Evidence map›Paper›PMID 32318853›Full record

ReviewHuman genetics2020

Genetic innovations and our understanding of stillbirth.

Louise Wilkins-Haug

Abstract readReview
PubMed Publisher
In one paragraph

Review in Human genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Genetics and Stillbirth.Clinics in perinatology · 2026
    Review
  2. Placental Pathology Findings in Unexplained Pregnancy Losses.Reproductive sciences (Thousand Oaks, Calif.) · 2024
    Article
  3. Article
  4. Familial aggregation of stillbirth: A pedigree analysis of a matched case-control study.BJOG : an international journal of obstetrics and gynaecology · 2023
    Article
  5. Article
  6. Article
  7. Extreme Heat and Pregnancy Outcomes: A Scoping Review of the Epidemiological Evidence.International journal of environmental research and public health · 2022
    Article
  8. Article
  9. Recurrent Pregnancy Loss and Concealed Long-QT Syndrome.Journal of the American Heart Association · 2021
    Article
  10. Article
  11. Article
  12. 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

1 author.

Louise Wilkins-HaugDivision of Maternal Fetal Medicine, Department of Obstetrics, Gynecology and Reproductive Biology, Brigham and Women's Hospital, Harvard Medical School, 75 Francis Street, Boston, MA, 01770, USA. LWilkinshaug@partners.org.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stillbirth after 20 weeks gestation happens in 1 in 200 pregnancies and occurs more commonly than neonatal loss and sudden infant death syndrome (SIDs) combined. The stillbirth rate is several times greater in low as opposed to high-resource countries. However, among high-resource countries, although a lower overall stillbirth rate exists, there has been little change for several decades. Molecular genetic technologies are emerging as important contributors to our understanding of stillbirth. Initially, genetic etiologies included alterations in chromosome number or structure such as aneuploidy and microduplications and deletions. More recently, next-generation sequencing analysis in two genetic conditions, Smith Lemli Optiz Syndrome (SLOs) and the channelopathy disorders (such as long QT syndrome (LQTS)) provide examples into the association of pathogenic gene variants with stillbirth. Although these specific conditions individually account for only a small number of stillbirths, investigating these disorders provides a new and innovative approach for further understanding genetic contributors to adverse pregnancy outcomes. Our knowledge of the role of genetic disease as an etiology for stillbirth is elementary. Genomic interrogation of maternal-fetal genotypes, gene-gene, and genotype-environment interaction is lacking in stillbirth research. At the DNA sequence level, further investigation of variants of unknown significance is an opportunity for exploration of biologic pathways of importance to pregnancy loss. This review concentrates on SLO as an example of a single gene disorder with a high carrier but low affected liveborn proband rate. The channelopathy disorders are included as initial examples of genetic conditions with variable presentation including an association with sudden infant death syndrome. Highlighted are the challenges when numerous genes and variants are involved, and the task of assigning pathogenicity. The advantages and limitations of genetic evaluations are presented and avenues for further research considered.

Indexed as

ChannelopathiesChromosome AberrationsExome SequencingFemaleGestational AgeHumansInfant, NewbornPregnancySmith-Lemli-Opitz SyndromeStillbirth

Identifiers

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.