Elevated levels of interleukin 18 in children with acute and chronic liver disease: further evidence of T cell-mediated liver injury

ABSTRACT

IL-18, derived from macrophages and kupffer cells, is the central pro-inflammatory cytokine leading to experimental liver failure. The objective of this study was to evaluate IL-18 in sera of infants and children suffering from acute hepatitis, chronic hepatitis and cirrhosis and to define its role as a predictive factor for chronicity of liver disease. Eighteen children suffering from acute viral hepatitis, 26 from chronic hepatitis and 15 suffering from cirrhosis were included in this study. They were attendants of the Hepatology Clinic of the New Children's Hospital, Cairo University. Twenty-three age and sex matched, clinically free infants and children, were also included as a control group. All studied infants and children, and the control group underwent quantitative determination of IL-18 in serum by ELISA. The mean IL-18 was found to be statistically significantly lower among the control group compared to the others. The mean IL-18 values were 38.65 +/- 15.46, 510.27 +/- 757, 305.03 +/- 647 and 257.86 +/- 395 pg/ml for the healthy control, acute hepatitis, chronic hepatitis and cirrhosis groups respectively. IL-18 level was not found to be predictive of pathology or etiology [P=0.067]. No correlation was found between IL-18 level and total bilirubin [P=0.70], direct bilirubin [P=0.79], ALT [P=0.29], AST [P=0.48] or alkaline phosphatase [P=0.222]. Higher levels of IL-18 were encountered in those children having more severe AIH. High IL-18 was present in children having various liver diseases. This supports the view that hepatocytes destruction is in part immune mediated. Immune modulation remains a potential future perspective for liver disease intervention