Malignant Vascular Tumors of the Liver Presenting as Liver Failure and Portal Hypertension

Sergio Rojter, Federico G. Villamil, Lidija M. Petrovic, Jeffrey M. Silverman, Graham M. Woolf, Luis G. Podesta, Leonard Makowka, John M. Vierling – 1 May 1995 – We describe three patients referred for orthotopic liver transplantation with liver failure and portal hypertension who were found to have malignant vascular tumors: two patients with angiosarcoma and one patient with epithelioid hemangioendothelioma. Their clinical presentation mimicked decompensated chronic liver disease. None had tumor masses on computed tomography and ultrasonography.

Hormone‐induced bile flow and hepatobiliary calcium fluxes are attenuated in the perfused liver of rats made cholestatic with ethynylestradiol in vivo and with phalloidin in vitro

Yuhki Hamada, Ari Karjalainen, Fyfe L. Bygravec – 1 May 1995 – The actions of vasopressin and glucagon, administered alone or together, were assessed on bile flow in perfused livers from rats made cholestatic by the injection of ethynylestradiol and from those allowed to recover from such treatment. Concomitant measurements were made of biliary calcium output as well as changes in the perfusate Ca2+ concentration, glucose output, and oxygen uptake. Experiments were also conducted where cholestasis was induced in vitro in the perfused liver by the infusion of phalloidin.

Increase of deoxycholate in supersaturated bile of patients with cholesterol gallstone disease and its correlation with de novo syntheses of cholesterol and bile acids in liver, gallbladder emptying, and small intestinal transit

Junichi Shoda, Bing‐Fang He, Naomi Tanaka, Yasushi Matsuzaki, Toshiaki Osuga, Shunji Yamamori, Hiroshi Miyazaki, Jan Sjövall – 1 May 1995 – A total of 100 nonobese and normolipidemic subjects (29 control subjects, 49 patients with cholesterol stones [CSs], and 22 patients with brown pigment stones) were studied to elucidate the pathogenetic contributions of deoxycholate (DC) to supersaturated bile formation with special reference to de novo syntheses of cholesterol and bile acids in the liver.

Hepatic and portal vein thrombosis in cirrhosis: Possible role in development of parenchymal extinction and portal hypertension

Ian R. Wanless, Florence Wong, Lawrence M. Blendis, Paul Greig, E. Jenny Heathcote, Gary Levy – 1 May 1995 – Obliterative lesions in portal veins (PVs) and hepatic veins (HVs) of all sizes are known to occur in cirrhotic livers. PV lesions have generally been attributed to thrombosis, but the pathogenesis of the HV (veno‐occlusive) lesions is unknown. We have studied 61 cirrhotic livers removed at transplantation to clarify the prevalence, distribution, and pathogenesis of venous lesions, as well as the association of these lesions with other morphological features and clinical morbidity.

Role of thrombosis in the pathogenesis of congestive hepatic fibrosis (cardiac cirrhosis)

Ian R. Wanless, Julia J. Liu, Jagdish Butany – 1 May 1995 – The pathogenesis of congestive cirrhosis is generally thought to be a reaction of the hepatic stroma to hypoxia, pressure, or necrosis. This does not explain the poor correlation between symptoms and severity of fibrosis and the irregular distribution of fibrosis within the liver. We have observed healed hepatic vein (HV) thrombosis in patients with congestive heart failure (CHF).

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