| Literature DB >> 28416349 |
Sandra Donkervoort1, Sophelia H S Chan2, Leslie H Hayes3, Nathaniel Bradley1, David Nguyen1, Meganne E Leach4, Payam Mohassel1, Ying Hu1, Mathula Thangarajh5, Diana Bharucha-Goebel4, Amanda Kan6, Ronnie S L Ho6, Christine A Reyes5, Jessica Nance7, Steven A Moore8, A Reghan Foley1, Carsten G Bönnemann9.
Abstract
Mutations in ACTA1 cause a group of myopathies with expanding clinical and histopathological heterogeneity. We describe three patients with severe ACTA1-related myopathy who have muscle fiber cytoplasmic bodies but no classic nemaline rods. Patient 1 is a five-year-old boy who presented at birth with severe weakness and respiratory failure, requiring mechanical ventilation. Whole exome sequencing identified a heterozygous c.282C>A (p.Asn94Lys) ACTA1 mutation. Patients 2 and 3 were twin boys with hypotonia, severe weakness, and respiratory insufficiency at birth requiring mechanical ventilation. Both died at 6 months of age. The same heterozygous c.282C>A (p.Asn94Lys) ACTA1 mutation was identified by whole exome sequencing. We conclude that clinically severe ACTA1-related myopathy can present with muscle morphological findings suggestive of cytoplasmic body myopathy in the absence of definite nemaline rods. The Asn94Lys mutation in skeletal muscle sarcomeric α-actin may be linked to this histological appearance. These novel ACTA1 cases also illustrate the successful application of whole exome sequencing in directly arriving at a candidate genetic diagnosis in patients with unexpected phenotypic and histologic features for a known neuromuscular gene.Entities:
Keywords: ACTA1; Congenital myopathies; Cytoplasmic bodies; Skeletal muscle α-actin
Mesh:
Substances:
Year: 2017 PMID: 28416349 PMCID: PMC5918412 DOI: 10.1016/j.nmd.2017.02.012
Source DB: PubMed Journal: Neuromuscul Disord ISSN: 0960-8966 Impact factor: 4.296