Serological markers of primary biliary cirrhosis: Diagnosis, prognosis and subsets
Margaret F. Bassendine, S. J. Yeaman – 1 March 1992
Margaret F. Bassendine, S. J. Yeaman – 1 March 1992
John Olynyk, Phillip Williams, Andrew Fudge, Steven Pulbrook, Rikki Kerr, Malcolm MacKinnon, Pauline Hall – 1 March 1992 – The potential application of fine‐needle aspiration liver biopsy in the documentation of hepatic iron overload has been assessed in iron‐loaded rats. Fineneedle aspiration and standard liver biopsy specimens were obtained from three groups of animals supplemented with oral and parenteral iron for 2 to 6 mo. The mean dry weights of standard and fine‐needle biopsy specimens were 7.41 ± 0.77 (± S.E.M.) and 0.57 ± 0.54 mg, respectively.
Jorge L. Poo, Alain Braillon, Antoine Hadengue, Christophe Gaudin, Didier Lebrec – 1 March 1992 – The hemodynamic responses to terbutaline – a selective β2‐adrenoceptor agonist – were studied in conscious normal rats and in conscious rats with secondary biliary cirrhosis. Compared with those of normal rats, dose‐response curves in cirrhotic rats indicated significantly decreased reactivity in arterial pressure and heart rate. Half‐maximal effective dose was not significantly different between the two groups.
Eugenio Grau, Vicente Felipo, María‐Dolores Miñana, Santiago Grisolía – 1 March 1992 – A protein‐free diet causes a paradoxical increase of blood ammonia levels that seems to be due to decreased liver content of acetylglutamate, the physiological activator of carbamylphosphate synthetase. The purpose of this study was to assess whether oral administration to rats of carbamylglutamate, a metabolically stable activator of carbamylphosphate synthetase, could decrease the blood ammonia levels increased by the protein‐free diet.
Ibrahim Yousef, Diane Mignault, Beatriz Tuchweber – 1 March 1992 – The effect of complete sulfation of conjugated cholic, chenodeoxycholic and deoxycholic acids on bile formation was investigated in rats. The sulfated bile acids were infused intravenously in stepwise increasing doses (1, 2, 3 and 4 μmol/min/100 gm body wt) in rats after 90 min of bile acid pool depletion. The effects of these bile acids on bile flow, bile salt, biliary phospholipid and cholesterol secretion rates were determined.
Hong‐Yuan Hsu, Mei‐Hwei Chang, Chin‐Yun Lee, Juei‐San Chen, Hey‐Chi Hsu, Ding‐Shinn Chen – 1 March 1992 – Spontaneous loss of HBsAg is infrequent in adult HBV carriers. Little is known about this serological change in children. In a prospective study of 420 hepatitis B virus–carrier children who were observed for 1 to 12 yr (mean = 4.3 yr), spontaneous loss of HBsAg occurred in 10 patients, with an average incidence of 0.6%/yr.
Santiago J. Muñoz – 1 March 1992 – The two main causes of gastrointestinal bleeding in cirrhosis are oesophageal varices and portal hypertensive gastropathy (PHG). Rebleeding from varices can be prevented by beta‐blockers, but it is not clear whether these drugs effectively reduce rebleeding from PHG. 54 cirrhotic patients with acute or chronic bleeding from severe PHG took part in a randomised, controlled trial to investigate the efficacy of propranolol in prevention of rebleeding from PHG.
Anthony Koo, Hirokazu Komatsu, Gongming Tao, Masayashu Inoue, Paul H. Guth, Neil Kaplowitz – 1 March 1992 – Controversy exists as to the role of oxygen‐derived free radicals in tissue injury and the no‐reflow phenomenon in reperfusion injury after ischemia. In this study using an experimental rat model, left hepatic lobar ischemia followed by reperfusion resulted in an increase of serum glutamic pyruvic transaminase at 30 min with concomitant histological evidence of hepatocellular necrosis at 24 hr.
Sanjeev Gupta, Douglas R. LaBrecque, David A. Shafritz – 1 March 1992 – We determined whether hepatic stimulator substance shares its mitogenic specificity for hepatocytes with nonparenchymal epithelial cells in the hepatocyte lineage. Cell lines designated HTC (derived from a rat hepatoma known to respond to hepatic stimulator substance) and FNRL, K‐16 and K‐22 (derived from rat liver nonparenchymal epithelial cells) were used.
Margaret Swain, Roger F. Butterworth, Andres T. Blei – 1 March 1992 – The pathogenesis of brain edema in acute liver failure is poorly understood. We have previously shown that rats with ischemic acute liver failure (portacaval anastomosis followed by hepatic artery ligation) exhibit brain edema and intracranial hypertension, with swelling of cortical astrocytes as the most prominent neuropathological abnormality.