V. Arroyo, A. Rimola, J. Felisart, J. Cabrera, William G. Rector – 1 January 1986

Guadalupe Garcia‐Tsao, Norman D. Grace, Roberto J. Groszmann, Harold O. Conn, Max M. Bermann, Michael J. C. Patrick, Steven S. Morse, Jeanne L. Alberts – 1 January 1986 – The present study was designed to investigate the effect of propranolol on portal pressure of patients with alcoholic cirrhosis and portal hypertension and to correlate these effects with clinical and laboratory parameters. The mean baseline hepatic venous pressure gradient in the 50 patients studied was of 18.2 ± 4.1 mm Hg.

Jean‐Charles Delchier, Paul Benfredj, Anne‐Marie Preaux, Jean‐Michel Metreau, Daniel Dhumeaux – 1 January 1986 – Gallbladder bile collected by duodenal intubation or during surgery was examined microscopically in patients who werefree of stones and in patients with proven stones. None of the 16 patients free of stones had cholesterol monohydrate crystals or calcium bilirubinate granules in bile.

Maud I. Cleton, Jan W. Sindram, Louk H. P. M. Rademakers, Floris M. J. Zuyderhoudt, Willem C. De Bruijn, Joannes J. M. Marx – 1 January 1986 – Ferritin‐like particles were observed in bile canaliculi of patients with iron overload. These particles have been further investigated by: (1) a staining method enhancing the size and contrast of ferritin protein, and (2) electronprobe microanalysis detecting the presence of the elements iron and phosphorus.

Marc L. Berger, Harshika Bhatt, Burton Combes, Ronald W. Estabrook – 1 January 1986 – CCl4 is proposed to induce cellular injury through its metabolites that are generated by a cytochrome P‐450 dependent step. These free radical products can interact with membrane structures, thereby generating lipid peroxides. The latter process has been implicated as a major mechanism of CCl4 hepatoxicity, although this relationship has been difficult to demonstrate when using isolated hepatocyte preparations.

Linus Chang, Peter Clifton, Philip Barter, Malcolm Mackinnon, M.D. – 1 January 1986 – Severe liver disease may be associated with a reduction in plasma concentration of high density lipoprotein and an impairment of plasma cholesterol esterification. These changes were confirmed in two patients with severe acute on chronic alcoholic liver disease.

Anton L. Boks, Emile J. P. Brommer, Solko W. Schalm, Huub H. D. M. Van Vliet – 1 January 1986 – In a study of severe, decompensated liver failure, we tried to find a correlation between hemorrhage and parameters ofhemostasis and fibrinolysis. Three groups of patients were studied: alcoholic cirrhosis; nonalcoholic cirrhosis, and acute liver failure without known prior liver disease. The two cirrhotic groups did not differ significantly from each other in coagulation or in fibrinolytic parameters, although liver function was more impaired in nonalcoholic cirrhosis.

Andres T. Blei – 1 January 1986

1 January 1986

Yukihisa Nagafuchi, Professor Peter J. Scheuer – 1 January 1986 – β2−Microglobulin display was examined in 131 liver biopsies from patients with acute and chronic type B hepatitis, using an indirect immunoperoxidase method. Enhanced expression of β2−microglobulin on hepatocyte membranes was observed in patients with acute hepatitis, chronic active hepatitis with moderate to severe activity and cirrhosis, when compared with normal liver. In acute hepatitis, β2−microglobulin‐positive hepatocytes were mainly observed in perivenular areas in association with bridging necrosis.