Journal of hepatology
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Journal of hepatology · Nov 1998
Randomized Controlled Trial Clinical TrialEffects of increasing blood hemoglobin levels on systemic hemodynamics of acutely anemic cirrhotic patients.
In experimental portal hypertension, blood hemoglobin levels have been shown to influence the hyperdynamic circulatory state. The aim of this study was to assess the hemodynamic effects of increasing hemoglobin concentration in human portal hypertension. ⋯ An increase in blood hemoglobin in acutely anemic cirrhotic patients attenuates their hyperdynamic circulation beyond viscosity-dependent changes, an effect which might be counteracted by the effects on portal venous pressure gradient.
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Journal of hepatology · Sep 1998
Clinical Trial Controlled Clinical TrialAbnormal accumulation of endotoxin in biliary epithelial cells in primary biliary cirrhosis and primary sclerosing cholangitis.
Previous studies have revealed the involvement of Kupffer cells and hepatocytes in the metabolism of endotoxin in the liver. The aim of this study was to investigate the in vivo localization of endotoxin in liver cells, including Kupffer cells, hepatocytes, and biliary epithelial cells, in primary biliary cirrhosis and primary sclerosing cholangitis. We also examined the effect of ursodeoxycholic acid on the intrahepatic distribution of endotoxin in primary biliary cirrhosis. ⋯ Our results revealed that in primary biliary cirrhosis and primary sclerosing cholangitis, endotoxin accumulates abnormally in biliary epithelial cells. In addition, we found that ursodeoxycholic acid treatment in primary biliary cirrhosis may provide a beneficial effect on the intrahepatic metabolism of endotoxin.
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Journal of hepatology · Jul 1998
Tumor necrosis factor genomic polymorphism and outcome of acetaminophen (paracetamol)-induced acute liver failure.
High levels of tumor necrosis factor-alpha are associated with an increased risk of severe encephalopathy in acute liver failure, and experimental studies suggest that tumor necrosis factor-alpha plays a role in the development of acetaminophen (paracetamol)-induced liver injury and associated multiple organ failure. Inter-individual variations in the production of tumor necrosis factor-alpha have been linked to genomic polymorphisms within the tumor necrosis factor-alpha locus. This study examined whether specific tumor necrosis factor polymorphisms are associated with variations in the severity of clinical features in acetaminophen-induced acute liver failure. ⋯ The development of acute liver failure is unlikely to be primarily sepsis driven. However, the apparent protective effect of the tumor necrosis factor B1B1 genotype on the development of severe encephalopathy may be related to the effects of this genotype on tumor necrosis factor-alpha production in sepsis.
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Journal of hepatology · Jun 1998
Letter Case ReportsSevere idiosyncratic acute hepatic injury caused by paracetamol.