Riordan Stephen M, Williams Roger
Gastrointestinal and Liver Unit, The Prince of Wales Hospital, Sydney, Australia.
Semin Liver Dis. 2003 Aug;23(3):203-15. doi: 10.1055/s-2003-42639.
Acute liver failure (ALF) occurs when the rate and extent of liver cell death are not adequately balanced by regenerative activity. Two forms of liver cell death are recognized: apoptosis and necrosis. A number of causes of ALF have been shown, predominantly in experimental animal models, to induce one or the other form of liver cell death. Nonetheless, an insult capable of inducing apoptosis may cause cell death by necrosis, particularly if the degree of mitochondrial damage is sufficient to exhaust stores of adenosine triphosphate. Here we consider mechanisms of liver cell injury in ALF, including evolving knowledge of signaling pathways leading to hepatocellular apoptosis and necrosis. Factors that have an impact on the adequacy of hepatic regeneration along with the pathophysiology of complicating multiorgan failure are also reviewed. Prognostic criteria are discussed, especially in relation to current concepts of mechanisms of liver cell death and multiorgan dysfunction.
当肝细胞死亡的速率和程度未被再生活动充分平衡时，就会发生急性肝衰竭（ALF）。肝细胞死亡有两种形式：凋亡和坏死。在实验动物模型中，已证实多种导致ALF的病因会诱导其中一种或另一种形式的肝细胞死亡。然而，一种能够诱导凋亡的损伤可能会导致细胞坏死，特别是如果线粒体损伤程度足以耗尽三磷酸腺苷储备时。在此，我们探讨急性肝衰竭中肝细胞损伤的机制，包括对导致肝细胞凋亡和坏死的信号通路的不断深入了解。还综述了影响肝再生充分性的因素以及并发多器官功能衰竭的病理生理学。讨论了预后标准，特别是与当前肝细胞死亡机制和多器官功能障碍概念相关的内容。
