| Literature DB >> 30140196 |
Pascaline Letard1, Dorien Schepers2, Juliette Albuisson3, Patrick Bruneval4, Emmanuel Spaggiari1, Gerarda Van de Beek2, Suonavy Khung-Savatovsky1, Nadia Belarbi5, Yline Capri6, Anne-Lise Delezoide1, Bart Loeys2, Fabien Guimiot1.
Abstract
EFEMP2 mutations are known to be responsible for autosomal recessive cutis laxa type 1B (ARCL1B), a rare multisystem disease affecting skin, skeleton, and vascular structures. We report 2 additional related cases of ARCL1B of particular severity leading to termination of pregnancy. Cardinal signs of this connective tissue disease were already seen during the second trimester of pregnancy, then confirmed and clarified at autopsy. Anomalies included cutis laxa, arachnodactyly, clubfoot, wormian bones, moderate bowing of long bones with slender bone trabeculae, rib fractures, undermuscularized diaphragm, hiatal hernia, and arterial tortuosity with thick vascular walls and disorganized elastic fibers. Sequencing of the EFEMP2 gene revealed a novel homozygous nonsense mutation: c.639C>A (p.Cys213*). We performed a thorough histological analysis and discuss differential diagnoses, genotype-phenotype correlations, and the challenge of prenatal diagnosis of this disease.Entities:
Keywords: Arterial tortuosity; Autopsy; Autosomal recessive cutis laxa type 1B; Bone fractures; EFEMP2; Elastic tissue; FBLN4; Fetus; Fibulin-4; Prenatal diagnosis
Year: 2018 PMID: 30140196 PMCID: PMC6103346 DOI: 10.1159/000489838
Source DB: PubMed Journal: Mol Syndromol ISSN: 1661-8769