Available online at www.sciencedirect.com
Neuromuscular Disorders 28 (2018) 633–638
www.elsevier.com/locate/nmd
Case report
A new mutation of the SCGA gene is the cause of a late onset mild
phenotype limb girdle muscular dystrophy type 2D with axial involvement
Lidia Gonzalez-Quereda
a,1
, Eduard Gallardo
b,1
, Ana Töpf
c
, Alicia Alonso-Jimenez
d
,
Volker Straub
c
, Maria Jose Rodriguez
e
, Cinta Lleixa
d
, Isabel Illa
b
, Pia Gallano
a,*
,
Jordi Diaz-Manera
b,*
a
Genetics Department, Centro de Investigación Biomédica en Red en Enfermedades Raras (CIBERER CB06/07/0011), Hospital de la Santa Creu I Sant Pau,
IIB Sant Pau, C/Sant Antoni Mª Claret 167, Barcelona, Spain
b
Neuromuscular disorders Unit, Neurology Department, Centro de Investigación Biomédica en Red en Enfermedades Raras (CIBERER CB06/05/0030),
Universitat Autònoma de Barcelona, Hospital de la Santa Creu I Sant Pau, C/Sant Antoni Mª Claret 167, Barcelona, Spain
c
The John Walton Muscular Dystrophy Research Centre, MRC Centre for Neuromuscular disorders, Institute of Genetic Medicine, Central Parkway,
Newcastle Upon Tyne, UK
d
Neuromuscular disorders Unit, Neurology department, Universitat Autònoma de Barcelona, Hospital de la Santa Creu I Sant Pau, Barcelona, Spain
e
Genetics Department, Hospital de la Santa Creu I Sant Pau, IIB Sant Pau, Barcelona, Spain
Received 25 March 2018; received in revised form 21 May 2018; accepted 7 June 2018
Abstract
Mutations in the SGCA gene cause limb girdle muscular dystrophy type 2D (LGMD2D). We report a family with three affected siblings
with a mild phenotype consisting of late onset glutei and axial muscle weakness produced by a new mutation in the SGCA gene leading to
a partial expression of the alpha-sarcoglycan protein. The MRI showed muscle atrophy involving paraspinal, pelvic and thigh muscles and
a dystrophic pattern was observed in the muscle biopsy. Exome sequencing revealed a homozygous intronic deletion of SGCA and mRNA
analysis showed the presence of three different transcripts. The presence, though in a lower proportion, of wild type transcript leads to a
milder presentation of the disease. Although clinical symptoms did not entirely correspond with a sarcoglycanopathy, a compatible muscle
MRI drove us to look for changes in the sarcoglycan genes. These cases are an example of how clinical, radiological and pathological data
enriches the interpretation of exome analysis.
© 2018 Elsevier B.V. All rights reserved.
Keywords: Axial myopathy; SGCA; Sarcoglycans; NGS.
1. Introduction
Mutations in the SGCA gene lead to a deficit or absence
of the alpha-sarcoglycan protein which is one of the members
of the dystrophin-glycoprotein complex (DGC) [1]. DGC
complex is involved in the stability of muscle fiber membrane
by linking the cytoskeleton to the extracellular matrix [2].
*
Corresponding authors.
E-mail addresses: pgallano@santpau.cat (P. Gallano),
jdiazm@santpau.cat (J. Diaz-Manera).
1
These authors have equally contributed to the work.
Mutations in DGC genes induce instability of the sarcolemma
during muscle contraction that leads to muscle injury [3].
Patients with mutations in SCGA gene develop an auto-
somal recessive muscle dystrophy known as LGMD2D [4].
Series reported show a homogeneous clinical picture charac-
terized by childhood onset, quick progression of muscle weak-
ness and loss of ambulation before the adulthood in most of
the cases [5]. However, some milder adult onset cases have
been reported. This clinical variability could be related with
the type of mutation [6]. Truncating mutations are commonly
associated with severe progression while missense mutations
are associated with milder clinical presentations.
https://doi.org/10.1016/j.nmd.2018.06.002
0960-8966/© 2018 Elsevier B.V. All rights reserved.
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