Evidence map›Paper›PMID 25266886›Full record

ArticlePediatric cardiology2015

Common variants in the CRP promoter are associated with a high C-reactive protein level in Kawasaki disease.

Jae-Jung Kim, Sin Weon Yun, Jeong Jin Yu, Kyung Lim Yoon, Kyung-Yil Lee, Hong-Ryang Kil, Gi Beom Kim, Myung Ki Han, Min Seob Song, Hyoung Doo Lee and 6 more

Abstract readMulticenter Study
PubMed Publisher
In one paragraph

Article in Pediatric cardiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 28% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. The Impact ofDiagnostics (Basel, Switzerland) · 2023
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Establishment of Kawasaki disease database based on metadata standard.Database : the journal of biological databases and curation · 2016
    Article
  12. 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

16 authors at 11 institutions in 1 country.

Jae-Jung KimAsan Institute for Life Sciences, University of Ulsan College of Medicine, 88 Olympic-Ro 43-Gil, Songpa-Gu, Seoul, 138-736, Korea.
Sin Weon Yun
Jeong Jin Yu
Kyung Lim Yoon
Kyung-Yil Lee
Hong-Ryang Kil
Gi Beom Kim
Myung Ki Han
Min Seob Song
Hyoung Doo Lee
Jung Hye Byeon
Saejung Sohn
Young Mi Hong
Gi Young Jang
Jong-Keuk Lee
Korean Kawasaki Disease Genetics Consortium
Ewha Womans University · KRKorea University Medical Center · KRUlsan College · KRUniversity of Ulsan · KRChung-Ang University Hospital · KRChungnam National University Hospital · KRInje University Busan Paik Hospital · KRKyung Hee University Hospital at Gangdong · KRPusan National University Hospital · KRSeoul National University Children's Hospital · KRThe Catholic University of Korea Daejeon St. Mary's Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Kawasaki disease (KD) is an acute self-limiting form of vasculitis that afflicts infants and children and manifests as fever and signs of mucocutaneous inflammation. Children with KD show various laboratory inflammatory abnormalities, such as elevations in their white blood cell (WBC) count, C-reactive protein (CRP) level, and erythrocyte sedimentation rate (ESR). We here performed a genome-wide association study (GWAS) of 178 KD patients to identify the genetic loci that influence 10 important KD laboratory markers: WBC count, neutrophil count, platelet count, CRP, ESR, hemoglobin, aspartate aminotransferase (AST), alanine aminotransferase (ALT), albumin, and total protein. A total of 165 loci passed our arbitrary stage 1 threshold for replication (p < 1 × 10(-5)). Of these, only 2 SNPs (rs12068753 and rs4786091) demonstrated a significant association with the CRP level in replication study of 473 KD patients (p < 0.05). The SNP located at the CRP locus (rs12068753) demonstrated the most significant association with CRP in KD patients (beta = 4.73 and p = 1.20 × 10(-6) according to the stage 1 GWAS; beta = 3.65 and p = 1.35 × 10(-8) according to the replication study; beta = 3.97 and p = 1.11 × 10(-13) according to combined analysis) and explained 8.1% of the phenotypic variation observed. However, this SNP did not demonstrate any significant association with CRP in the general population (beta = 0.37 and p = 0.1732) and only explained 0.1% of the phenotypic variation in this instance. Furthermore, rs12068753 did not affect the development of coronary artery lesions or intravenous immunoglobulin resistance in KD patients. These results indicate that common variants in the CRP promoter can play an important role in the CRP levels in KD.

Indexed as

Alanine TransaminaseAspartate AminotransferasesBlood SedimentationChild, PreschoolC-Reactive ProteinFemaleGenetic LociGenome-Wide Association StudyGenotyping TechniquesGranulomatous Disease, ChronicHemoglobinsHumansInfantLeukocyte CountMaleMucocutaneous Lymph Node SyndromeAlanine TransaminaseAspartate AminotransferasesC-Reactive ProteinHemoglobinsNADPH OxidasesSerum Albumin

Identifiers

PMID25266886
OpenAlexW2091631658

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.