CIRROSIS HEPATICA POR NASH PDF

Ayuda con un problema específico de un paciente (Recibirá por correo electrónico una breve encuesta de la OMGE aproximadamente una semana después. OWL es una empresa biotecnológica, basada en la metbolómica, con aplicaciones (en inglés, NASH), que puede evolucionar a cirrosis y cáncer hepático. “La EHNA (NASH) es una enfermedad grave con unos resultados . de una disminución de la funcionalidad hepática, produciendo cirrosis no.

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Clinical trials

Gene expression in obese patients with non-alcoholic steatohepatitis. Servicio de Aparato Digestivo. Los resultados se confirmaron mediante PCR en tiempo real.

Although the molecular basis for the pathophysiology of non-alcoholic steatohepatitis NASH is poorly understood, we evaluate the hepatic gene expression of cytokines, chemokines, cell receptors, growth factors, intracellular transducers and extracellular communication proteins in liver tissue of obese patients with and without NASHand we determine the specific intrahepatic gene expression profiles associated with histological severe NASH.

Biopsy specimen samples were snap-frozen in liquid nitrogen. Hepatic gene expression was determined in liver biopsy specimens from 3 groups: Genes were considered to be expressed differentially in NASH only if there was a greater than 2-fold difference in abundance of mRNA when compared with each of the control group.

Enfermedad del hígado graso no alcohólico y esteatohepatitis no alcohólica

These results were confirmed by real-time PCR. Fourteen genes were differentially expressed 10 overexpressed and 4 underexpressed in patients with NASH. Insulin growth factor-1, insulin growth factor-2, interleukin-2 and tyrosine-receptor were underexpressed in NASH patients. The obese patients with NASH without fibrosis show an overexpression of proinflammatory and proapoptotic genes.

Also, the NASH patients with fibrosis show an overexpression of fibrogenic cirroosis, including the leptin receptor Ob-Rb. The up-regulated gene expression of prohibitin suggests mitochondrial dysfunction in NASH patients.

Non-alcoholic fatty liver disease.

Consumo de alcohol diario superior a 30 gramos en los varones o 20 gramos en las mujeres. La historia de la ausencia de consumo de alcohol fue confirmada por, al menos, dos familiares del paciente.

Esteatosis hepática no alcohólica – Artículos – IntraMed

Asimismo, se determinaron HBsAg, anti-VHC, autoanticuerpos, metabolismo del hierro, ceruloplasmina y alfa 1 antitripsina. Se obtuvo el consentimiento informado en todos los casos antes de la misma.

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Estos se dividieron en 3 grupos: Los ensayos TaqMan se realizaron en un volumen total de 20 ml. Las diferencias entre los grupos se calcularon usando la t de Student para muestras independientes.

Los genes sobreexpresados fueron: Los genes sobreexpresados son: El gen inhibido fue el IGFI -2,5relacionado con la resistencia a la insulina. La prohibitina es una chaperona que interviene en el ensamblaje de la cadena respiratoria mitocondrial Semin Liver Dis ; An expanded clinical entity. Advances in the understanding and treatment of nonalcoholic fatty liver disease.

Rev Esp Enferm Dig ; A tale of two “hits”? Wanless IR, Shiota K. The pathogenesis of nonalcoholic steatohepatitis and other fatty liver diseases: A four-step model including the role of lipid release and hepatic venular obstruction in the progression to cirrhosis. Choudhury J, Sanyal AJ. Insulin resistance and the pathogenesis of nonalcoholic fatty liver disease.

Clin Liver Dis ; 8: Oxidative stress and depletion of hepatic long-chain polyunsaturated fatty acids may contribute to nonalcoholic fatty liver disease. Free Radic Biol Med ; Association of nonalcoholic fatty liver disease with insulin resistance. Am J Med ; Association of insulin resistance and mitochondrial abnormalities.

