We measured the levels of tumor necrosis factor alpha (TNF-α), interleukins (IL)-6 and -18, and soluble Fas (sFas) in 11 patients with postoperative hepatic failure and assessed whether IL-18-mediated apoptosis is involved in the onset of liver dysfunction. The serum TNF-α, IL-18, and sFas levels were significantly higher in patients with sepsis as a complication than in those without sepsis. The TNF-α and IL-18 levels were significantly higher in nonsurvivors than in survivors. Significant correlations were observed between TNF-α and IL-6, between TNF-α and IL-18, and between TNF-α and sFas levels. These results showed that Fas-mediated hepatocyte apoptosis functions as an important mechanism responsible for the onset of postoperative hepatic failure in humans. They especially suggested that IL-18 and TNF-α function both as apoptosis-promoting factors and as apoptosis-inhibiting factors, depending on the conditions to which hepatocytes are subjected.
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