FISIOPATOLOGIA CIRROSIS HEPATICA PDF

En ciertos casos es mas complicado determinar cuales han sido las causas que han desencadenado la cirrosis. Esta fase es irreversible. Lo mas importante es prevenirla no abusando en la ingesta de alcohol y previniendo las hepatitis B o C, dos de sus causas mas frecuentes. I was very happy to uncover this page.

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Liver fibrogenesis is the result of excessive tissue repair of chronic liver damage. This entity consists of the progressive extracellular matrix deposition in the liver parenchyma that is observed in most chronic liver diseases and which precedes the development of cirrhosis. In the last few years, several studies have identified activated stellate cells, portal fibroblasts, and myofibroblasts from distinct cell populations as the main collagen-producing cells in the damaged liver.

Likewise, the main cytokines and molecules involved in liver fibrogenesis have been identified. The finding that advanced liver fibrogenesis can be reversed has stimulated research into possible antifibrogenic therapies. Nevertheless, the only effective treatment is elimination of the causal agent.

The present article summarizes the progress made in the study of the pathogenesis of liver fibrogenesis and discusses the possible therapeutic targets for the development of antifibrogenic agents.. ISSN: Liver fibrogenesis: physiopathology. Descargar PDF. Autor para correspondencia. Palabras clave:. The present article summarizes the progress made in the study of the pathogenesis of liver fibrogenesis and discusses the possible therapeutic targets for the development of antifibrogenic agents.

Hepatic inflammation. Bataller, D. J Clin Invest, , pp. Roulot, J. Costes, J. Buyck, U. Warzocha, N. Gambier, S. Czernichow, et al. Transient elastography as a screening tool for liver fibrosis and cirrhosis in a community-based population aged over 45 years. Gut, 60 , pp. Springer Semin Immunopathol, 21 , pp. Hepatic stellate cells: protean, multifunctional, and enigmatic cells of the liver.

Physiol Rev, 88 , pp. Kalluri, E. Epithelial-mesenchymal transition and its implications for fibrosis. Interactions between hepatic stellate cells and the immune system. Semin Liver Dis, 21 , pp. Notas, T. Kisseleva, D. NK and NKT cells in liver injury and fibrosis. Clin Immunol, , pp. Li, S. Qiu, W. She, F. Wang, H. Gao, L. Li, et al. Significance of the balance between regulatory T Treg and T helper 17 Th17 cells during hepatitis B virus related liver fibrosis. PLoS One, 7 , pp.

Santodomingo-Garzon, M. Role of NKT cells in autoimmune liver disease. Autoimmun Rev, 10 , pp. Gressner, R. Weiskirchen, K. Breitkopf, S. Front Biosci, 7 , pp. Shek, R. How can transforming growth factor beta be targeted usefully to combat liver fibrosis?.

Eur J Gastroenterol Hepatol, 16 , pp. Yoshiji, S. Kuriyama, J. Yoshii, Y. Ikenaka, R. Noguchi, T. Nakatani, et al. Tissue inhibitor of metalloproteinases-1 attenuates spontaneous liver fibrosis resolution in the transgenic mouse. Hepatology, 36 , pp. Tsukamoto, S. Current concepts in the pathogenesis of alcoholic liver injury. Wanless, 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.

Semin Liver Dis, 24 , pp. Semin Gastrointest Dis, 11 , pp. Bataller, Y. Paik, J. Lindquist, J. Lemasters, D. Hepatitis C virus core and nonstructural proteins induce fibrogenic effects in hepatic stellate cells.

Gastroenterology, , pp. Pathogenesis of liver fibrosis: role of oxidative stress. Mol Aspects Med, 21 , pp. Reversibility of liver fibrosis and cirrhosis following treatment for hepatitis C. Bruguera, M. Torres, J. Histological course of alcoholic hepatitis. Influence of abstinence, sex and extent of hepatic damage. J Hepatol, 2 , pp.

Dixon, P. Bhathal, N. Hughes, P. Nonalcoholic fatty liver disease: Improvement in liver histological analysis with weight loss. Hepatology, 39 , pp.

Hammel, A. Couvelard, D. Ratouis, A. Sauvanet, J. Flejou, et al. Regression of liver fibrosis after biliary drainage in patients with chronic pancreatitis and stenosis of the common bile duct.

N Engl J Med, , pp. Camma, D. Di Bona, F. Schepis, E. Heathcote, S. Zeuzem, P. Pockros, et al.

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Cirrosis hepática

We report a case of a 63 year old male patient with history of chronic hepatopathy with cirrhosis. During his medical control and last hospitalization no cirrhosis etiology was found. On autopsy, excess iron was found with histochemical stains in liver, pancreas, myocardium and gastric mucosa. These findings, along with the clinical history and laboratory tests, showed that the origin of cirrhosis was primary hemochromatosis. Hepatic cirrosis , primary and secondary hemochromatosis , hemosiderosis , HME gene, transferrin , ferritin , serum iron, bronzed diabetes. Churchill Livingstone. USA : Elsevier.

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Hyponatremia is the most common electrolyte disorder in patients with cirrhosis. In dilutional or hypervolemic hyponatremia, serum sodium concentration is reduced, plasma volume is increased although the effective plasma volume is decreased due to marked arterial vasodilation in the splanchnic circulation and extracellular fluid volume is increased, with ascites and edema in the absence of signs of dehydration. This is a result of the marked deterioration in renal excretion of solute-free water, leading to disproportionate water retention in relation to sodium retention. Since hypervolemic hyponatremia is by far the most frequent form of this disorder, the present chapter will concentrate specifically on hypervolemic hyponatremia in cirrhosis.. ISSN:

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