Liver international : official journal of the International Association for the Study of the Liver
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Hepatic hydrothorax is defined as the accumulation of significant pleural effusion in a cirrhotic patient without primary pulmonary or cardiac disease. Hydrothorax is uncommon occurring in up to 4-6% of all patients with cirrhosis and up to 10% in patients with decompensated cirrhosis. Although ascites is usually present, hydrothorax can occur in the absence of ascites. ⋯ Over the last few years, new insights into the pathogenesis of this entity have lead to improved treatment modalities such as portosystemic shunts (TIPS) and video-assisted thoracoscopy for closure of diaphragmatic defects. These modalities may be of help as a bridge to transplantation. The aim of this review is to describe recent developments in the pathogenesis, diagnosis and treatment of hepatic hydrothorax.
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The role of endothelial nitric oxide synthase 3 (NOS-3) in the hyperdynamic circulation associated with cirrhosis is established but not that of the neuronal (NOS-1) isoform. We therefore investigated aortic NOS-1 levels in NOS-3 knock-out (KO) and wildtype (WT) mice and in hepatic arteries of patients. ⋯ Increased NOS-1 mRNA and protein levels and partially maintained in vitro NO-production in aortae of NOS-3 KO mice suggest that NOS-1 may partially compensate for NOS-3 deficiency. BDL-induced increase in aortic NOS-1 mRNA and protein levels hint that not only NOS-3, but also NOS-1 may be involved in the regulation of systemic hyperdynamic circulation and portal hypertension. Upregulation of NOS-1 mRNA levels in hepatic arteries of portal hypertensive patients suggests possible clinical significance for these experimental findings.
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Bile salts take part in an efficient enterohepatic circulation in which most of the secreted bile salts are reclaimed by absorption in the terminal ileum. In the liver, the sodium-dependent taurocholate transporter at the basolateral (sinusoidal) membrane and the bile salt export pump at the canalicular membrane mediate hepatic uptake and hepatobiliary secretion of bile salts. Canalicular secretion is the driving force for the enterohepatic cycling of bile salts and most genetic diseases are caused by defects of canalicular secretion. ⋯ Serum gamma-GT activity is elevated in these patients. Ursodeoxycholic acid therapy is useful for patients with a partial defect. Liver transplantation is a more definitive therapy for these patients.
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Tumor necrosis factor (TNF)-alpha itself does not induce liver injury in normal mice or hepatocytes. Rather, this event, especially in vitro, is explained by the fact that the TNF-alpha/TNF receptor system not only triggers downstream signals leading to apoptosis but also induces an antiapoptotic pathway through the activation of nuclear factor (NF)-kappaB. The aim of this study was to determine whether inhibition of antiapoptotic pathways influences the susceptibility of mice to TNF-alpha. Here, we focused on the roles of NF-kappaB and phosphatidylinositol 3-kinase (PI3K)-regulated serine/threonine kinase Akt. ⋯ The inducible activation of NF-kappaB and constitutive activation of Akt regulate hepatocyte survival against TNF-alpha, which occurs independent of Bcl-2 families.
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Comparative Study
Direct measurement of hepatic tissue hypoxia by using a novel tcpO2/pCO2 monitoring system in comparison with near-infrared spectroscopy.
Hepatic hypoxia occurs during liver surgery and transplantation and it may also appear within liver tumours, correlating with prognosis and efficacy of the treatment. The present study measured liver tissue hypoxia by directly using near-infrared spectroscopy (NIRS) and a novel tcpO2/pCO2 monitoring system. ⋯ The data from the present study suggest that, like NIRS, the tcpO2/pCO2 monitoring system can be reliably used for the direct monitoring of hepatic tissue oxygenation in vivo.