Serum hyaluronate in primary biliary cirrhosis—A biochemical marker for progressive liver damage

Anders Nyberg, Anna Engström‐Làurent, Lars Lööf – 1 January 1988 – To evaluate serum hyaluronate as a marker for progressive liver injury in patients with primary biliary cirrhosis, a longitudinal study including 48 patients was conducted with a mean follow‐up time of 40 months. The patients were examined every 6 months with a standardized set of conventional liver function tests, and a liver biopsy was performed every year.

IgA deposition and synthesis in alcoholic liver injury

D. R. Triger – 1 January 1988 – Immunoglobulin deposition in alcoholic and non‐alcoholic liver disease was studied using an indirect immunoperoxidase technique. A continuous pattern of IgA deposition, with IgA outlining the sinusoids, was shown to be a specific and sensitive marker for liver disease caused by alcohol in both cirrhotic and non‐cirrhotic livers. The sensitivity was lowest in cases of alcoholic disease showing fatty change alone.

Tissue localization and kinetics of pit cells or large granular lymphocytes in the liver of rats treated with biological response modifiers

Luc Bouwens, Eddie Wisse – 1 January 1988 – The numbers of Kupffer cells (macrophages) and pit cells (large granular lymphocytes) were counted by light and electron microscopy in perfusion‐fixed liver sinusoids. After a single intravenous injection of the biological response modifiers zymosan, Propionibacterium acnes and OK‐432, a 4‐ to 6‐fold increase in the number of pit cells and a 2‐ to 4‐fold increase in the number of Kupffer cells were observed within a period of 4 to 7 days.

The epidemiology and clinical outcome of hepatitis D virus (delta) infection in Jordan

Ala U. Toukan, Omayma A. Abu‐El‐Rub, Salwa A. Abu‐Laban, Musleh S. Tarawneh, M. Feisal Kamal, Stephen C. Hadler, Krzysztof Krawczynski, Harold S. Margolis, James E. Maynard – 1 November 1987 – The epidemiology and clinical outcome of hepatitis D viral infection in HBsAg‐positive acute hepatitis, chronic liver disease, primary hepatocellular carcinoma and the symptomless carrier state was studied in Jordan.

Graft‐versus‐host‐induced cirrhosis: Possible mechanisms

Howard M. Shulman – 1 November 1987 – A 28‐yr‐old woman with severe idiopathic aplastic anemia received an HLA‐identical mixed lymphocyte culture nonreactive bone marrow transplant from her brother. In the months after successful engraftment, she developed cutaneous and hepatic graft‐versus‐host disease, associated with marked cholestatic jaundice. Despite a series of therapeutic maneuvers, cholestasis persisted but remained relative stable over the enuing 10 yr. However, serial liver biopsies revealed progressive biliary‐type firbrosis culminating in cirrhosis.

Increase in the number of fenestrae in mouse endothelial liver cells by altering the cytoskeleton with cytochalasin B

Anne‐Marie Steffan, Jean‐Louis Gendrault, André Kirn – 1 November 1987 – Endothelial cells of the hepatic sinusoid isolated from mice livers and maintained in culture display typical fenestrae grouped in sieve plates. Treatment with cytochalasin B led to no significant change in the mean diameter of the fenestrae but to an increase in their number and in the porosity of the cells (percentage of the cellular surface opened by the fenestrae) which attained up to 300% of that of the controls.

Electron microscopic evaluation of brain edema in rabbits with galactosamine‐induced fulminant hepatic failure: Ultrastructure and integrity of the blood‐brain barrier

Peter G. Traber, Mauro Dal Canto, Daniel R. Ganger, Andres T. Blei – 1 November 1987 – Brain edema is a major complication of fulminant hepatic failure and is responsible for death in a large percentage of patients. We previously demonstrated the progressive accumulation of water in grey matter areas of the brain in the rabbit with galactosamine‐induced fulminant hepatic failure.

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