Evidence map›Paper›PMID 26590821›Full record

ArticleRheumatology international2016

Determination of IL1 R2, ANTXR2, CARD9, and SNAPC4 single nucleotide polymorphisms in Iranian patients with ankylosing spondylitis.

Parisa Momenzadeh, Mahdi Mahmoudi, Maani Beigy, Masoud Garshasbi, Mahdi Vodjdanian, Ali Farazmand, Ahmad Reza Jamshidi

Abstract read
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In one paragraph

Article in Rheumatology international, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 2 pooled it
3.5field-weighted citation impact, top 8% 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

13 citing papers in PubMed, 2 syntheses or guidelines pooled it, 26 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. CARD9 in the pathogenesis of axial spondyloarthritis.Best practice & research. Clinical rheumatology · 2024
    Review
  5. Review
  6. CARD9 Signaling, Inflammation, and Diseases.Frontiers in immunology · 2022
    Review
  7. Review
  8. Review
  9. Article
  10. 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

7 authors at 3 institutions in 1 country.

Parisa MomenzadehDepartment of Cellular and Molecular Biology, Kish International Campus, University of Tehran, Kish Island, Iran.
Mahdi MahmoudiRheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran. mahmoudim@tums.ac.ir.
Maani BeigyRheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Masoud GarshasbiDepartment of Medical Genetics, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
Mahdi VodjdanianRheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Ali FarazmandDepartment of Cellular and Molecular Biology, Kish International Campus, University of Tehran, Kish Island, Iran. afarazmand@khayam.ut.ac.ir.
Ahmad Reza JamshidiRheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Tehran University of Medical Sciences · IRUniversity of Tehran · IRTarbiat Modares University · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ankylosing spondylitis (AS) is a chronic inflammatory disease of unknown origin, while both genetic and environmental factors have been demonstrated to be etiologically involved. Recent genome-wide association and replication studies have suggested that anthrax toxin receptor 2 (ANTXR2), interleukin-1 receptor 2 (IL1R2), caspase recruitment domain-containing protein 9 (CARD9), and small nuclear RNA-activating complex polypeptide 4 (SNAPC4) seem to be associated with AS pathogenesis. This case-control study was performed on 349 unrelated AS patients and 469 age- and gender-matched healthy controls, to investigate whether these non-MHC genes (IL1R2 rs2310173, ANTXR2 rs4333130, CARD9 rs4077515, and SNAPC4 rs3812571) influence the AS risk in Iranian population. ANTXR2 rs4333130 allele C (p = 0.0328; OR 0.744, 95% CI 0.598-0.927) and genotype CC (p = 0.0108; OR 0.273, 95% CI 0.123-0.605) were found to be significantly protective against AS. No other associations were found between AS and studied genes. The association between ANTXR2 rs4333130 and AS was independent of HLA-B27 status. Moreover, we found clinical disease severity scores (BASDAI and BASFI) and pain score were higher in ANTXR2 rs4333130 CT genotype. However, we observed that CARD9 allele C (p = 0.012) and genotype CC (p = 0.012) were significant protective factors against AS only in HLA-B27-negative patients, and IL1R2 rs2310173 genotype GT was mildly protective against AS only in HLA-B27-negative status. These findings support the role of non-MHC pathogenic pathways in susceptibility to AS and warrants more comprehensive studies focusing on these non-MHC pathways for developing novel therapeutic strategies.

Indexed as

Polymorphism, Single NucleotideAdultCARD Signaling Adaptor ProteinsCase-Control StudiesChi-Square DistributionDNA-Binding ProteinsFemaleGene FrequencyGenetic Association StudiesGenetic Predisposition to DiseaseHeterozygoteHLA-B27 AntigenHomozygoteHumansIranLogistic ModelsANTXR2 protein, humanCARD9 protein, humanCARD Signaling Adaptor ProteinsDNA-Binding ProteinsHLA-B27 AntigenIL1R2 protein, humanReceptors, Interleukin-1 Type IIReceptors, PeptideSNAPC4 protein, humanTranscription FactorsAnkylosing spondylitisANTXR2CARD9IL1R2SNAPC4

Identifiers

PMID26590821
OpenAlexW2284881030

What OpenQuestion holds

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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.