A Case of Osteogenesis Imperfecta Type II With Additional Balanced Translocation t(1;20)(p13;p11.2).


Journal

Fetal and pediatric pathology
ISSN: 1551-3823
Titre abrégé: Fetal Pediatr Pathol
Pays: England
ID NLM: 101230972

Informations de publication

Date de publication:
Jun 2019
Historique:
pubmed: 4 4 2019
medline: 18 12 2019
entrez: 4 4 2019
Statut: ppublish

Résumé

Osteogenesis imperfect (OI) type II is a genetic disorder of bone characterized by bone fragility, multiple fractures, severe bowing and shortening of long bones, and perinatal death due to respiratory insufficiency. It is mainly caused by mutations in the COL1A1 or COL1A2 genes, inherited in an autosomal dominant manner. A fetal form of this disorder that included brachydactyly, macrocephaly, frontal bossing, soft calvarium, saddle nose, micrognathia, low set ears, and narrow thoracic cavity is described. A postmortem skeletal survey revealed multiple fractures, unossified skull, and long crumpled bones. The fetal karyotype revealed a balanced translocation t(1;20)(p13;p11.2). DNA sequencing detected a c.3065G > T transversion in exon 42 of the COL1A1 gene, a mutation associated with OI type II. Although the balanced translocation t(1:20)(p13;p11.2) appears to be incidental in our case, identification of the specific mutation and translocation is important for estimation of genetic risk for another afflicted child.

Sections du résumé

BACKGROUND BACKGROUND
Osteogenesis imperfect (OI) type II is a genetic disorder of bone characterized by bone fragility, multiple fractures, severe bowing and shortening of long bones, and perinatal death due to respiratory insufficiency. It is mainly caused by mutations in the COL1A1 or COL1A2 genes, inherited in an autosomal dominant manner.
CASE REPORT METHODS
A fetal form of this disorder that included brachydactyly, macrocephaly, frontal bossing, soft calvarium, saddle nose, micrognathia, low set ears, and narrow thoracic cavity is described. A postmortem skeletal survey revealed multiple fractures, unossified skull, and long crumpled bones. The fetal karyotype revealed a balanced translocation t(1;20)(p13;p11.2). DNA sequencing detected a c.3065G > T transversion in exon 42 of the COL1A1 gene, a mutation associated with OI type II.
CONCLUSION CONCLUSIONS
Although the balanced translocation t(1:20)(p13;p11.2) appears to be incidental in our case, identification of the specific mutation and translocation is important for estimation of genetic risk for another afflicted child.

Identifiants

pubmed: 30942118
doi: 10.1080/15513815.2019.1579877
doi:

Substances chimiques

Collagen Type I 0
Collagen Type I, alpha 1 Chain 0

Types de publication

Case Reports Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

263-271

Auteurs

Nasma K Majeed (NK)

a Pathology Department , University of Illinois at Chicago , Chicago , IL , USA.

Diana Oramas (D)

a Pathology Department , University of Illinois at Chicago , Chicago , IL , USA.

Valerie Lindgren (V)

a Pathology Department , University of Illinois at Chicago , Chicago , IL , USA.

Steven Garzon (S)

a Pathology Department , University of Illinois at Chicago , Chicago , IL , USA.

Dr Elizabeth Wiley (DE)

a Pathology Department , University of Illinois at Chicago , Chicago , IL , USA.

Christopher Enakpene (C)

a Pathology Department , University of Illinois at Chicago , Chicago , IL , USA.

Rajyasree Emmadi (R)

a Pathology Department , University of Illinois at Chicago , Chicago , IL , USA.

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Classifications MeSH