Evidence map›Paper›PMID 31712860›Full record

ArticlePediatric cardiology2020

Identification of Gene Mutations in Primary Pediatric Cardiomyopathy by Whole Exome Sequencing.

Kitiwan Rojnueangnit, Boonchu Sirichongkolthong, Ratthapon Wongwandee, Thanitchet Khetkham, Saisuda Noojarern, Arthaporn Khongkraparn, Duangrurdee Wattanasirichaigoon

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Article in Pediatric cardiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Article
  2. Familial glucocorticoid deficiency due to a novelFrontiers in endocrinology · 2026
    Article
  3. Review
  4. Article
  5. Review
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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

7 authors.

Kitiwan RojnueangnitDepartment of Pediatrics, Faculty of Medicine, Thammasat University, Pathumthani, Thailand. rkitiwan@tu.ac.th.ORCID http://orcid.org/0000-0002-9488-4470
Boonchu SirichongkolthongDepartment of Pediatrics, Faculty of Medicine, Thammasat University, Pathumthani, Thailand.
Ratthapon WongwandeeDepartment of Pediatrics, Faculty of Medicine, Thammasat University, Pathumthani, Thailand.
Thanitchet KhetkhamDivison of Forensic Medicine, Thammasat University Hospital, Pathumthani, Thailand.
Saisuda NoojarernDivision of Medical Genetics, Department of Pediatrics, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand.
Arthaporn KhongkraparnDivision of Medical Genetics, Department of Pediatrics, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand.
Duangrurdee WattanasirichaigoonDivision of Medical Genetics, Department of Pediatrics, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand.

Funding

Thammasat University TP.2-10/2559
6 · The paper itself

Abstract

Pediatric primary cardiomyopathy is rare but serious, having high mortality; hypertrophic and dilated types are the most common. Its etiology has been mainly considered idiopathic; however, next generation sequencing techniques have revealed nearly half of idiopathic pediatric cases arose from specific genetic mutations. Therefore, our study aimed to identify the genetic causes of primary idiopathic cardiomyopathy. Newborns to 15-year old patients with this condition were recruited between March 2016 and May 2017 at Thammasat University Hospital. Complete patient history and physical examination data were collected by a geneticist with cardiac examinations and echocardiograms by pediatric cardiologists. Whole exome sequencing was performed for all. Of the 12 patients enrolled, 5 cases were dilated type and 7 hypertrophic. Two with dilated type were excluded during follow-up as cause was determined (hypocalcemia and pacemaker induced). A list of 118 genes for cardiomyopathy was analyzed in the remaining 10 cases. Pathogenic and likely pathogenic mutations were identified in 5 patients: HRAS, PTPN11, SOS1, FLNC and TXNRD2; half our patients were not actually idiopathic. Despite its high cost, genetic testing is useful for determining familial risk as well as predicting patient cardiomyopathy progress.

Indexed as

Exome SequencingAdolescentCardiomyopathiesChildChild, PreschoolEchocardiographyFemaleHumansInfantInfant, NewbornMaleMutationPedigreeProspective StudiesMutationsPediatricPrimary cardiomyopathyWhole exome sequencing

Identifiers

What OpenQuestion holds

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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.