HADHA and HADHB gene associated phenotypes - Identification of rare variants in a patient cohort by Next Generation Sequencing.


Journal

Molecular and cellular probes
ISSN: 1096-1194
Titre abrégé: Mol Cell Probes
Pays: England
ID NLM: 8709751

Informations de publication

Date de publication:
04 2019
Historique:
received: 13 12 2018
revised: 17 01 2019
accepted: 20 01 2019
pubmed: 27 1 2019
medline: 7 5 2019
entrez: 26 1 2019
Statut: ppublish

Résumé

The heterooctameric mitochondrial trifunctional protein (MTP), composed of four α- and β-subunits harbours three enzymes that each perform a different function in mitochondrial fatty acid β-oxidation. Pathogenic variants in the MTP genes (HADHA and HADHB) cause MTP deficiency, a rare autosomal recessive metabolic disorder characterized by phenotypic heterogeneity ranging from severe, early-onset, cardiac disease to milder, later-onset, myopathy and neuropathy. Since metabolic myopathies and neuropathies are a group of rare genetic disorders and their associated muscle symptoms may be subtle, the diagnosis is often delayed. Here we evaluated data of 161 patients with myopathy and 242 patients with neuropathy via next generation sequencing (NGS) and report the diagnostic yield in three patients of this cohort by the detection of disease-causing variants in the HADHA or HADHB gene. The mitigated phenotypes of this treatable disease were missed by the newborn screening, highlighting the importance of phenotype-based NGS analysis in patients with rare and clinically very variable disorders such as MTP deficiency.

Identifiants

pubmed: 30682426
pii: S0890-8508(18)30322-0
doi: 10.1016/j.mcp.2019.01.003
pii:
doi:

Substances chimiques

HADHA protein, human EC 1.1.1.211
Mitochondrial Trifunctional Protein, alpha Subunit EC 1.1.1.211
HADHB protein, human EC 2.3.1.16
Mitochondrial Trifunctional Protein EC 2.3.1.16
Mitochondrial Trifunctional Protein, beta Subunit EC 2.3.1.16

Types de publication

Case Reports Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

14-20

Subventions

Organisme : Medical Research Council
ID : G1000848
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/N010035/1
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/N025431/1
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/N025431/2
Pays : United Kingdom

Informations de copyright

Copyright © 2019. Published by Elsevier Ltd.

Auteurs

Isabel Diebold (I)

Medical Genetics Center, Munich, Germany.

Ulrike Schön (U)

Medical Genetics Center, Munich, Germany.

Rita Horvath (R)

Department of Clinical Neuroscience, University of Cambridge, Cambridge, UK.

Oliver Schwartz (O)

Department of Neuropediatrics, University Children's Hospital Muenster, Muenster, Germany.

Elke Holinski-Feder (E)

Medical Genetics Center, Munich, Germany.

Heike Kölbel (H)

Department of Pediatric Neurology, Developmental Neurology and Social Pediatrics, University of Essen, Germany.

Angela Abicht (A)

Medical Genetics Center, Munich, Germany; Department of Neurology, Friedrich-Baur-Institute, Klinikum der Ludwig-Maximilians-University, Munich, Germany. Electronic address: angela.abicht@mgz-muenchen.de.

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Classifications MeSH