Evidence map›Paper›PMID 24465786›Full record

ArticlePloS one2014

A CARD9 polymorphism is associated with decreased likelihood of persistent conjugated hyperbilirubinemia in intestinal failure.

Karolina Maria Burghardt, Vishal Avinashi, Christina Kosar, Wei Xu, Paul W Wales, Yaron Avitzur, Aleixo Muise

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. 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
1.2field-weighted citation impact, top 23% 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, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. CARD9Nature immunology · 2018
    Article
  6. Review
  7. Article
  8. 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

7 authors at 3 institutions in 1 country.

Karolina Maria BurghardtGroup for Improvement of Intestinal Function and Treatment (GIFT), Transplant Centre, Toronto, Ontario, Canada ; Division of Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, Toronto, Ontario, Canada.
Vishal AvinashiDivision of Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, BC Children Hospital, Vancouver, British Columbia, Canada.
Christina KosarGroup for Improvement of Intestinal Function and Treatment (GIFT), Transplant Centre, Toronto, Ontario, Canada.
Wei XuDalla Lana School of Public Health, University of Toronto, Toronto, Ontario, Canada.
Paul W WalesGroup for Improvement of Intestinal Function and Treatment (GIFT), Transplant Centre, Toronto, Ontario, Canada.
Yaron AvitzurGroup for Improvement of Intestinal Function and Treatment (GIFT), Transplant Centre, Toronto, Ontario, Canada ; Division of Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, Toronto, Ontario, Canada.
Aleixo MuiseDivision of Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, Toronto, Ontario, Canada ; SickKids IBD Centre, Program in Cell Biology, Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada.
British Columbia Children's Hospital · CASickKids Foundation · CAUniversity of Toronto · CA

Funding

Canadian Institutes of Health Research MOP119457
6 · The paper itself

Abstract

Recently, genetic associations have been described in intestinal transplants. Namely, Crohn's disease susceptibility gene NOD2 polymorphisms have been reported to be more prevalent in patients with graft failure following intestinal transplantation (IT). Therefore, we sought to determine if polymorphisms in the NOD2 signaling cascade, including NOD2, CARD9, RAC1 and ATG16L1 are associated with intestinal failure (IF) or its complications. We carried out a cross-sectional study of 59 children with IF and 500 healthy Caucasian controls. Using the Taqman platform we determined the prevalence of NOD2 as well as ATG16L1, RAC1 and CARD9 SNPs. NOD2 pathway polymorphisms were evaluated in relation to outcomes of episodes of sepsis, ICU admissions, hyperbilirubinemia and need for IT. We found that the minor allele of a CARD9 SNP was associated with protection from developing IF when compared to healthy controls and was also associated with decreased odds of sustained conjugated hyperbilirubinemia. Therefore, IF patients with CARD9 polymorphism are less likely to develop progressive liver disease and suggests that host innate immunity may play a role in IF associated liver disease.

Indexed as

Genetic Predisposition to DiseaseAdolescentAutophagy-Related ProteinsCARD Signaling Adaptor ProteinsCarrier ProteinsCase-Control StudiesChildChild, PreschoolDemographyFemaleGene FrequencyHumansHyperbilirubinemiaInfantIntestinesMaleATG16L1 protein, humanAutophagy-Related ProteinsCARD9 protein, humanCARD Signaling Adaptor ProteinsCarrier ProteinsNod2 Signaling Adaptor Proteinrac1 GTP-Binding ProteinRAC1 protein, human

Identifiers

PMID24465786
PMCPMC3897546
OpenAlexW2004597234

What OpenQuestion holds

Textmetadata
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.