Evidence map›Paper›PMID 25101798›Full record

ArticleGenes and immunity2014

High-density genotyping of immune loci in Kawasaki disease and IVIG treatment response in European-American case-parent trio study.

A Shendre, H W Wiener, D Zhi, A I Vazquez, M A Portman, S Shrestha

Open access · bronzeAbstract read
In one paragraph

Article in Genes and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 11% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Homozygous ofFrontiers in genetics · 2021
    Article
  6. Article
  7. Article
  8. Article
  9. Observational
  10. Review
  11. Dissecting Kawasaki disease: a state-of-the-art review.European journal of pediatrics · 2017
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
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

6 authors at 2 institutions in 1 country.

A ShendreDepartment of Epidemiology, University of Alabama at Birmingham, Birmingham, AL, USA.
H W WienerDepartment of Epidemiology, University of Alabama at Birmingham, Birmingham, AL, USA.
D ZhiDepartment of Biostatistics, University of Alabama at Birmingham, Birmingham, AL, USA.
A I VazquezDepartment of Biostatistics, University of Alabama at Birmingham, Birmingham, AL, USA.
M A PortmanDepartment of Pediatrics, University of Washington, Seattle Children's Research Institute, Seattle, WA, USA.
S ShresthaDepartment of Epidemiology, University of Alabama at Birmingham, Birmingham, AL, USA.
University of Alabama at Birmingham · USSeattle Children's Hospital · US

Funding

FcR Mutations in Kawasaki DiseaseR21HL090558 · NHLBI · SEATTLE CHILDREN'S HOSPITAL · PI PORTMAN, MICHAEL A · 2007 to 2008
$466k
NHLBI NIH HHS R21 HL090558PHS HHS NHLBI-R21-HL90558
6 · The paper itself

Abstract

Kawasaki disease (KD) is a diffuse and acute small-vessel vasculitis observed in children, and has genetic and autoimmune components. We genotyped 112 case-parent trios of European decent (confirmed by ancestry informative markers) using the immunoChip array, and performed association analyses with susceptibility to KD and intravenous immunoglobulin (IVIG) non-response. KD susceptibility was assessed using the transmission disequilibrium test, whereas IVIG non-response was evaluated using multivariable logistic regression analysis. We replicated single-nucleotide polymorphisms (SNPs) in three gene regions (FCGR, CD40/CDH22 and HLA-DQB2/HLA-DOB) that have been previously associated with KD and provide support to other findings of several novel SNPs in genes with a potential pathway in KD pathogenesis. SNP rs838143 in the 3'-untranslated region of the FUT1 gene (2.7 × 10(-5)) and rs9847915 in the intergenic region of LOC730109 | BRD7P2 (6.81 × 10(-7)) were the top hits for KD susceptibility in additive and dominant models, respectively. The top hits for IVIG responsiveness were rs1200332 in the intergenic region of BAZ1A | C14orf19 (1.4 × 10(-4)) and rs4889606 in the intron of the STX1B gene (6.95 × 10(-5)) in additive and dominant models, respectively. Our study suggests that genes and biological pathways involved in autoimmune diseases have an important role in the pathogenesis of KD and IVIG response mechanism.

Indexed as

3' Untranslated RegionsChildChild, PreschoolFemaleFucosyltransferasesGalactoside 2-alpha-L-fucosyltransferaseGenetic Predisposition to DiseaseGenotypeGenotyping TechniquesHumansImmunoglobulins, IntravenousInfantIntronsLogistic ModelsMaleMucocutaneous Lymph Node Syndrome3' Untranslated RegionsFucosyltransferasesGalactoside 2-alpha-L-fucosyltransferaseImmunoglobulins, IntravenousSyntaxin 1

Identifiers

PMID25101798
PMCPMC4257866
OpenAlexW2044562002

What OpenQuestion holds

Textmetadata
LicenceTDM
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.