Serum tumor necrosis factor (TNF) in the pathogenesis of clinical hepatic failure of HCV and/or HBV infection.

Serum TNF and IL-6 levels were measured in 48 patients with liver disease positive for anti-HCV only or concurrent HBV infection. High serum TNF levels were observed in patients with liver disease positive for anti-HCV and/or HBV infection (P < 0.001). Serum TNF levels varied with the severity of liver disease. Serum TNF levels of anti-HCV positive patients with hepatic failure were higher than those with CAH (P < 0.01). Serum TNF levels of patients infected with HCV or concurrent HBV were also significantly higher than those with HBV infection alone (P < 0.001). However, no difference in serum IL-6 levels was observed in either group of patients. Serum TNF in the deceased patients with hepatic failure induced by HBV and HCV infection was higher than in those who survived (P < 0.05), and it also seemed significantly different in patients with and without multiple organ failure (P < 0.05). In vitro, HSS showed marked inhibitory activity on TNF production from PBM induced by endotoxin, but had no significant effect on the TNF cytotoxicity of L929 cells. It seems that high serum TNF level is an important mediator in the pathogenesis of liver necrosis and failure of microcirculation in HCV and/or HBV infection. These observations favor the attempt to treat hepatic failure with HSS or anti-TNF. Encouraging results were achieved using HSS in the treatment of subacute liver necrosis in our institute.(ABSTRACT TRUNCATED AT 250 WORDS)