (FIOCRUZ), Salvador, Bahia, Brazil.
Rodrigo Mota de OliveiraLaboratório de Investigação em Genética e Hematologia Translacional, Instituto Gonçalo Moniz, Fundação Oswaldo Cruz (FIOCRUZ), Salvador, Bahia, Brazil.
Camylla Vilas Boas FigueiredoLaboratório de Investigação em Genética e Hematologia Translacional, Instituto Gonçalo Moniz, Fundação Oswaldo Cruz (FIOCRUZ), Salvador, Bahia, Brazil.
Suéllen Pinheiro CarvalhoLaboratório de Investigação em Genética e Hematologia Translacional, Instituto Gonçalo Moniz, Fundação Oswaldo Cruz (FIOCRUZ), Salvador, Bahia, Brazil.
Sètondji Cocou Modeste Alexandre YahouédéhouLaboratório de Investigação em Genética e Hematologia Translacional, Instituto Gonçalo Moniz, Fundação Oswaldo Cruz (FIOCRUZ), Salvador, Bahia, Brazil.
Luciana Magalhães FiuzaLaboratório de Investigação em Genética e Hematologia Translacional, Instituto Gonçalo Moniz, Fundação Oswaldo Cruz (FIOCRUZ), Salvador, Bahia, Brazil.
Corynne Stéphanie Ahouefa AdanhoLaboratório de Investigação em Genética e Hematologia Translacional, Instituto Gonçalo Moniz, Fundação Oswaldo Cruz (FIOCRUZ), Salvador, Bahia, Brazil.
Thassila Nogueira PitangaLaboratório de Investigação em Genética e Hematologia Translacional, Instituto Gonçalo Moniz, Fundação Oswaldo Cruz (FIOCRUZ), Salvador, Bahia, Brazil.
Isa Menezes LyraFundação de Hematologia e Hemoterapia do Estado da Bahia (HEMOBA), Salvador, Bahia, Brazil.
Valma Maria Lopes NascimentoFundação de Hematologia e Hemoterapia do Estado da Bahia (HEMOBA), Salvador, Bahia, Brazil.
Alberto Augusto Noronha-DutraUniversity College of London, UCL, London, UK.
Marilda Souza GoncalvesLaboratório de Investigação em Genética e Hematologia Translacional, Instituto Gonçalo Moniz, Fundação Oswaldo Cruz (FIOCRUZ), Salvador, Bahia, Brazil. marilda.goncalves@fiocruz.br.
Fundação Oswaldo Cruz · BRUniversidade Federal da Bahia · BRFundação de Amparo à Pesquisa do Estado da Bahia · BRFundação Hospitalar de Hematologia e Hemoterapia do Amazonas · BRUniversity College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sickle cell disease (SCD) patients often exhibit a dyslipidemic sub-phenotype. Paraoxonase 1 (PON 1) is a serum glycoprotein associated with the high-density lipoproteins cholesterol (HDL-C), and variability in PON1 activity depends on the PON1 genotypes. We investigated the influence of PON1c.192Q > R and PON1c.55L > M polymorphisms on PON1 activity and laboratory parameters and the association between PON1 activity and clinical manifestations in SCD patients. We recruited 350 individuals, including 154 SCD patients and 196 healthy volunteers, which comprised the control group. Laboratory parameters and molecular analyses were investigated from the participants' blood samples. We have found increased PON1 activity in SCD individuals compared to the control group. In addition, carriers of the variant genotype of each polymorphism presented lower PON1 activity. SCD individuals carrying the variant genotype of PON1c.55L > M polymorphism had lower platelet and reticulocyte counts, C-reactive protein, and aspartate aminotransferase levels; in addition to higher creatinine levels. SCD individuals carrying the variant genotype of PON1c.192Q > R polymorphism had lower triglyceride, VLDL-c, and indirect bilirubin levels. Furthermore, we observed an association between PON1 activity history of stroke and splenectomy. The present study confirmed the association between PON1c.192Q > R and PON1c.55L > M polymorphisms and PON1 activity, in addition to demonstrate their effects on markers of dislipidemia, hemolysis and inflammation, in SCD individuals. Moreover, data suggest PON1 activity as a potential biomarker related to stroke and splenectomy.

Indexed as

Anemia, Sickle CellStrokeAryldialkylphosphataseGenotypeHumansPolymorphism, GeneticAryldialkylphosphatasePON1 protein, human

Identifiers

PMID37137941
PMCPMC10156724
OpenAlexW4367856323

What OpenQuestion holds

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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 OpenQuestion graph.