Ascites in cirrhosis: A medical or surgical problem?

Leroy Shear – 1 February 1990 – Fifty‐seven cirrhotic patients with intractable ascites had a portosystemic shunt. In 35 patients, a peritoneovenous shunt had previously failed. Forty‐six patients were in Pugh's class B and 11 were in class C. There were three operative deaths (5.3%). Fifty‐three (98.2%) of the 54 survivors were cleared of ascites. In one patient, ascites persisted because of postshunt heart failure that resulted in a marked increase of caval pressure. Twenty‐seven patients (50%) had late encephalopathy, which was severe and disabling in 12 (22%).

Immunocytochemical and electron microscopic study of hepatitis B virus antigen and complete particle production in hepatitis B virus DNA transfected HepG2 cells

Philippe Roingeard, Shilun Lu, Camille Sureau, Marianne Freschlin, Brigi, Max Essex, Jean‐Loup Romet‐Lemonne – 1 February 1990 – The relationship between the presence of hepatitis B virus antigens, their localization and hepatitis B virus replication was studied in different clones of cultured HepG2 hepatoblastoma cells transfected with cloned hepatitis B virus DNA. Intracellular hepatitis B virus antigens were detected by immunofluorescence. The production of these antigens was evaluated in the culture media by enzyme‐linked immunoassay.

Enhancement of portal pressure reduction by the association of isosorbide‐5‐mononitrate to propranolol administration in patients with cirrhosis

Joan Carles Garcia‐Pagan, Miquel Navasa, Jaime Bosch, Conxita Bru, Pilar Pizcueta, Joan Rodes – 1 February 1990 – This study investigated whether oral doses of isosorbide‐5‐mononitrate, a preferential venous dilator that decreases portal pressure, could enhance the effects of propranolol on portal hypertension. Taking part in the stuty were 28 patients with cirrhosis and portal hypertension.

An additional argument for a toxic mechanism of peliosis hepatis in man

Elie Serge Zafrani – 1 February 1990 – A patient with acute myeloblastic leukaemia developed jaundice revealing peliosis hepatis after receiving 6‐thioguanine for two months. Peliosis hepatis was severe and was associated with mild lesions of centrilobular veins. Withdrawal of 6‐thioguanine was followed by a progressive improvement of liver dysfunction. This report shows that 6‐thioguanine, a thiopurine already reported to be responsible for veno‐occlusive disease of the liver, can induce peliosis hepatis.

Volume regulation in liver: Further characterization by inhibitors and ionic substitutions

Dieter Häussinger, Thomas Stehle, Florian Lang – 1 February 1990 – The present study has been performed to elucidate the mechanisms of volume regulation in isolated perfused liver. Reduction of extracellular osmolarity by 80 mOsm/L leads to a release of potassium and a sustained alkalinization of effluent. Reexposure to isotonic perfusate leads to reuptake of potassium by the liver and acidification of effluent. Part of the alkalinization could be due to release of bicarbonate parallel to potassium release.

The effect of liver dysfunction on colchicine pharmacokinetics in the rat

Jonathan A. Leighton, Michael K. Bay, Alma L. Maldonado, Raymond F. Johnson, Steven Schenker, K. V. Speeg – 1 February 1990 – Recent work has shown that colchicine may benefit patients with primary biliary or alcoholic cirrhosis. However, very little is known about its pharmacokinetics in the presence of impaired liver function. To study this we examined the effects of three models of experimental liver dysfunction and one of cytochrome P‐450 inhibition on colchicine elimination in the rat.

S‐Adenosyl‐L‐methionine attenuates alcohol‐induced liver injury in the baboon

Charles S. Lieber, Alessandro Casini, Leonore M. Decarli, Cho‐Il Kim, Nancy Lowe, Rika Sasaki, Maria A. Leo – 1 February 1990 – Chronic ethanol consumption by baboons (50% of energy from a liquid diet) for 18 to 36 mo resulted in significant depletion of hepatic S‐adenosyl‐L‐methionine concentration: 74.6 ± 2.4 nmol/gm vs. 108.9 ± 8.2 nmol/gm liver in controls (p < 0.005). The depletion was corrected with S‐adenosyl‐L‐methionine (0.4 mg/kcal) administration (102.1 ± 15.4 nmol/gm after S‐adenosyl‐L‐methionine–ethanol, with 121.4 ± 11.9 nmol/gm in controls).

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