Evidence map›Paper›PMID 26071874›Full record

ArticleRheumatology international2016

CCR5Δ32 (rs333) polymorphism is associated with the susceptibility to systemic lupus erythematosus in female Brazilian patients.

Thiago Hissnauer Leal Baltus, Ana Paula Kallaur, Marcell Alysson Batisti Lozovoy, Helena Kaminami Morimoto, Francieli Delongui, Daniela Frizon Alfieri, Tatiane Mayumi Veiga Iriyoda, Isaias Dichi, Andrea Name Colado Simão, Edna Maria Vissoci Reiche

Abstract read
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Article in Rheumatology international, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

5 citing papers in PubMed, 15 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

10 authors at 1 institution in 1 country.

Thiago Hissnauer Leal BaltusHealth Sciences Postgraduate Program, Health Sciences Center, State University of Londrina, Londrina, Paraná, Brazil.
Ana Paula KallaurHealth Sciences Postgraduate Program, Health Sciences Center, State University of Londrina, Londrina, Paraná, Brazil.
Marcell Alysson Batisti LozovoyDepartment of Pathology, Clinical Analysis, and Toxicology, Health Sciences Center, State University of Londrina, Av. Robert Koch, 60, CEP 86.038-440, Londrina, Paraná, Brazil.
Helena Kaminami MorimotoDepartment of Pathology, Clinical Analysis, and Toxicology, Health Sciences Center, State University of Londrina, Av. Robert Koch, 60, CEP 86.038-440, Londrina, Paraná, Brazil.
Francieli DelonguiHealth Sciences Postgraduate Program, Health Sciences Center, State University of Londrina, Londrina, Paraná, Brazil.
Daniela Frizon AlfieriHealth Sciences Postgraduate Program, Health Sciences Center, State University of Londrina, Londrina, Paraná, Brazil.
Tatiane Mayumi Veiga IriyodaOutpatient Clinic for Rheumatology, University Hospital, State University of Londrina, Londrina, Paraná, Brazil.
Isaias DichiDepartment of Internal Medicine, Health Sciences Center, State University of Londrina, Londrina, Paraná, Brazil.
Andrea Name Colado SimãoDepartment of Pathology, Clinical Analysis, and Toxicology, Health Sciences Center, State University of Londrina, Av. Robert Koch, 60, CEP 86.038-440, Londrina, Paraná, Brazil.
Edna Maria Vissoci ReicheDepartment of Pathology, Clinical Analysis, and Toxicology, Health Sciences Center, State University of Londrina, Av. Robert Koch, 60, CEP 86.038-440, Londrina, Paraná, Brazil. reiche@sercomtel.com.br.
Universidade Estadual de Londrina · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The role of CCR5Δ32 (rs333) polymorphism in the pathogenesis of systemic lupus erythematosus (SLE) has been evaluated worldwide. The aim of this study was to determine the association between CCR5Δ32 polymorphism with the susceptibility to SLE and the activity of disease in female Southern Brazilian patients. The study enrolled 169 female SLE patients and 132 unrelated female healthy individuals. Baseline clinical, laboratorial characteristics, and the SLE activity (determined using the SLEDAI) were evaluated according to the CCR5Δ32 genotypes. The CCR5Δ32 polymorphism was determined from genomic DNA using a polymerase chain reaction. The frequencies of the genotypes CCR5/CCR5, CCR5/CCR5Δ32, and CCR5Δ32/CCR5Δ32 were 87.6, 11.8, and 0.6 %, respectively, among the patients and 96.2, 3.8, and 0.0 %, respectively, among the controls [CCR5/CCR5 vs. CCR5/CCR5Δ32 + CCR5Δ32/CCR5Δ32: p = 0.0081, odds ratio 3.604 (95 % confidence interval 1.321-9.4836)]. The frequencies of the CCR5 and the CCR5Δ32 alleles were 93.2 and 6.8 % among the patients, and 98.1 and 1.9 % among the controls, respectively (p = 0.0047, OR 3.758, 95 % CI 1.409-10.80). Patients carrying the genotypes with the CCR5Δ32 allele presented earlier age of onset of disease (p = 0.0293) and higher levels of anti-dsDNA (p = 0.0255) than those carrying the wild-type genotype. When the analysis was adjusted for ethnicity, only the age at onset of disease remained significant (p > 0.05). The results suggest that the CCR5Δ32 polymorphism might be associated with SLE genetic predisposition among female Brazilian patients and the age at onset of the disease; however, this genetic variant was not associated with the activity of SLE in this population.

Indexed as

Genetic Predisposition to DiseasePolymorphism, Single NucleotideAdultAge of OnsetAllelesBrazilFemaleGene FrequencyGenotypeHumansLupus Erythematosus, SystemicMiddle AgedReceptors, CCR5CCR5 protein, humanReceptors, CCR5CCR5Chemokine receptorGenetic polymorphismSystemic lupus erythematosus

Identifiers

PMID26071874
OpenAlexW656664808

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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.