A randomized trial comparing transjugular intrahepatic portosystemic stent‐shunt with variceal band ligation in the prevention of rebleeding from esophageal varices

R Jalan, E H Forrest, A J Stanley, D N Redhead, J Forbes, J F Dillon, A J MacGilchrist, N D Finlayson, P C Hayes – 30 December 2003 – The aim of this study was to compare transjugular intrahepatic portosystemic stent‐shunt (TIPSS) with variceal band ligation (VBL) in the secondary prophylaxis of esophageal variceal hemorrhage in patients with cirrhosis. Fifty‐eight patients with cirrhosis who presented with the first episode of esophageal variceal hemorrhage were randomized to TIPSS (31) or VBL (27), 24 hours after control of bleeding.

Effect of moderate exercise on insulin sensitivity and substrate metabolism during post‐exercise recovery in cirrhosis

A S Petrides, D E Matthews, U Eßer – 30 December 2003 – We examined whether a single bout of moderate exercise has a beneficial effect on insulin sensitivity and fuel homeostasis in cirrhosis. Clinically stable cirrhotic patients and age‐, sex‐, and weight‐matched controls participated in insulin clamp studies (either euglycemic hyperinsulinemic or hyperglycemic hyperinsulinemic) in combination with indirect calorimetry and [6,6‐2H2]glucose.

Cycloheximide prevents apoptosis, reactive oxygen species production, and glutathione depletion induced by transforming growth factor β in fetal rat hepatocytes in primary culture

A Sanchez, A M Alvarez, M Benito, I Fabregat – 30 December 2003 – We have previously reported that transforming growth factor‐beta (TGF‐β) induces apoptosis in fetal hepatocytes in primary culture. This effect was found to be associated with an increase in intracellular reactive oxygen species (ROS) and a lowering of total cellular reduced glutathione (GSH). In this study, we investigated whether protein synthesis plays a role in these TGF‐β‐induced effects.

Exhaled nitric oxide and oxygenation abnormalities in hepatic cirrhosis

G Rolla, L Brussino, P Colagrande, L Dutto, S Polizzi, E Scappaticci, S Bergerone, M Morello, A Marzano, G Martinasso, M Salizzoni, C Bucca – 30 December 2003 – Impaired arterial oxygenation, ranging from increased alveolar‐arterial oxygen gradient (AaDo2) to hypoxemia, is commonly present in patients with cirrhosis. Nitric oxide (NO), through pulmonary vasodilatation, may play a major role in the oxygen abnormalities of cirrhosis.

Defects of the respiratory chain in the normal human liver and in cirrhosis during aging

J Muller‐Hocker, D Aust, H Rohrbach, J Napiwotzky, A Reith, T A Link, P Seibel, D Holzel, B Kadenbach – 30 December 2003 – Defects of the respiratory chain are a typical feature of mitochondrial diseases and occur also during normal aging where they have been described in postmitotic tissues. The present study addresses the question of defect expression in the normal and cirrhotic liver.

Intercellular adhesion molecule‐1 and CD18 are involved in neutrophil adhesion and its cytotoxicity to cultured sinusoidal endothelial cells in rats

S Sakamoto, T Okanoue, Y Itoh, K Sakamoto, K Nishioji, Y Nakagawa, N Yoshida, T Yoshikawa, K Kashima – 30 December 2003 – The expression of several adhesion molecules is increased on the hepatic sinusoidal endothelial cells (SECs) in various liver diseases. The objective of this study is to assess the roles of intercellular adhesion molecule 1 (ICAM‐1) and of CD18 in the interaction between the neutrophils (polymorphonuclear leukocytes [PMNs]) and SECs and in the injury to SECs mediated by PMNs.

Role of ischemia in causing apoptosis, atrophy, and nodular hyperplasia in human liver

K Shimamatsu, I R Wanless – 30 December 2003 – Ischemia is known to be a cause of hepatocellular apoptosis and atrophy in experimental animals, but the effect of vascular obstruction on such lesions in the normal or cirrhotic human liver has not been studied. The purpose of this study was to investigate the role of ischemia in the development of apoptosis, atrophy, and nodular hyperplasia in cirrhotic and noncirrhotic human livers. Apoptosis, focal atrophy, and nodular hyperplasia were semiquantitated in 203 liver specimens obtained at transplantation, segmental resection, or autopsy.

S‐adenosyl‐L‐methionine protects the liver against the cholestatic, cytotoxic, and vasoactive effects of leukotriene D4: A study with isolated and perfused rat liver

R N Cincu, C M Rodriguez‐Ortigosa, I Vesperinas, J Quiroga, J Prieto – 30 December 2003 – Cysteinyl‐leukotrienes can cause cholestasis and liver damage when administered at nanomolar concentrations. Using the isolated and perfused rat liver we analyzed whether S‐adenosyl‐L‐methionine (SAMe) may protect this organ against the noxious effects of leukotriene‐D4 (LTD4).

Subscribe to