Hepatitis C y resistencia a la insulina: Beyond insulin resistance in NASH: Defective hepatic mitochondrial respiratory chain in patients with nonalcoholic steatohepatitis. Gene expression of tumor necrosis factor alpha and TNF-receptors, p55 and p75, in nonalcoholic steatohepatitis patients.

Role of transforming growth factor beta TGF-b in hepatic fibrosis of non-alcoholic steatohepatitis patients. Adiponectin and its receptors in nonalcoholic steatohepatitis. A genomic and proteomic study of the spectrum of nonalcoholic fatty liver disease. Hepatic gene expression in patients with obesity-related non-alcoholic steatohepatitis.

Liver Int ; A proposal for grading and staging the histological lesions. Am J Gastroenterol ; Chomczynski P, Sacchi V. Single step method of RNA isolation by acid guanidium thiocynate-phenol-chloroform extraction. Anal Biochem ; Prohibitins act as a membrane-bound chaperone for the stabilization of mitochondrial proteins.

EMBO J ; 19 Prohibitins and Ras2 protein cooperate in the maintenance of mitochondrial function during yeast aging.

Acta Biochim Pol ; The mitochondrial PHB complex: Roles in mitochondrial respiratory complex assembly, ageing and degenerative disease.

Cell Mol Life Sci ; Mammalian prohibitin proteins respond to mitochondrial stress and decrease during cellular senescence. Exp Cell Res ; Functional proteomics of nonalcoholic steatohepatitis: Mitochondrial proteins as targets of S-adenosylmethionine. Identification of oxidized mitochondrial proteins in alcohol-exposed human hepatoma cells and mouse liver.

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The ins and outs of mitochondrial dysfunction in NASH. Diabetes Metab ; Effects of recombinant human macrophage colony-stimulating factor on proliferation, differentiation and survival of Kupffer cells in the liver of adult mice.

Anal Quant Cytol Histol ; Regulation of macrophagecolony stimulating factor in liver fat-storing cells by peptide growth factors. Am J Physiol ; 4 Pt 1: Hepatic damage induced by transcatheter arterial chemoembolization elevates serum concentrations of macrophage-colony stimulating factor.

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Hepstica ; 19 2: Serum levels of macrophage colony stimulating factor M-CSF in liver disease. J Hepatol ; 21 4: Hepatology ; 37 1: Increased transforming growth factor beta 1 gene expression in human liver disease.

J Hepatol ; Transforming growth factor-beta 1 TGF-beta 1 and TGF-beta 1 receptors in normal, cirrhotic, and neoplastic human livers.

In situ expression of transforming growth factor betalatent transforming growth factor beta binding protein and tumor necrosis factor alpha in liver tissue from patients with chronic hepatitis C. Scand J Gastroenterol ; Endocr Rev ; The modular architecture of a new family of growth regulators related to connective tissue growth factor. FEBS Lett ; Connective tissue hepaitca factor gene expression in tissue sections from localized scleroderma, keloid, and other fibrotic skin disease.

J Invest Dermatol ; Expression of connective tissue growth factor in human renal ppor. Kidney Int ; Expression of connective tissue growth factor in experimental rat and human liver fibrosis. High glucose and hiperinsulinemia stimulate connective tissue growth factor expression: A potential mechanism involved in progression to fibrosis in nonalcoholic steatohepatitis.

Transforming growth factor beta and tumor necrosis factor alpha hepaticw both apoptosis and proliferation of activated rat hepatic stellate cells. Effect of tumor necrosis factor alpha on proliferation, activation, plr protein synthesis of rat hepatic stellate cells.

Effects of tumor necrosis factor alpha on the expression of connective tissue growth factor in hepatic stellate cells. Expression patterns of matrix metalloproteinases and their inhibitors in parenchymal and non-parenchymal cells of rat liver: Fibroblast growth factor 2 and transforming growth factor beta 1 interactions in human liver myofibroblasts. Gastroenterology ; 6: