الفهرس 
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Abstract
A host of immunological abnormalities have been documented in chronic liver disease, for example, decreased production of Interferon, lnterleukin 2 and decrease of T lymphocyte response to interleukin 2 (Dudley et aL, 1972).
DNA recombinant technology provides us with large quantities of pure biologically active materials for scientific and clinical evaluation. it seems likely that studies evaluating their treatment value will also yield insights into the biological processes which they control (Wang et aL, 1985).
Tumour Necrosis Factor (TNF) is considered one of the mediators of the metabolic and immunological consequences that lead to cytotoxicity and ultimately organ failure in endotoxemia or sepsis. The cytotoxic potential of TNF appears to involve the production of oxygen derived radicals. The release of such radicals may induce tissue injury that could lead to organ failure (Bautista et (IL, 1991).
Lehmann et at., (1987) suggested that TNFa is responsible for liver injury mediated by galactosarnine.
Muto et (z1.,(1988)haVe observed increased production of TNF by mononuclear cells in patients with fulminant hepatic failure.
‘oshioka et a/.,(1989. showed that TNF production is increased in chronic liver diseases.
Jones et aL, (1990) noted that when exogenous TNF was administered as a potential anti-cancer agent abnormal liver enzymes with transient hyperbilirubinaemia were seen.
The present study was undertaken to highlight the state of TNF production in chronic liver disease, to evaluate its relation to the development of vascular or parenchymatous decompensation with special emphasis on its relation to different histopathological processes.