Evidence map›Paper›PMID 27044681›Full record

ArticleThe pharmacogenomics journal2017

FCGR3A-V158F polymorphism is a disease-specific pharmacogenetic marker for the treatment of psoriasis with Fc-containing TNFα inhibitors.

E Mendrinou, A Patsatsi, E Zafiriou, D Papadopoulou, L Aggelou, C Sarri, Z Mamuris, A Kyriakou, D Sotiriadis, A Roussaki-Schulze and 2 more

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Article in The pharmacogenomics journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

10 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  10. AInternational journal of medical sciences · 2018
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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.

E MendrinouLaboratory of Genetics, Comparative and Evolutionary Biology, Department of Biochemistry and Biotechnology, University of Thessaly, Larissa, Greece.
A Patsatsi2nd Dermatology Department, Medical School, Papageorgiou Hospital, Aristotle University, Thessaloniki, Greece.
E ZafiriouDepartment of Dermatology, University General Hospital Larissa, University of Thessaly, Larissa, Greece.
D PapadopoulouLaboratory of Genetics, Comparative and Evolutionary Biology, Department of Biochemistry and Biotechnology, University of Thessaly, Larissa, Greece.
L AggelouLaboratory of Genetics, Comparative and Evolutionary Biology, Department of Biochemistry and Biotechnology, University of Thessaly, Larissa, Greece.
C SarriLaboratory of Genetics, Comparative and Evolutionary Biology, Department of Biochemistry and Biotechnology, University of Thessaly, Larissa, Greece.
Z MamurisLaboratory of Genetics, Comparative and Evolutionary Biology, Department of Biochemistry and Biotechnology, University of Thessaly, Larissa, Greece.
A Kyriakou2nd Dermatology Department, Medical School, Papageorgiou Hospital, Aristotle University, Thessaloniki, Greece.
D Sotiriadis2nd Dermatology Department, Medical School, Papageorgiou Hospital, Aristotle University, Thessaloniki, Greece.
A Roussaki-SchulzeDepartment of Dermatology, University General Hospital Larissa, University of Thessaly, Larissa, Greece.
T SarafidouLaboratory of Genetics, Comparative and Evolutionary Biology, Department of Biochemistry and Biotechnology, University of Thessaly, Larissa, Greece.
Y VasilopoulosLaboratory of Genetics, Comparative and Evolutionary Biology, Department of Biochemistry and Biotechnology, University of Thessaly, Larissa, Greece.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Psoriasis is a multifactorial skin disease affecting ~2% of world's population, causing a dramatic decrease in patients' quality of life and a significant increase in health-care expenses. Biological agents such as the anti-TNFα ones had an enormous impact in patients' therapy; however, a significant proportion of them do not respond well, an outcome attributed mainly to genetic factors. Recently, in a large European cohort of rheumatoid arthritis patients we have shown association with variation in the receptors that correspond to the Fc portion of the biological agents. As both diseases share common immunological fingerprints, we examined the hypothesis that they share common pharmacogenetic markers. Analysis of FCGR2A-H131R and FCGR3A-V158F polymorphisms in 100 psoriasis patients showed association only with respect to FCGR3A-V158F and response to etanercept (P=0.018). Interestingly, no association was found between FCGR2A-H131R and response to anti-TNFα therapy (P=0.882). This study suggests a role for FCGR3A-V158F polymorphism unique for psoriasis.

Indexed as

Pharmacogenomic VariantsPolymorphism, Single NucleotideAdultAnti-Inflammatory AgentsDrug ResistanceEtanerceptFemaleGenotypeHumansImmunoglobulin Fc FragmentsMaleMiddle AgedPharmacogeneticsPharmacogenomic TestingPhenotypePsoriasisAnti-Inflammatory AgentsEtanerceptFCGR3A protein, humanImmunoglobulin Fc FragmentsReceptors, IgGTumor Necrosis Factor-alpha

Identifiers

PMID27044681

What OpenQuestion holds

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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.