Hypoxia: A teratogen underlying a range of congenital disruptions, dysplasias, and malformations.
brain malformation
carbon monoxide poisoning
hypoxia
stroke
teratogen
Journal
American journal of medical genetics. Part A
ISSN: 1552-4833
Titre abrégé: Am J Med Genet A
Pays: United States
ID NLM: 101235741
Informations de publication
Date de publication:
09 2021
09 2021
Historique:
revised:
12
03
2021
received:
08
12
2020
accepted:
15
04
2021
pubmed:
4
5
2021
medline:
21
1
2022
entrez:
3
5
2021
Statut:
ppublish
Résumé
In this review, we explore evidence that hypoxia in the developing human fetus can lead not only to the more commonly accepted disruptive-type defects, but also patterns of anomalies that suggest that hypoxia can exert a more classic teratogenic effect, using the brain as one example. We review neuropathology in the context of intrauterine hypoxia, particularly as it relates to carbon monoxide poisoning, in utero strokes, and homozygous alpha-thalassemia. In general, the associated brain injuries resemble those seen with other causes of hypoxic-ischemic injury. Fetal strokes during development usually lead to loss of brain tissue in areas that do not follow a typical embryologic pattern, and therefore are considered disruptions. However, there is also evidence that fetal brain ischemia can cause more classically recognized patterns of abnormal embryonic neuronal migration and organization such as polymicrogyria, cortical dysplasia, or dysgenesis, including select types of focal cortical dysplasia. This study summarizes available literature and evidence to raise clinicians' awareness regarding the association between hypoxia and congenital anomalies, including brain malformations.
Identifiants
pubmed: 33938618
doi: 10.1002/ajmg.a.62235
pmc: PMC8683554
mid: NIHMS1761695
doi:
Substances chimiques
Teratogens
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
2801-2808Subventions
Organisme : NICHD NIH HHS
ID : P50 HD103524
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS092772
Pays : United States
Informations de copyright
© 2021 Wiley Periodicals LLC.
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