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Gut and Liver ; : 411-416, 2013.
Artigo em Inglês | WPRIM | ID: wpr-163966

RESUMO

BACKGROUND/AIMS: The primary pathophysiologic abnormality in achalasia is known to be a loss of inhibitory myenteric ganglion cells, which may result from an immune-mediated response or neuronal degeneration. The aim of this study was to identify proteins suggestive of an immune-mediated response or neuronal degeneration in the serum of achalasia patients using a proteomic analysis. METHODS: Blood samples were collected from five symptomatic achalasia patients and five sex- and age-matched healthy controls. Serum proteomic analysis was conducted, and the protein spots were identified using matrix-assisted laser desorption ionization/time-of-flight and a proteomics analyzer. The serum level of C3 was measured by enzyme-linked immunosorbent assay in nine patients with achalasia and 18 sex- and age-matched healthy controls. RESULTS: Of the 658 matched protein spots, 28 spots were up-regulated over 2-fold in the serum from achalasia patients compared with that from controls. The up-regulated proteins included complement C4B5, complement C3, cyclin-dependent kinase 5, transthyretin, and alpha 2 macroglobulin. The serum levels of C3 in achalasia patients were significantly higher than those of controls. CONCLUSIONS: The serum proteomic analysis of achalasia patients suggests an immune-mediated response or neuronal degeneration. Further validation studies in larger samples and the esophageal tissue of achalasia patients are required.


Assuntos
Humanos , alfa-Macroglobulinas , Complemento C3 , Proteínas do Sistema Complemento , Quinase 5 Dependente de Ciclina , Ensaio de Imunoadsorção Enzimática , Acalasia Esofágica , Cistos Glanglionares , Neurônios , Pré-Albumina , Proteínas , Proteômica
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