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 dise ase 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 wit h 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 we re also significantly higher than those with HBV infection alone (P<0. 001). However, no difference in serum IL-6 levels was observed in eith er 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 patie nts with and without multiple organ failure (P<0.05). In vitro, HSS sh owed marked inhibitory activity on TNF production from PBM induced by endotoxin, but had no significant effect on the TNF cytotoxicity of L9 29 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. Since HSS exerts growth factor-like activity in addition t o inhibiting TNF production, further study of the mutual action of TNF and HSS may provide better understanding of liver necrosis and develo p new immunomodulating therapeutic options.