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Glycogenin-1 deficiency mimicking limb-girdle muscular dystrophy.
Lefeuvre, Claire; Schaeffer, Stéphane; Carlier, Robert-Yves; Fournier, Maxime; Chapon, Françoise; Biancalana, Valérie; Nicolas, Guillaume; Malfatti, Edoardo; Laforêt, Pascal.
Afiliación
  • Lefeuvre C; Neurology Department, Raymond Poincaré University Hospital, Garches, APHP, France.
  • Schaeffer S; Centre de Référence de Pathologie Neuromusculaire Nord-Est-Ile-de-France, France.
  • Carlier RY; Neurology department, Caen University Hospital, France.
  • Fournier M; Radiology Department, DMU Smart Imaging Raymond Poincaré Hospital, Garches, GH, Université Paris Saclay, APHP, France.
  • Chapon F; U 1179 INSERM, Université Versailles Saint Quentin en Yvelines, Paris, Saclay, France.
  • Biancalana V; Neurology department, Caen University Hospital, France.
  • Nicolas G; Anatomo-pathology Department, Caen Universitary Hospital, INSERM U 1075, France.
  • Malfatti E; Laboratoire Diagnostic Génétique, Faculté de Médecine-CHRU, Strasbourg, France.
  • Laforêt P; Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), INSERM U964, CNRS UMR 7104, Fédération de Médecine Translationnelle de Strasbourg, Université de Strasbourg, Illkirch, France.
Mol Genet Metab Rep ; 24: 100597, 2020 Sep.
Article en En | MEDLINE | ID: mdl-32477874
Glycogen storage disease type XV (GSD XV) is a recently described muscle glycogenosis due to glycogenin-1 (GYG1) deficiency characterized by the presence of polyglucosan bodies on muscle biopsy (Polyglucosan body myopathy-2, PGBM2). Here we describe a 44 year-old man with limb-girdle muscle weakness mimicking a limb-girdle muscular dystrophy (LGMD), and early onset exertional myalgia. Neurologic examination revealed a waddling gait with hyperlordosis, bilateral asymmetric scapular winging, mild asymmetric deltoid and biceps brachii weakness, and pelvic-girdle weakness involving the gluteal muscles and, to a lesser extent, the quadriceps. Serum creatine kinase levels were slightly elevated. Electrophysiological examination showed a myopathic pattern. There was no cardiac or respiratory involvement. Whole-body muscle MRI revealed atrophy and fat replacement of the tongue, biceps brachii, pelvic girdle and erector spinae. A deltoid muscle biopsy showed the presence of PAS-positive inclusions that remained non-digested with alpha-amylase treatment. Electron microscopy studies confirmed the presence of polyglucosan bodies. A diagnostic gene panel designed by the Genetic Diagnosis Laboratory of Strasbourg University Hospital (France) for 210 muscular disorders genes disclosed two heterozygous, pathogenic GYG1 gene mutations (c.304G>C;p.(Asp102His) + c.164_165del). Considering the clinical heterogeneity found in the previously described 38 GYG-1 deficient patients, we suggest that GYG1 should be systematically included in targeted NGS gene panels for LGMDs, distal myopathies, and metabolic myopathies.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Mol Genet Metab Rep Año: 2020 Tipo del documento: Article País de afiliación: Francia

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Mol Genet Metab Rep Año: 2020 Tipo del documento: Article País de afiliación: Francia
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