Long read sequencing overcomes challenges in the diagnosis of SORD neuropathy.


Journal

Journal of the peripheral nervous system : JPNS
ISSN: 1529-8027
Titre abrégé: J Peripher Nerv Syst
Pays: United States
ID NLM: 9704532

Informations de publication

Date de publication:
06 2022
Historique:
revised: 13 02 2022
received: 05 11 2021
accepted: 22 02 2022
pubmed: 1 3 2022
medline: 9 6 2022
entrez: 28 2 2022
Statut: ppublish

Résumé

Biallelic mutations in sorbitol dehydrogenase (SORD) have been recently identified as a common cause of recessive axonal Charcot-Marie-Tooth neuropathy (CMT2). We aimed to assess a novel long-read sequencing approach to overcome current limitations in SORD neuropathy diagnostics due to the SORD2P pseudogene and the phasing of biallelic mutations in recessive disease. We conducted a screen of our Australian whole exome sequencing (WES) CMT cohort to identify individuals with homozygous or compound heterozygous SORD variants. Individuals detected with SORD mutations then underwent long-read sequencing, clinical assessment, and serum sorbitol analysis. An individual was detected with compound heterozygous truncating mutations in SORD exon 7, NM_003104.5:c.625C>T (p.Arg209Ter) and NM_003104.5:c.757del (p.Ala253GlnfsTer27). Subsequent Oxford Nanopore Tech (ONT) long-read sequencing was used to successfully differentiate SORD from the highly homologous non-functional SORD2P pseudogene and confirmed that the mutations were biallelic through haplotype-resolved analysis. The patient presented with axonal sensorimotor polyneuropathy (CMT2) and ulnar neuropathy without compression at the elbow. Burning neuropathic pain in the forearms and feet was also reported and was exacerbated by alcohol consumption and improved with alcohol cessation. UPLC-tandem mass spectrometry confirmed that the patient had elevated serum sorbitol levels (12.0 mg/L) consistent with levels previously observed in patients with biallelic SORD mutations. This represents a novel clinical presentation and expands the phenotype associated with biallelic SORD mutations causing CMT2. Our study is the first report of long-read sequencing for an individual with CMT and demonstrates the utility of this approach for clinical genomics.

Identifiants

pubmed: 35224818
doi: 10.1111/jns.12485
doi:

Substances chimiques

Sorbitol 506T60A25R
L-Iditol 2-Dehydrogenase EC 1.1.1.14

Types de publication

Case Reports Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

120-126

Subventions

Organisme : Medical Research Council
ID : MR/T001712/1
Pays : United Kingdom

Commentaires et corrections

Type : CommentIn

Informations de copyright

© 2022 Peripheral Nerve Society.

Références

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Auteurs

Bianca R Grosz (BR)

Northcott Neuroscience Laboratory, ANZAC Research Institute, Concord, New South Wales, Australia.

Igor Stevanovski (I)

Kinghorn Centre for Clinical Genomics, Garvan Institute of Medical Research, Sydney, New South Wales, Australia.

Sara Negri (S)

Istituiti Clinici Scientifici Maugeri IRCCS, Environmental Research Center, Pavia, Italy.

Melina Ellis (M)

Northcott Neuroscience Laboratory, ANZAC Research Institute, Concord, New South Wales, Australia.
Sydney Medical School, University of Sydney, Camperdown, New South Wales, Australia.

Stephanie Barnes (S)

Sydney Medical School, University of Sydney, Camperdown, New South Wales, Australia.
Department of Neurology, Concord Repatriation General Hospital, Concord, New South Wales, Australia.
Faculty of Medicine, University of Notre Dame, Sydney, New South Wales, Australia.
Department of Neurology, Hornsby Ku-Ring-Gai Hospital, Sydney, New South Wales, Australia.

Stephen Reddel (S)

Sydney Medical School, University of Sydney, Camperdown, New South Wales, Australia.
Department of Neurology, Concord Repatriation General Hospital, Concord, New South Wales, Australia.

Steve Vucic (S)

Sydney Medical School, University of Sydney, Camperdown, New South Wales, Australia.
Department of Neurology, Concord Repatriation General Hospital, Concord, New South Wales, Australia.

Garth A Nicholson (GA)

Sydney Medical School, University of Sydney, Camperdown, New South Wales, Australia.
Department of Neurology, Concord Repatriation General Hospital, Concord, New South Wales, Australia.
Molecular Medicine Laboratory, Concord Repatriation General Hospital, Concord, New South Wales, Australia.

Andrea Cortese (A)

MRC Center for Neuromuscular Diseases, Department of Neuromuscular Diseases, UCL Queen Square Institute of Neurology, London, UK.
Department of Brain and Behavioral Sciences, University of Pavia, Pavia, Italy.

Kishore R Kumar (KR)

Kinghorn Centre for Clinical Genomics, Garvan Institute of Medical Research, Sydney, New South Wales, Australia.
Sydney Medical School, University of Sydney, Camperdown, New South Wales, Australia.
Department of Neurology, Concord Repatriation General Hospital, Concord, New South Wales, Australia.
Molecular Medicine Laboratory, Concord Repatriation General Hospital, Concord, New South Wales, Australia.

Ira W Deveson (IW)

Kinghorn Centre for Clinical Genomics, Garvan Institute of Medical Research, Sydney, New South Wales, Australia.
St Vincent's Clinical School, University of New South Wales, Sydney, New South Wales, Australia.

Marina L Kennerson (ML)

Northcott Neuroscience Laboratory, ANZAC Research Institute, Concord, New South Wales, Australia.
Sydney Medical School, University of Sydney, Camperdown, New South Wales, Australia.
Molecular Medicine Laboratory, Concord Repatriation General Hospital, Concord, New South Wales, Australia.

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