MHC antigen expression in human liver grafts: Its role in rejection

Dale C. Snover – 1 April 1990 – The present study documents major histocompatibility complex (MHC) Class I and II expression during early acute rejection of human liver grafts. Serial graft biopsies (pretransplant, time zero, and 1 week) were studied. Ten patients received azathioprine (AZA) and prednisone; the other six patients were treated with quadruple therapy (azathioprine, cyclosporine A, prednisone, and cyclophosphamide). To study the specificity of changes in MHC antigen expression, biopsies of six patients with minor or no morphologic abnormalities served as controls.

Fate of Mallory body‐containing hepatocytes: Disappearance of Mallory bodies and restoration of the hepatocytic intermediate filament cytoskeleton after drug withdrawal in the griseofulvin‐treated mouse

Kurt Zatloukal, Gerlinde Spurej, Ingrid Rainer, Elisabeth Lackinger, Helmut Denk – 1 April 1990 – Mallory bodies are characteristic morphological features of alcoholic hepatitis in man and can be produced in the mouse by chronic griseofulvin intoxication. The appearance of Mallory bodies in hepatocytes is associated with derangement of the cytokeratin intermediate filament cytoskeleton, at least as revealed by immunofluorescence and suggested by immunoelectron microscopy.

Reversal of the behavioral and electrophysiological abnormalities of an animal model of hepatic encephalopathy by benzodiazepine receptor ligands

Sergio H. Gammal, Anthony S. Basile, David Geller, Phil Skolnick, E. Anthony Jones – 1 March 1990 – Behavioral and electrophysiological evidence implicating the GABA‐benzodiazepine receptor complex in the pathogenesis of hepatic encephalopathy was obtained using an improved rat model of hepatic encephalopathy caused by thioacetamide‐induced fulminant hepatic failure. After the administration of thioacetamide together with supportive therapy, acute hepatocellular failure developed in rats as a result of massive hepatocellular necrosis without evidence of renal failure or hypoglycemia.

Hyperprolinemia and lactatemia in alcoholic liver disease: Relationships to abstinence and histological findings

Marcos Rojking – 1 March 1990 – It has not yet been established whether serum proline and blood lactate levels are increased in alcoholic liver disease. We measured serum proline and blood lactate in controls and in patients with different stages of alcoholic liver disease in the absence of hepatic failure. Samplings were done in both abstinent and drinking alcoholics. Compared to controls, there was a striking increase in serum proline levels in 52 abstinent alcoholics with little or no hepatic fibrosis by histological assessment (0.10 ± 0.01 vs. 0.155 ± 0.008; p < 0.005).

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