Evidence map›Paper›PMID 17570063›Full record

ArticleDigestive diseases and sciences2008

Analysis of the NOD2/CARD15 gene in patients affected with the aseptic abscesses syndrome with or without inflammatory bowel disease.

Marc François Jean André, Olivier Aumaître, Jean-Charles Piette, Gilles Grateau, Marie-Céleste Cardoso, Lemlih Ouchchane, Jean-Louis Kémény, Bernard Dastugue, Marc Delpech, Isabelle Creveaux

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Article in Digestive diseases and sciences, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.2field-weighted citation impact, top 40% 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

8 citing papers in PubMed, 17 citations in OpenAlex.

  1. Effects of pentasa-combined probiotics on the microflora structure and prognosis of patients with inflammatory bowel disease.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2019
    Trial
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  7. JAAD case reports · 2018
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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

10 authors at 4 institutions in 1 country.

Marc François Jean AndréInserm, U384, Clermont-Ferrand, 63001, France. mandre@chu-clermontferrand.fr
Olivier Aumaître
Jean-Charles Piette
Gilles Grateau
Marie-Céleste Cardoso
Lemlih Ouchchane
Jean-Louis Kémény
Bernard Dastugue
Marc Delpech
Isabelle Creveaux
Centre Hospitalier Universitaire de Clermont-Ferrand · FRInserm · FRUniversité Paris Cité · FRAssistance Publique – Hôpitaux de Paris · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesNOD2/CARD15 is a susceptibility gene for Crohn's disease (CD). It is also involved, via different mutations, in the Blau syndrome. The syndrome of aseptic abscesses (AA) is characterized by visceral sterile collections of mature neutrophils that do not respond to antibiotics but regress quickly with corticosteroids. It is associated in two cases out of three with inflammatory bowel disease (IBD), and in particular with CD. We wanted to assess if changes on gene NOD2/CARD15 could contribute to the development of AA in patients with and without IBD.

methodsSeventeen unrelated patients with AA from the French national register were genotyped for c.802C>T (p.Pro268Ser) and the three main CD associated variants, c.2104C>T (p.Arg702Trp), c.2722G>C (p.Gly908Arg) and c.3019_3020insC (p.Leu1007fsX1008), and 16 were screened for the 11 coding exons of NOD2/CARD15.

resultsThe main variants associated with CD were found at a similar frequency in patients free of IBD and in those with CD. There was no significant difference in the main variants between patients with CD and those without IBD in our study and patients with CD and controls, respectively, from a large study of an ethnically similar population. No rare variant was found. A significant association between carriers of the silent variant c.1377 C>T and markers of severity of AA was observed.

conclusionsThese results suggest that the emergence of AA is not closely related to gene NOD2/CARD15. NOD2/CARD15 and other susceptibility genes might enhance the expression of AA as the result of a combination of polymorphisms.

Indexed as

AbdomenAbscessAdultCrohn DiseaseFemaleGene FrequencyGenetic Predisposition to DiseaseHumansMaleMiddle AgedNod2 Signaling Adaptor ProteinPolymorphism, GeneticSyndromeNod2 Signaling Adaptor Protein

Identifiers

PMID17570063
OpenAlexW2001777851

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.