Evidence map›Paper›PMID 16606645›Full record

Trial reportAnnals of the rheumatic diseases2006

Polymorphism at position +896 of the toll-like receptor 4 gene interferes with rapid response to treatment in rheumatoid arthritis.

K Kuuliala, A Orpana, M Leirisalo-Repo, H Kautiainen, M Hurme, P Hannonen, M Korpela, T Möttönen, L Paimela, K Puolakka and 2 more

Open access · greenAbstract readRandomized Controlled Trial
In one paragraph

Trial report in Annals of the rheumatic diseases, 2006. 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
1.5field-weighted citation impact, top 18% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Association of Toll-like receptor 4 single-nucleotide polymorphisms Asp299Gly and Thr399Ile with the risk of primary open angle glaucoma.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2017
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. 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

12 authors at 7 institutions in 1 country.

K KuulialaDepartment of Bacteriology and Immunology, Haartman Institute, University of Helsinki, PO Box 21 (Haartmaninkatu 3), FIN-00014 Helsinki, Finland. krista.anttonen@helsinki.fi
A Orpana
M Leirisalo-Repo
H Kautiainen
M Hurme
P Hannonen
M Korpela
T Möttönen
L Paimela
K Puolakka
A Karjalainen
H Repo
Helsinki University Hospital · FIOulu University Hospital · FICentral Finland Health Care District · FIInvalidisäätiö · FISouth Karelia Central Hospital · FITampere University Hospital · FIUniversity of Helsinki · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of this study was to determine whether the +896 A-->G substitution of the Toll-like receptor 4 (TLR4) gene, causing the Asp299-->Gly change in the extracellular domain of TLR4, influences treatment response in recent-onset rheumatoid arthritis. 169 patients with rheumatoid arthritis were genotyped from the Finnish Rheumatoid Arthritis Combination Therapy trial, in which they were treated either with only one disease-modifying antirheumatic drug (DMARD) with or without prednisolone (single group), or with three DMARDs and prednisolone (combination group). Patients homozygotic for the wild-type +896A allele were compared with those having the polymorphic G allele in terms of early clinical response (at 6 months) by the 28-joint Disease Activity Score (DAS28). 1 of 20 (5%; (95% (confidence interval (CI) 1 to 5)) patients of the single group with TLR4 +896AG or GG and 29 of 67 (43%; (95% CI 31 to 56)) patients with AA were in remission (p = 0.001). DAS28 of the single group with TLR4 +896AG or GG was higher than with AA (p = 0.019). In the combination group, remission rates and DAS28 values were comparable between the genotypes. The polymorphic TLR4 +896G allele may impair treatment response to single DMARD treatment in recent-onset rheumatoid arthritis.

Indexed as

Polymorphism, GeneticAntirheumatic AgentsArthritis, RheumatoidDrug Therapy, CombinationFemaleGenotypeGlucocorticoidsHumansLogistic ModelsMalePrednisolonePrognosisSeverity of Illness IndexToll-Like Receptor 4Treatment OutcomeAntirheumatic AgentsGlucocorticoidsPrednisoloneTLR4 protein, humanToll-Like Receptor 4

Identifiers

PMID16606645
PMCPMC1798301
OpenAlexW2134936041

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.