Intestinal mucosal proliferation, apoptosis and oxidative stress in patients with liver cirrhosis



Título del documento: Intestinal mucosal proliferation, apoptosis and oxidative stress in patients with liver cirrhosis
Revista: Annals of hepatology
Base de datos: PERIÓDICA
Número de sistema: 000416666
ISSN: 1665-2681
Autores: 1
2
3
1
4
5
2
4
2
3
Instituciones: 1University Hospital of Patras, Department of Internal Medicine, Patras. Grecia
2University Hospital of Patras, Department of Pathology, Patras. Grecia
3University Hospital of Patras, Division of Gastroenterology, Patras. Grecia
4University Hospital of Patras, Department of Biology, Patras. Grecia
5University Hospital of Patras, Department of Surgery, Patras. Grecia
Año:
Periodo: Mar-Abr
Volumen: 12
Número: 2
Paginación: 301-307
País: México
Idioma: Inglés
Tipo de documento: Artículo
Enfoque: Experimental, analítico
Resumen en inglés Intestinal mucosal barrier dysfunction in liver cirrhosis and its implicated mechanisms is of great clinical importance because it is associated with the development of serious complications from diverse organs through promotion of systemic endotoxemia. Aim. The present study was designed to investigate whether enterocytes’ proliferation, apoptosis and intestinal oxidative stress are altered in the intestinal mucosa of patients with compensated and decompensated liver cirrhosis. Material and methods. Twelve healthy controls (group A) and twenty four cirrhotic patients at a compensated (n = 12, group B) or decompensated condition (n = 12, group C) were subjected to duodenal biopsy. In intestinal specimens mucosal apoptotic and mitotic activity and their ratio were recorded by means of morphological assessment and mucosal lipid hydroperoxides were measured. Plasma endotoxin concentration, an index of gut barrier function, was also determined. Results. Cirrhotic patients presented significantly higher serum endotoxin concentrations as compared to healthy controls (P < 0.001), whilst endotoxemia was higher in decompensated disease (P < 0.05 vs. compensated cirrhosis). Intestinal mucosal mitotic count was significantly lower in patients with compensated and decompensated cirrhosis compared to controls (P < 0.01, respectively), whilst a trend towards increased apoptosis was recorded. The mitotic/apoptotic ratio was significantly reduced in groups B (P < 0.05) and C (P < 0.01) as compared to controls. Intestinal lipid peroxidation was significantly increased in decompensated cirrhotics (P < 0.001 vs. groups A and B). Conclusions. The present study demonstrates for the first time that human liver cirrhosis is associated with decreased intestinal mucosal proliferation and proliferation/apoptosis ratio even at early stages of cirrhosis and increased intestinal oxidative stress in advanced liver disease
Disciplinas: Medicina
Palabras clave: Gastroenterología,
Bioquímica,
Cirrosis,
Hígado,
Permeabilidad intestinal,
Endotoxemia,
Homeostasis,
Tejido epitelial,
Peroxidación lipídica
Keyword: Gastroenterology,
Biochemistry,
Cirrhosis,
Liver,
Intestinal permeability,
Endotoxemia,
Homeostasis,
Epithelial tissues,
Lipid peroxidation
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