Novel pathogenic variants in GBE1 causing fetal akinesia deformation sequence and severe neuromuscular form of glycogen storage disease type IV.
Journal
Clinical dysmorphology
ISSN: 1473-5717
Titre abrégé: Clin Dysmorphol
Pays: England
ID NLM: 9207893
Informations de publication
Date de publication:
Jan 2019
Jan 2019
Historique:
pubmed:
12
10
2018
medline:
26
3
2019
entrez:
11
10
2018
Statut:
ppublish
Résumé
Glycogen storage disease IV (GSD IV), caused by a defect in GBE1, is a clinically heterogeneous disorder. A classical hepatic form and a neuromuscular form have been described. The severe neuromuscular form presents as a fetal akinesia deformation sequence or a congenital subtype. We ascertained three unrelated families with fetuses/neonates who presented with fetal akinesia deformation sequence to our clinic for genetic counseling. We performed a detailed clinical evaluation, exome sequencing, and histopathology examination of two fetuses and two neonates from three unrelated families presenting with these perinatally lethal neuromuscular forms of GSD IV. Exome sequencing in the affected fetuses/neonates identified four novel pathogenic variants (c.1459G>T, c.144-1G>A, c.1680C>G, and c.1843G>C) in GBE1 (NM_000158). Histopathology examination of tissues from the affected fetuses/neonate was consistent with the diagnosis. Here, we add three more families with the severe perinatally lethal neuromuscular forms of GSD IV to the GBE1 mutation spectrum.
Identifiants
pubmed: 30303820
doi: 10.1097/MCD.0000000000000248
doi:
Substances chimiques
Glycogen Debranching Enzyme System
0
GBE1 protein, human
EC 2.4.1.18
Types de publication
Case Reports
Journal Article
Langues
eng
Sous-ensembles de citation
IM