Df. Zhang et al., SERUM TUMOR-NECROSIS-FACTOR (TNF) IN THE PATHOGENESIS OF CLINICAL HEPATIC-FAILURE OF HCV AND OR HBV INFECTION, Chinese medical journal, 106(5), 1993, pp. 335-338
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.