Evidence map›Paper›PMID 15647186›Full record

ArticleGut2005

Epithelioid granulomas, pattern recognition receptors, and phenotypes of Crohn's disease.

M Pierik, G De Hertogh, S Vermeire, G Van Assche, P Van Eyken, S Joossens, G Claessens, R Vlietinck, P Rutgeerts, K Geboes

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 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
4.6field-weighted citation impact, top 5% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. New insights into gastrointestinal and hepatic granulomatous disorders.Nature reviews. Gastroenterology & hepatology · 2011
    Review
  13. Review
  14. Granuloma-positive Crohn's disease.Canadian journal of gastroenterology = Journal canadien de gastroenterologie · 2007
    Article
  15. Article
  16. Review
  17. Review
  18. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 1 institution in 1 country.

M PierikDepartment of Gasteroenterology, University Hospitals, Katholieke Universiteit, Leuven, Belgium.
G De Hertogh
S Vermeire
G Van Assche
P Van Eyken
S Joossens
G Claessens
R Vlietinck
P Rutgeerts
K Geboes
KU Leuven · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionCrohn's disease is a chronic inflammatory disorder of the gut. It is assumed that a defective interaction between the bacterial flora of the gut and the innate immune system plays a key role in the pathogenesis of the disease. This may lead to specific histological lesions. The epithelioid granuloma is particularly interesting in this regard as it is also observed in several bacterial infections of the gut. AIMS AND

methodsWe hypothesised that genetic or environmental factors with a known influence on inflammation or immunity would lead to an increased prevalence of granulomas. Therefore, surgical specimens from 161 patients were evaluated for the presence of granulomas. Patients were genotyped for the three single nucleotide polymorphisms in caspase recruitment domain 15 (CARD15)/NOD2 associated with CD and for Asp299Gly in Toll-like receptor 4 (TLR4).

resultsThe overall prevalence of granulomas was 68.9%. We did not find a significant correlation between granulomas and TLR4 or CARD15 variants. The frequency of granulomas increased with more distal disease (63% small bowel, 72% right colon, 88% left colon, 90% rectum; p=0.01). Granulomas were more frequent in younger patients (odds ratio 0.95 (95% confidence interval 0.92-0.98) p=0.007).

conclusionIn this study of 161 well documented CD patients, we found no significant association between CARD15 and TLR4 variants and granulomas. This finding seems to refute our initial hypothesis. However, it may be that additional factors are needed for granuloma development. Granulomas may develop only when specific bacterial components are present. Therefore, future research on granuloma pathogenesis should be orientated towards detection and identification of bacterial components in these lesions.

Indexed as

AdultAge FactorsCrohn DiseaseFemaleGenetic Predisposition to DiseaseGenotypeGranulomaHumansIntestinal DiseasesIntracellular Signaling Peptides and ProteinsMaleMembrane GlycoproteinsMiddle AgedNod2 Signaling Adaptor ProteinPhenotypePolymorphism, GeneticIntracellular Signaling Peptides and ProteinsMembrane GlycoproteinsNOD2 protein, humanNod2 Signaling Adaptor ProteinReceptors, Cell SurfaceTLR4 protein, humanToll-Like Receptor 4Toll-Like Receptors

Identifiers

PMID15647186
PMCPMC1774832
OpenAlexW2004582112

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.