RESUMO
Liver fibrosis occurs in response to chronic injury of any etiology. Kupffer cell [macrophage] activation accompanies liver injury with altered cytokine metabolism. This study aimed to investigate serum levels of tumour necrosis factor alpha [TNFa] and interleukin-6 [IL -6] as proinflammatory and profibrogenic cytokines in cirrhotic patients and relate them with the degree of liver disease and with the level of type -I plasminogen activator inhibitor [PAI-1] as a marker of fibrinolytic activity. The study included 20 cirrhotic patients and 15 healthy controls. After performing clinical and ultrasonic evaluation, liver function tests and hepatitis viral markers, patients were divided according to Child's Pugh classification of severity of liver disease into 3 groups, [group I] compensated cirrhosis, [group II] cirrhosis with ascites, [group III] decompensated cirrhosis. Serum levels of tumour necrosis factor alpha and interleukin-6 and plasma levels of type -I plasminogen activator inhibitor were measured. All patients showed significant positivity with hepatitis C virus antibodies. The Child-Pugh score of severity of liver disease was significantly increased in groups II and III compared to group I and control subjects. Serum TNFa. was significantly increased in all three groups of cirrhotic patients compared to control group. [P<0.05].Serum IL-6 was significantly increased in groups II and III [class B and C] compared to control group and there was significant difference between groups II and III and I and III So levels of IL-6 increased progressively with evolution of the disease. There was no statistical significant difference in plasma levels of PA1-1 between patients and controls. A positive significant correlation existed between TNFa and IL-6 in group II of patients [r= 0. 784 P=0.065] and between IL-6 and PAI-1 in groups II and III [r=0.78 P=0.067 and r= 0.000 P= 0.999 respectively]. In conclusion, this study revealed that in cirrhotic patients, serum levels of TNFa and IL-6 were significantly higher than control group, and IL-6 increased in advanced stages of the disease compared to early ones. There was positive correlation between TNFa and IL-6 in group II of patients. We suggested that the profibrogenic cytokines TNFa and IL-6 are implicated in fibrogenesis in cirrhotic patients and can be used as indicators for its progression. Further studies are needed to evaluate the use of their inhibitors as novel therapeutic agents to control undesirable fibrosis