Abstract
Massive hepatic necrosis is a key event underlying acute liver failure, a serious clinical syndrome with high mortality. Massive hepatic necrosis in acute liver failure has unique pathophysiological characteristics including extremely rapid parenchymal cell death and removal. On the other hand, massive necrosis rapidly induces the activation of liver progenitor cells, the so-called “second pathway of liver regeneration.” The final clinical outcome of acute liver failure depends on whether liver progenitor cell-mediated regeneration can efficiently restore parenchymal mass and function within a short time. This review summarizes the current knowledge regarding massive hepatic necrosis and liver progenitor cell-mediated regeneration in patients with acute liver failure, the two sides of one coin.
Highlights
Pathological characteristics of massive hepatic necrosis (MHN)Two elegant studies investigated detailed pathological features of MHN (Lucke, 1944; Lucke and Mallory, 1946)
The following should be emphasized at the end of this review: Massive hepatic necrosis and liver progenitor cell-mediated regeneration are not isolated events during acute liver failure that occurs either in healthy or in diseased liver
Whether liver progenitor cells (LPC) can provide enough functional hepatocytes within a short time to restore liver mass and function determines destiny of patients who are suffering from acute liver failure (ALF) or acute-on-chronic liver failure (ACLF)
Summary
Two elegant studies investigated detailed pathological features of MHN (Lucke, 1944; Lucke and Mallory, 1946). In patients with a clinical history of more than 10 days, destruction of the liver was less uniform. Remarkable inflammatory cell infiltration into destructive areas (Figure 1B) with endophlebitis of the terminal veins (Figure 1C) is observed. Strong ductular reaction can be detected at this moment (Figure 1D) These two seminal studies, which included 296 dead patients with autopsy (most of whom were USA soldiers), represent the most complete and thorough investigations into MHN so far. In a clinical study to investigate the role of auxiliary liver transplantation in treating 30 patients with ALF, Chenard-Neu and colleagues showed that the percentage and distribution of necrosis at the time of transplantation was not associated with the final outcome (Chenard-Neu et al, 1996). We separated patients with serious necrosis into two groups according to area of necrosis (15–33% or 33–90%) and compared critical clinical parameters, including creatinine, serum total bilirubin, international normalized ratio
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