Glycogen Debrancher Enzyme Deficiency Myopathy.


Journal

Journal of clinical neuromuscular disease
ISSN: 1537-1611
Titre abrégé: J Clin Neuromuscul Dis
Pays: United States
ID NLM: 100887391

Informations de publication

Date de publication:
01 Jun 2021
Historique:
entrez: 21 5 2021
pubmed: 22 5 2021
medline: 16 11 2021
Statut: ppublish

Résumé

Glycogen storage disease type III is a rare inherited disease caused by decreased activity of glycogen debranching enzyme. It affects primarily the liver, cardiac muscle, and skeletal muscle. Pure involvement of the skeletal muscle with adult onset is extremely rare. We report on a patient with myopathy due to glycogen storage disease III, and describe the clinical features, and pathologic and genetic findings.

Identifiants

pubmed: 34019008
doi: 10.1097/CND.0000000000000339
pii: 00131402-202106000-00007
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

224-227

Informations de copyright

Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved.

Déclaration de conflit d'intérêts

The authors report no conflicts of interest.

Références

Endo Y, Horinishi A, Vorgerd M, et al. Molecular analysis of the AGL gene: heterogeneity of mutations in patients with glycogen storage disease type III from Germany, Canada, Afghanistan, Iran, and Turkey. J Hum Genet. 2006;51:958–963.
Van Hoof F, Hers HG. The subgroups of type 3 glycogenosis. Eur J Biochem. 1967;2:265–270.
Aoyama Y, Ozer I, Demirkol M, et al. Molecular features of 23 patients with glycogen storage disease type III in Turkey: a novel mutation p.R1147G associated with isolated glucosidase deficiency, along with 9 AGL mutations. J Hum Genet. 2009;54:681–686.
Sugie H, Fukuda T, Ito M, et al. Novel exon 11 skipping mutation in a patient with glycogen storage disease type IIId. J Inherit Metab Dis. 2001;24:535–545.
Endo Y, Fateen E, El Shabrawy M, et al. Egyptian glycogen storage disease type III - identification of six novel AGL mutations, including a large 1.5 kb deletion and a missense mutation p.L620P with subtype IIId. Clin Chem Lab Med. 2009;47:1233–1238.
DiMauro S, Hartwig GB, Hays A, et al. Debrancher deficiency: neuromuscular disorder in 5 adults. Ann Neurol. 1979;5:422–436.
Cornelio F, Bresolin N, Singer PA, et al. Clinical varieties of neuromuscular disease in debrancher deficiency. Arch Neurol. 1984;41:1027–1032.
Goldstein JL, Austin SL, Boyette K, et al. Molecular analysis of the AGL gene: identification of 25 novel mutations and evidence of genetic heterogeneity in patients with Glycogen Storage Disease Type III. Genet Med. 2010;12:424–430.
Sentner CP, Hoogeveen IJ, Weinstein DA, et al. Glycogen storage disease type III: diagnosis, genotype, management, clinical course and outcome. J Inherit Metab Dis. 2016;39:697–704.
Dagli AI, Zori RT, McCune H, et al. Reversal of glycogen storage disease type IIIa-related cardiomyopathy with modification of diet. J Inherit Metab Dis. 2009;32(suppl 1):S103–S106.
Valayannopoulos V, Bajolle F, Arnoux JB, et al. Successful treatment of severe cardiomyopathy in glycogen storage disease type III with D,L-3-hydroxybutyrate, ketogenic and high-protein diet. Pediatr Res. 2011;70:638–641.

Auteurs

Menachem Sadeh (M)

Department of Neurology, Wolfson Medical Center Holon, Affiliated with Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel; and.

Keren Yosovich (K)

Molecular Genetic Laboratory, Edith Wolfson Medical Center, Holon, Israel .

Ron Dabby (R)

Department of Neurology, Wolfson Medical Center Holon, Affiliated with Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel; and.

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