Evidence map›Paper›PMID 36355253›Full record

ArticleClinical rheumatology2023

Association of - 717 A > G (rs2794521) CRP polymorphism with high cardiovascular risk by C-reactive protein in systemic lupus erythematosus patients.

Karen Pesqueda-Cendejas, Isela Parra-Rojas, Mónica R Meza-Meza, Paulina E Mora-García, Bertha Campos-López, Adolfo I Ruiz-Ballesteros, Margarita Montoya-Buelna, Melissa Rivera-Escoto, José M Moreno-Ortiz, Luis A Bautista-Herrera and 2 more

Abstract read
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Article in Clinical rheumatology, 2023. 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
0.5field-weighted citation impact, top 33% 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, 3 citations in OpenAlex.

  1. Article
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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

12 authors at 2 institutions in 1 country.

Karen Pesqueda-CendejasRed de Inmunonutrición Y Genómica Nutricional en Las Enfermedades Autoinmunes, Centro Universitario de Ciencias de La Salud, Universidad de Guadalajara, 44340, Guadalajara, Jalisco, Mexico.ORCID http://orcid.org/0000-0002-6849-5965
Isela Parra-RojasRed de Inmunonutrición Y Genómica Nutricional en Las Enfermedades Autoinmunes, Centro Universitario de Ciencias de La Salud, Universidad de Guadalajara, 44340, Guadalajara, Jalisco, Mexico.ORCID http://orcid.org/0000-0002-9213-8263
Mónica R Meza-MezaRed de Inmunonutrición Y Genómica Nutricional en Las Enfermedades Autoinmunes, Centro Universitario de Ciencias de La Salud, Universidad de Guadalajara, 44340, Guadalajara, Jalisco, Mexico.ORCID http://orcid.org/0000-0003-4991-4965
Paulina E Mora-GarcíaRed de Inmunonutrición Y Genómica Nutricional en Las Enfermedades Autoinmunes, Centro Universitario de Ciencias de La Salud, Universidad de Guadalajara, 44340, Guadalajara, Jalisco, Mexico.ORCID http://orcid.org/0000-0002-5452-6222
Bertha Campos-LópezRed de Inmunonutrición Y Genómica Nutricional en Las Enfermedades Autoinmunes, Centro Universitario de Ciencias de La Salud, Universidad de Guadalajara, 44340, Guadalajara, Jalisco, Mexico.ORCID http://orcid.org/0000-0002-1667-8794
Adolfo I Ruiz-BallesterosRed de Inmunonutrición Y Genómica Nutricional en Las Enfermedades Autoinmunes, Centro Universitario de Ciencias de La Salud, Universidad de Guadalajara, 44340, Guadalajara, Jalisco, Mexico.ORCID http://orcid.org/0000-0001-8993-6312
Margarita Montoya-BuelnaRed de Inmunonutrición Y Genómica Nutricional en Las Enfermedades Autoinmunes, Centro Universitario de Ciencias de La Salud, Universidad de Guadalajara, 44340, Guadalajara, Jalisco, Mexico.ORCID http://orcid.org/0000-0001-9309-1957
Melissa Rivera-EscotoRed de Inmunonutrición Y Genómica Nutricional en Las Enfermedades Autoinmunes, Centro Universitario de Ciencias de La Salud, Universidad de Guadalajara, 44340, Guadalajara, Jalisco, Mexico.ORCID http://orcid.org/0000-0001-9069-7478
José M Moreno-OrtizInstituto de Genética Humana "Dr. Enrique Corona Rivera, Departamento de Biología Molecular Y Genómica, Centro Universitario de Ciencias de La Salud, Universidad de Guadalajara, 44340, Guadalajara, Jalisco, Mexico.ORCID http://orcid.org/0000-0001-7555-9851
Luis A Bautista-HerreraDepartamento de Farmacobiología, Centro Universitario de Ciencias Exactas E Ingenierías, Universidad de Guadalajara, 44430, Guadalajara, Jalisco, Mexico.ORCID http://orcid.org/0000-0002-3599-3909
Sergio Cerpa-CruzDepartamento de Reumatología, O.P.D. Hospital Civil de Guadalajara Fray Antonio Alcalde, 44280, Guadalajara, Jalisco, Mexico.ORCID http://orcid.org/0000-0002-0755-0289
Ulises De la Cruz-MossoRed de Inmunonutrición Y Genómica Nutricional en Las Enfermedades Autoinmunes, Centro Universitario de Ciencias de La Salud, Universidad de Guadalajara, 44340, Guadalajara, Jalisco, Mexico. ulises_cdm@hotmail.com.ORCID http://orcid.org/0000-0003-4579-2294
Universidad de Guadalajara · MXHospital Civil de Guadalajara · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionSystemic lupus erythematosus (SLE) is an autoimmune disease where genetic factors have been related to SLE susceptibility and disease severity. CRP polymorphisms have been associated with high C-reactive protein (CRP) serum levels, cardiovascular disease (CVD), and high clinical disease activity in SLE patients; however, the evidence is still inconclusive.

objectiveThis study was aimed to assess the association of the - 717 A > G, - 409 G > A, + 1444 C > T, and + 1846 C > T CRP polymorphisms with genetic susceptibility, clinical disease activity, and CVD risk in Mexican-mestizo SLE patients.

methodsA comparative cross-sectional study was conducted on 369 unrelated women: 183 with SLE according to the 1997 SLE-ACR criteria and 186 healthy subjects (HS). The clinical disease activity was assessed by the Mex-SLEDAI score; CRP and lipid profile were quantified by turbidimetry and colorimetric-enzymatic assays, respectively. The CRP polymorphisms genotyping was carried out by allelic discrimination.

resultsSLE patients with - 717 AA genotype had higher CRP serum levels than SLE carriers of AG and GG genotypes (AA = 5 mg/L vs. AG = 3.2 mg/L vs. GG = 2.4 mg/L; p = 0.01), and the AA genotype was associated with high CVD risk by CRP in SLE patients (OR = 3; CI: 1.2-7.6; p < 0.01).

conclusionsThe - 717 A > G CRP polymorphism is a risk factor for high CRP levels and high CVD risk in Mexican-mestizo SLE patients. Key Points • Cardiovascular disease is one of the major causes of death in SLE patients due to the higher prevalence of traditional and non-traditional cardiovascular risk factors. • C-reactive protein is a liver-derived acute-phase protein suggested as one powerful independent risk predictor factor for cardiovascular disease. • Single nucleotide polymorphisms in CRP have been suggested as genetic susceptibility factors that could modify the SLE pathophysiology outcomes. • Mexican-mestizo SLE patients carrying the -717 A>G CRP AA genotype had 3-fold high cardiovascular disease risk than SLE patients with AG or GG genotypes.

Indexed as

Cardiovascular DiseasesLupus Erythematosus, SystemicCase-Control StudiesC-Reactive ProteinCross-Sectional StudiesFemaleGene FrequencyGenetic Predisposition to DiseaseGenotypeHeart Disease Risk FactorsHumansPolymorphism, Single NucleotideRisk FactorsC-Reactive ProteinCardiovascular riskC-reactive proteinCRP polymorphismSystemic lupus erythematosus

Identifiers

PMID36355253
OpenAlexW4308683204

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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.