Evidence map›Paper›PMID 25548430›Full record

ArticleDisease markers2014

The CCR5Δ32 polymorphism in Brazilian patients with sickle cell disease.

Mariana Pezzute Lopes, Magnun Nueldo Nunes Santos, Eliel Wagner Faber, Marcos André Cavalcanti Bezerra, Betânia Lucena Domingues Hatzlhofer, Dulcinéia Martins Albuquerque, Tânia Regina Zaccariotto, Daniela Maria Ribeiro, Aderson da Silva Araújo, Fernando Ferreira Costa and 1 more

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

Article in Disease markers, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 36% 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

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
  2. 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

11 authors at 2 institutions in 1 country.

Mariana Pezzute LopesDepartment of Clinical Pathology, School of Medical Sciences, State University of Campinas (UNICAMP), 13083-970 Campinas, SP, Brazil.
Magnun Nueldo Nunes SantosDepartment of Clinical Pathology, School of Medical Sciences, State University of Campinas (UNICAMP), 13083-970 Campinas, SP, Brazil.
Eliel Wagner FaberDepartment of Clinical Pathology, School of Medical Sciences, State University of Campinas (UNICAMP), 13083-970 Campinas, SP, Brazil.
Marcos André Cavalcanti BezerraPernambuco Hematology and Hemotherapy Center, HEMOPE Foundation, 52011-900 Recife, PE, Brazil.
Betânia Lucena Domingues HatzlhoferPernambuco Hematology and Hemotherapy Center, HEMOPE Foundation, 52011-900 Recife, PE, Brazil.
Dulcinéia Martins AlbuquerqueHematology and Hemotherapy Center, UNICAMP, 13083-878 Campinas, SP, Brazil.
Tânia Regina ZaccariottoDepartment of Clinical Pathology, School of Medical Sciences, State University of Campinas (UNICAMP), 13083-970 Campinas, SP, Brazil.
Daniela Maria RibeiroDepartment of Clinical Pathology, School of Medical Sciences, State University of Campinas (UNICAMP), 13083-970 Campinas, SP, Brazil.
Aderson da Silva AraújoPernambuco Hematology and Hemotherapy Center, HEMOPE Foundation, 52011-900 Recife, PE, Brazil.
Fernando Ferreira CostaHematology and Hemotherapy Center, UNICAMP, 13083-878 Campinas, SP, Brazil.
Maria de Fátima SonatiDepartment of Clinical Pathology, School of Medical Sciences, State University of Campinas (UNICAMP), 13083-970 Campinas, SP, Brazil.ORCID 0000-0002-5193-8854
Universidade Estadual de Campinas (UNICAMP) · BRFundação Hemopa · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPrevious studies on the role of inflammation in the pathophysiology of sickle cell disease (SCD) suggested that the CCR5Δ32 allele, which is responsible for the production of truncated C-C chemokine receptor type 5 (CCR5), could confer a selective advantage on patients with SCD because it leads to a less efficient Th1 response. We determined the frequency of the CCR5Δ32 polymorphism in 795 Afro-Brazilian SCD patients followed up at the Pernambuco Hematology and Hemotherapy Center, in Northeastern Brazil, divided into a pediatric group (3 months-17 years, n = 483) and an adult group (18-70 years, n = 312). The adult patients were also compared to a healthy control group (blood donors, 18-61 years, n = 247).

methodsThe CCR5/CCR5Δ32 polymorphism was determined by allele-specific PCR.

resultsNo homozygous patient for the CCR5Δ32 allele was detected. The frequency of heterozygotes in the study population (patients and controls) was 5.8%, in the total SCD patients 5.1%, in the children 5.4%, in the adults with SCD 4.8%, and in the adult controls 8.1%. These differences did not reach statistical significance.

conclusionsOur findings failed to demonstrate an important role of the CCR5Δ32 allele in the population sample studied here.

Indexed as

AdolescentAdultAgedAnemia, Sickle CellBrazilCase-Control StudiesChildChild, PreschoolFemaleGene FrequencyGenetic Association StudiesGenetic Predisposition to DiseaseHumansInfantMaleMiddle AgedCCR5 protein, humanReceptors, CCR5

Identifiers

PMID25548430
PMCPMC4274860
OpenAlexW2157875498

What OpenQuestion 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 OpenQuestion graph.