Evidence map›Paper›PMID 23856853›Full record

ArticleThe pharmacogenomics journal2014

Association of a complement receptor 1 gene variant with baseline erythrocyte sedimentation rate levels in patients starting anti-TNF therapy in a UK rheumatoid arthritis cohort: results from the Biologics in Rheumatoid Arthritis Genetics and Genomics Study Syndicate cohort.

J Bluett, I Ibrahim, D Plant, K L Hyrich, A W Morgan, A G Wilson, J D Isaacs, BRAGGSS, A Barton

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

Article in The pharmacogenomics journal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.2field-weighted citation impact, top 46% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Trial
  2. Article
  3. The Impact ofDiagnostics (Basel, Switzerland) · 2023
    Article
  4. 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

9 authors at 3 institutions in 1 country.

J BluettArthritis Research UK Epidemiology Unit, Manchester Academy of Health Science, University of Manchester, Manchester, UK.
I IbrahimArthritis Research UK Epidemiology Unit, Manchester Academy of Health Science, University of Manchester, Manchester, UK.
D PlantNIHR Manchester Musculoskeletal Biomedical Research Unit, Central Manchester NHS Foundation Trust, Manchester Academic Health Science Centre, Manchester, UK.
K L HyrichArthritis Research UK Epidemiology Unit, Manchester Academy of Health Science, University of Manchester, Manchester, UK.
A W Morgan1] NIHR Leeds Musculoskeletal Biomedical Research Unit, Chapel Allerton Hospital, The Leeds Teaching Hospitals NHS Trust, Leeds, UK [2] Leeds Institute of Molecular Medicine, Wellcome Trust Brenner Building, St. James's University Hospital, Leeds, UK.
A G WilsonDepartment of Infection and Immunity, University of Sheffield Medical School, Sheffield, UK.
J D IsaacsMusculoskeletal Research Group, Newcastle upon Tyne NHS Foundation Trust, Institute of Cellular Medicine, Newcastle University and NIHR Newcastle Biomedical Research Centre, Newcastle-upon-Tyne, UK.
BRAGGSS
A Barton1] Arthritis Research UK Epidemiology Unit, Manchester Academy of Health Science, University of Manchester, Manchester, UK [2] NIHR Manchester Musculoskeletal Biomedical Research Unit, Central Manchester NHS Foundation Trust, Manchester Academic Health Science Centre, Manchester, UK.
Manchester Academic Health Science Centre · GBChapel Allerton Hospital · GBNIHR Newcastle Biomedical Research Centre · GB

Funding

Arthritis Research UK 17552Arthritis Research UK 18475Arthritis Research UK 20385Department of Health MANMKBRU-2012-1Medical Research Council G0902272Medical Research Council G1000417Medical Research Council G1000758Medical Research Council G1001518Medical Research Council MR/K015346/1Versus Arthritis 20088
6 · The paper itself

Abstract

Eligibility for anti-tumour necrosis factor (TNF) therapy in most European countries is restricted to severe, active rheumatoid arthritis (RA). The DAS28 score is a marker of disease severity and incorporates one of two inflammatory markers, erythrocyte sedimentation rate (ESR) or C-reactive protein. We aimed to determine the relation between genetic variants known to affect ESR and levels of ESR in patients with active RA. DNA samples were genotyped for four single-nucleotide polymorphisms (SNPs) rs7527798 (CR1L), rs6691117 (CR1), rs10903129 (TMEM57) and rs1043879 (C1orf63). The association between SNPs and baseline ESR, baseline DAS28-ESR, and change in DAS28-ESR was evaluated. Baseline ESR was significantly associated with CR1 rs6691117 genotype (P=0.01). No correlation was identified between baseline DAS28-ESR or change in DAS28-ESR. In conclusion, genetic variation in the gene encoding CR1 may alter ESR levels but not DAS28-ESR, indicating no adjustment for CR1 genotype is required in the assessment of patients with severe active RA.

Indexed as

Blood SedimentationAdultAgedArthritis, RheumatoidC-Reactive ProteinEuropeFemaleGenomicsHumansMaleMiddle AgedPolymorphism, Single NucleotideReceptors, Complement 3bTreatment OutcomeTumor Necrosis Factor-alphaCR1 protein, humanC-Reactive ProteinReceptors, Complement 3bTumor Necrosis Factor-alpha

Identifiers

PMID23856853
PMCPMC3965567
OpenAlexW2089124417

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.