Ousama E. Moussa, Harold O. Conn – 1 September 1987 – Since 1976, we have compared the end‐to‐side portacaval shunt (PCS) with the distal splenorenal shunt (DSRS) in patients with alcoholic liver disease and recurrent variceal bleeding. Fifty‐four patients were randomly assigned to receive either shunt procedure. There were 27 patients in each group and both groups were highly comparable in clinical and laboratory characteristics. Median follow‐up was 31 mo in each group. Postoperative complications and operative mortality (7% after PCS, 12% after DSRS) were comparable.

Michael Bennick – 1 September 1987

Cynthia Cohen – 1 September 1987 – Liver cell dysplasia (LCD) is a premalignant cytologic change of hepatocytes that has been statistically linked to cirrhosis, hepatocellular carcinoma (HCC), and chronic liver disease related to hepatitis B virus. The relationship of LCD to non‐A, non‐B (NANB) hepatitis is currently unknown. We studied liver biopsy and surgical resection specimens from 36 patients with NANB hepatitis, and identified LCD in 17 (42.5%) of 40 specimens, most often associated with cirrhosis.

Guadalupe Garcia‐Tsao, Roberto J. Groszmann – 1 September 1987 – Nitroglycerin is a potent venous dilator and a mild arterial vasodilator that has been shown to improve the hemodynamic response to vasopressin in portal hypertensive patients and to decrease portal pressure in experimental animals. In order to determine the effect of nitroglycerin on portal venous hemodynamics, we studied 11 patients with alcoholic cirrhosis before and during the administration of sublingual nitroglycerin (0.4 and 0.6 mg).

Raf Sciot, Alan C. Paterson, Joost J. Van Den Oord, Valeer J. Desmet – 1 September 1987 – The major part of hepatocellular iron is derived from uptake of transferrin‐bound iron by means of nonspecific fluid‐phase endocytosis and specific, saturable binding on high‐affinity transferrin receptors. We investigated the expression of transferrin receptors on hepatocytes in liver biopsies of 22 cases of hemochromatosis (21 primary hemochromatosis and 1 secondary hemochromatosis), using immunohistochemical demonstration of the human transferrin receptor with the specific monoclonal antibody OKT9.

Heidrun Matern, Heinz‐Herbert Fiebig, Siegfried Matern – 1 September 1987 – Human hepatoma which had been xenografted into nude mice have been estimated for their ability to catalyze glucuronic acid and glucose conjugation of endogenous compounds and p‐nitrophenol. The xenobiotic p‐nitrophenol was glucuronidated with a comparable rate in microsomes from human hepatoma, human liver and host liver.

Helmut Denk – 1 September 1987 – Livers from 12 mice fed griseofulvin for 4 to 6 months were perfused in situ with a detergent solution to extract lipid membranes leaving the cytoskeleton intact. Seven control mice were similarly studied. After 30 to 120 minutes perfusion, liver samples were examined by scanning electron microscopy and transmission electron microscopy. By light microscopy, Mallory bodies (MBs) were observed in pericentral hepatocytes. These were confirmed by transmission electron microscopy. Intermediate filaments (IFs) were observed in close apposition to MBs.

1 September 1987

Seigo Kitano, Nobuhiro Koyanagi, Yasunori Iso, Hidefumi Higashi, Keizo Sugimachi – 1 September 1987 – Endoscopic injection sclerotherapy was given to 155 patients with esophageal varices mainly related to non‐alcoholic liver cirrhosis. The formation of a superficial ulcer in the lower esophagus was achieved in 141 (91.0%) of the 155 patients, with an average of 4.1 sessions of endoscopic injection sclerotherapy during an average time of 4.9 weeks.

Udaya M. Kabadi – 1 September 1987 – Hyperammonemia is a well‐recognized metabolic abnormality which occurs in cirrhotic patients with advanced liver dysfunction. We recently documented that hyperglucagonemia that occurs as a result of hepatic glycogen depletion may be responsible for this hyperammonemia by promoting gluconeogenesis to provide glucose as a fuel for functioning of several organ systems. Thus, hepatic glycogen depletion may be the initial process responsible for hyperammonemia.