Evidence map›Paper›PMID 37482595›Full record

ArticleInternational journal of legal medicine2024

Clinical exome sequencing elucidates underlying cause of death in sudden unexpected death of infants: two case reports.

Laura Jane Heathfield, Lorna Jean Martin, Yolande van der Heyde, Itumeleng Molefe, Raj Ramesar

Open access · hybridAbstract readCase Reports
In one paragraph

Article in International journal of legal medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed, 1 pooled it
0.5field-weighted citation impact, top 41% 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

2 citing papers in PubMed, 1 synthesis or guideline pooled it, 3 citations in OpenAlex.

  1. Pooled it
  2. 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

5 authors at 1 institution in 1 country.

Laura Jane HeathfieldDivision of Forensic Medicine and Toxicology, Department of Pathology, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa. laura.heathfield@uct.ac.za.ORCID http://orcid.org/0000-0002-4860-9419
Lorna Jean MartinDivision of Forensic Medicine and Toxicology, Department of Pathology, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa.
Yolande van der HeydeDivision of Forensic Medicine and Toxicology, Department of Pathology, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa.
Itumeleng MolefeDivision of Forensic Medicine and Toxicology, Department of Pathology, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa.
Raj RamesarMRC/UCT Research Unit for Genomic and Precision Medicine, Division of Human Genetics, Institute of Infectious Diseases and Molecular Medicine, Department of Pathology, University of Cape Town, Cape Town, South Africa.
University of Cape Town · ZA

Funding

National Health Laboratory Service GRANT004 94623University of Cape Town Research Office
6 · The paper itself

Abstract

Sudden unexpected death in infants (SUDI) is a traumatic event for families, and unfortunately its occurrence remains high in many parts of the world. Whilst cause of death is resolved for most cases, others remain undetermined following postmortem investigations. There has been a recognition of the role of genetic testing in unexplained cases, where previous studies have demonstrated the resolution of cases through DNA analyses. Here we present two case reports of SUDI cases admitted to Salt River Mortuary, South Africa, and show that underlying causes of death were determined for both infants using clinical exome sequencing. The first infant was heterozygous for a variant (rs148175795) in COL6A3, which suggested a bronchopulmonary dysplasia phenotype. This hypothesis led to finding of a second candidate variant in DMP1 (rs142880465), which may contribute towards a digenic/polygenic mechanism of a more severe phenotype. Histological analysis of retained tissue sections showed an asphyxial mechanism of death, where bronchiolar muscle weakness from an underlying bronchopulmonary dysplasia may have contributed to the asphyxia by affecting respiration. In the second infant, a homozygous variant (rs201340753) was identified in MASP1, which was heterozygous in each parent, highlighting the value of including parental DNA in genetic studies. Whilst mannose-binding lectin deficiency could not be assessed, it is plausible that this variant may have acted in combination with other risk factors within the triple-risk model to result in sudden death. These results may have genetic implications for family members, and represent possible new candidate variants for molecular autopsies.

Indexed as

Bronchopulmonary DysplasiaSudden Infant DeathAsphyxiaCause of DeathDNAExome SequencingHumansInfantInfant, NewbornDNABronchopulmonary dysplasiaMannose-binding lectin deficiencyMolecular autopsyPolygenic mechanismPostmortem forensic geneticsSudden unexpected death in infants (SUDI)

Identifiers

PMID37482595
PMCPMC10861614
OpenAlexW4385175052

What OpenQuestion holds

Textmetadata
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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.