Serum levels of vascular endothelial growth factor elevated in patients with muscular dystrophy.
Brain Dev
; 31(8): 612-7, 2009 Sep.
Article
em En
| MEDLINE
| ID: mdl-18980821
ABSTRACT
In patients with muscular dystrophy, such as Duchenne muscular dystrophy (DMD), microcirculation abnormalities and hypoxic ischemic conditions in muscle tissues are suspected to be induced by non-symptomatic coagulation fibrinolysis abnormalities and vascular dysfunction. Vascular endothelial growth factor (VEGF) is a critical regulating factor in angiogenesis that is known to be induced by hypoxic and/or ischemic conditions. To examine whether VEGF is associated with muscular dystrophy, we measured serum levels of VEGF in 52 patients with DMD, 15 with Becker muscular dystrophy (BMD), 20 with Fukuyama congenital muscular dystrophy (FCMD), eight with myotonic dystrophy (DM), and four with spinal muscular atrophy (SMA), as well as in 15 healthy and eight disease controls. The serum level of VEGF in the DMD patients was 267.7+/-25.3 pg/ml (10.5-800.0), while it was 358.8+/-96.3 pg/ml (0.2-1320.0) in the BMD patients, 261.4+/-45.6 pg/ml (0.1-758.0) in the FCMD patients, 165.0+/-63.4 pg/ml (2.6-479.0) in the DM patients, 96.0+/-30.3 pg/ml (41.0-168.0) in the SMA patients, 148.3+/-20.1 pg/ml (46.5-298.0) in the healthy controls, and 154.1+/-54.0 pg/ml (7.2-343.0) in the disease controls. The level of VEGF in BMD was significantly elevated, as compared with DM, SMA, and control groups. Further, the level of VEGF in the bedridden sub-group of DMD patients was significantly elevated as compared with chair-bound DMD, DM, SMA, and control groups. We concluded that VEGF may reflect hypoxic and/or ischemic conditions in muscle tissue, and have a relationship with the process of disease progression in DMD and BMD patients.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Fator A de Crescimento do Endotélio Vascular
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Distrofias Musculares
Limite:
Adolescent
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Adult
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Female
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Humans
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Male
Idioma:
En
Revista:
Brain Dev
Ano de publicação:
2009
Tipo de documento:
Article