Treatment modalities in experimentally induced acute liver failure

The findings made in the presented study suggest that one or more still unknown factors inherent in the experimental models currently in use are of critical importance and that only a certain limited type of model of acute hepatic failure is suitable for the evaluation of the effectiveness of methods intended to promote regeneration of diseased livers. It does not seem unreasonable to conclude that 40 x 106 liver cells injected into the abdominal cavity or the spleen would not improve survival, since ca. 300xlo6 (representing 30% of a normal liver) did not do so. It is conceivable that in a given model the use of hepatocytes and/or hepatocyte fractions triggers a non-specific reaction leading to survival. It is then also conceivable that when the hepatocytes or hepatocyte fractions are injected, the ongoing damage caused by galactosamine is arrested before it becomes lethal. This means that in cases of real fulminant hepatic failure the only chance of survival lies in the ability of the graft either to induce regeneration in the diseased liver or to take over all of the functions of the damaged liver. Because of the excessive risk associated with waiting to see whether the organ will recover is too great, it is preferable to aim at a transplantation enabling the graft to take over functions of the host's liver completely

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