Evidence map›Paper›PMID 23365659›Full record

ArticlePloS one2013

IRGM variants and susceptibility to inflammatory bowel disease in the German population.

Jürgen Glas, Julia Seiderer, Stephanie Bues, Johannes Stallhofer, Christoph Fries, Torsten Olszak, Eleni Tsekeri, Martin Wetzke, Florian Beigel, Christian Steib and 5 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 5 pooled it
9.0field-weighted citation impact, top 2% 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

30 citing papers in PubMed, 5 syntheses or guidelines pooled it, 61 citations in OpenAlex.

  1. Pooled it
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  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Crohn's disease IRGM risk alleles are associated with altered gene expression in human tissues.American journal of physiology. Gastrointestinal and liver physiology · 2019
    Article
  13. Article
  14. A haplotypic variant at the IRGM locus and rs11747270 are related to the susceptibility for chronic periodontitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018
    Article
  15. Article
  16. Review
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  18. Correlations of Promoter Methylation in WIF-1, RASSF1A, and CDH13 Genes with the Risk and Prognosis of Esophageal Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2016
    Article
  19. MicroRNAs: how many in inflammatory bowel disease?Current opinion in gastroenterology · 2016
    Review
  20. 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

15 authors at 4 institutions in 1 country.

Jürgen GlasDepartment of Medicine II - Grosshadern, Ludwig-Maximilians-University, Munich, Germany.
Julia Seiderer
Stephanie Bues
Johannes Stallhofer
Christoph Fries
Torsten Olszak
Eleni Tsekeri
Martin Wetzke
Florian Beigel
Christian Steib
Matthias Friedrich
Burkhard Göke
Julia Diegelmann
Darina Czamara
Stephan Brand
Ludwig-Maximilians-Universität München · DEMax Planck Institute of Psychiatry · DEMedizinische Hochschule Hannover · DERWTH Aachen University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND &

aimsGenome-wide association studies identified the autophagy gene IRGM to be strongly associated with Crohn's disease (CD) but its impact in ulcerative colitis (UC), its phenotypic effects and potential epistatic interactions with other IBD susceptibility genes are less clear which we therefore analyzed in this study. METHODOLOGY/PRINCIPAL

findingsGenomic DNA from 2060 individuals including 817 CD patients, 283 UC patients, and 961 healthy, unrelated controls (all of Caucasian origin) was analyzed for six IRGM single nucleotide polymorphisms (SNPs) (rs13371189, rs10065172 = p.Leu105Leu, rs4958847, rs1000113, rs11747270, rs931058). In all patients, a detailed genotype-phenotype analysis and testing for epistasis with the three major CD susceptibility genes NOD2, IL23R and ATG16L1 were performed. Our analysis revealed an association of the IRGM SNPs rs13371189 (p = 0.02, OR 1.31 [95% CI 1.05-1.65]), rs10065172 = p.Leu105Leu (p = 0.016, OR 1.33 [95% CI 1.06-1.66]) and rs1000113 (p = 0.047, OR 1.27 [95% CI 1.01-1.61]) with CD susceptibility. There was linkage disequilibrium between these three IRGM SNPs. In UC, several IRGM haplotypes were weakly associated with UC susceptibility (p<0.05). Genotype-phenotype analysis revealed no significant associations with a specific IBD phenotype or ileal CD involvement. There was evidence for weak gene-gene-interaction between several SNPs of the autophagy genes IRGM and ATG16L1 (p<0.05), which, however, did not remain significant after Bonferroni correction. CONCLUSIONS/SIGNIFICANCE: Our results confirm IRGM as susceptibility gene for CD in the German population, supporting a role for the autophagy genes IRGM and ATG16L1 in the pathogenesis of CD.

Indexed as

Genetic Predisposition to DiseasePolymorphism, Single NucleotideAdolescentAdultAgedAged, 80 and overAutophagy-Related ProteinsCarrier ProteinsCase-Control StudiesColitis, UlcerativeCrohn DiseaseEpistasis, GeneticFemaleGene FrequencyGenome-Wide Association StudyGermanyATG16L1 protein, humanAutophagy-Related ProteinsCarrier ProteinsGTP-Binding ProteinsIRGM protein, human

Identifiers

PMID23365659
PMCPMC3554777
OpenAlexW2140541163

What OpenQuestion holds

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LicenceCC BY
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.