Evidence map›Paper›PMID 15955786›Full record

ArticleGut2005

Polymorphisms in the DLG5 and OCTN cation transporter genes in Crohn's disease.

H-P Török, J Glas, L Tonenchi, P Lohse, B Müller-Myhsok, O Limbersky, C Neugebauer, F Schnitzler, J Seiderer, C Tillack and 10 more

Open access · bronzeAbstract read
In one paragraph

Article in Gut, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 3 pooled it
18.9field-weighted citation impact, top 1% 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

44 citing papers in PubMed, 3 syntheses or guidelines pooled it, 161 citations in OpenAlex.

  1. Pooled it
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  3. Pooled it
  4. Article
  5. Article
  6. The role of heredity in pterygium development.International journal of ophthalmology · 2014
    Review
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  16. Crohn's disease: an immune deficiency state.Clinical reviews in allergy & immunology · 2010
    Review
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  18. Article
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  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

20 authors at 7 institutions in 2 countries.

H-P TörökChirurgische Klinik und Poliklinik-Standort Innenstadt, and Medizinische Poliklinik-Standort Innenstadt, Ludwig-Maximilians-Universität München, Germany.
J Glas
L Tonenchi
P Lohse
B Müller-Myhsok
O Limbersky
C Neugebauer
F Schnitzler
J Seiderer
C Tillack
S Brand
G Brünnler
P Jagiello
J T Epplen
T Griga
W Klein
U Schiemann
M Folwaczny
T Ochsenkühn
C Folwaczny
Ludwig-Maximilians-Universität München · DEKlinik und Poliklinik für Orthopädie, Physikalische Medizin und Rehabilitation · DEPoliklinik für Zahnerhaltung und Parodontologie · DERuhr University Bochum · DEBG University Hospital Bergmannsheil Bochum · DEMax Planck Institute of Psychiatry · DEUniversity Hospital of Bern · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimsRecent data suggest identification of causal genetic variants for inflammatory bowel disease in the DLG5 gene and in the organic cation transporter (OCTN) cluster, both situated in previously described linkage regions. PATIENTS AND

methodsThe polymorphisms in DLG5 (113 G-->A, 4136 C-->A, and DLG5_e26), SLC22A4 (1672 C-->T), and SLC22A5 (-207 G-->C) were assessed in 625 patients with Crohn's disease (CD), 363 patients with ulcerative colitis (UC), and 1012 healthy controls. Association with disease susceptibility, clinical phenotypes, and possible genetic interactions of these polymorphisms with disease associated CARD15/NOD2 mutations was analysed.

resultsNo significant association of DLG5 polymorphisms with CD or UC was observed. Homozygosity for the OCTN-TC haplotype was associated with an increased CD risk (OR = 1.65), which was even greater in the presence of CARD15 mutations. Genotype-phenotype analysis revealed that this association was particularly strong in patients with colonic disease. The TC haplotype was associated with non-fistulising non-fibrostenotic disease, an earlier age of disease onset, and reduced need for surgery.

conclusionOur observations argue against a role of DLG5 polymorphisms in the susceptibility for inflammatory bowel disease, whereas the OCTN polymorphisms are associated with CD. However, due to the comparable weak association observed herein, extended linkage disequilibrium analyses of these variants with the IBD5 haplotype tagged single nucleotide polymorphims might be advisable before definitive conclusions about their causative role in CD can be drawn.

Indexed as

AdolescentAdultAgedChildColitis, UlcerativeCrohn DiseaseFemaleGenetic MarkersGenetic Predisposition to DiseaseGenotypeHaplotypesHumansIntracellular Signaling Peptides and ProteinsLinkage DisequilibriumMaleMembrane ProteinsDLG5 protein, humanGenetic MarkersIntracellular Signaling Peptides and ProteinsMembrane ProteinsNOD2 protein, humanNod2 Signaling Adaptor ProteinOrganic Cation Transport ProteinsTumor Suppressor Proteins

Identifiers

PMID15955786
PMCPMC1774699
OpenAlexW2100749285

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.