Evidence map›Paper›PMID 24594669›Full record

ArticleThe Journal of investigative dermatology2014

TNF-α gene polymorphisms: association with disease susceptibility and response to anti-TNF-α treatment in psoriatic arthritis.

Giuseppe Murdaca, Rossella Gulli, Francesca Spanò, Francesca Lantieri, Martina Burlando, Aurora Parodi, Paola Mandich, Francesco Puppo

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in The Journal of investigative dermatology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 7 pooled it
7.1field-weighted citation impact, top 3% 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

51 citing papers in PubMed, 7 syntheses or guidelines pooled it, 99 citations in OpenAlex.

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  17. Journal of personalized medicine · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Giuseppe MurdacaClinical Immunology Unit, Department of Internal Medicine, University of Genoa, Genoa, Italy. Electronic address: Giuseppe.Murdaca@unige.it.
Rossella GulliDepartment of Neuroscience, Rehabilitation, Ophthalmology, Genetics and Maternal Child Health, Section of Medical Genetics, University of Genoa, Genoa, Italy.
Francesca SpanòClinical Immunology Unit, Department of Internal Medicine, University of Genoa, Genoa, Italy.
Francesca LantieriBiostatistic Unit, Department of Health Sciences, University of Genoa, Genoa, Italy.
Martina BurlandoDermatology Unit, Department of Health Sciences, University of Genoa, Genoa, Italy.
Aurora ParodiDermatology Unit, Department of Health Sciences, University of Genoa, Genoa, Italy.
Paola MandichDepartment of Neuroscience, Rehabilitation, Ophthalmology, Genetics and Maternal Child Health, Section of Medical Genetics, University of Genoa, Genoa, Italy.
Francesco PuppoClinical Immunology Unit, Department of Internal Medicine, University of Genoa, Genoa, Italy.
University of Genoa · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The tumor necrosis factor-α (TNF-α) gene has been proposed as a major candidate gene in psoriatic arthritis (PsA). TNF-α is a therapeutic target for patients responding poorly to conventional treatments. We investigated the role of single-nucleotide polymorphisms (SNPs) at positions -238, -308, and +489 of the TNF-α gene in the genetic susceptibility to PsA, in the severity of the disease, and, finally, in the response to TNF-α inhibitors (adalimumab, etanercept, or infliximab). Fifty-seven Caucasian PsA patients and 155 healthy matched controls were studied. The SNP +489 variant allele A was significantly associated with PsA susceptibility (P=0.0136) and severity of clinical (Psoriasis Area and Severity Index score, American College of Rheumatology criteria, Disease Activity Score 28, and Disability Index Health Assessment Questionnaire) and laboratory (C-reactive protein and erythrocyte sedimentation rate) parameters (P-values ranging from 0.016 to 2.908 × 10(-12)). The difference in severity was accounted for by the differences between the AA and GA genotypes with respect to the GG genotype. The SNP +489A allele shows a trend of association with the response to PsA treatment with etanercept. These findings suggest a role of the SNP +489A allele in the susceptibility and severity of PsA.

Indexed as

AdalimumabAdultAllelesAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedArthritis, PsoriaticCase-Control StudiesEtanerceptFemaleGenetic Predisposition to DiseaseGenotypeHumansImmunoglobulin GInfliximabMaleMiddle AgedAdalimumabAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedEtanerceptImmunoglobulin GInfliximabReceptors, Tumor Necrosis FactorTumor Necrosis Factor-alpha

Identifiers

PMID24594669
OpenAlexW2033081114

What OpenQuestion holds

Textmetadata
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.