Enhanced tumour necrosis factor and interleukin-1 in fulminant hepatic failure

Y Muto, A Meager, KT Nouri-Aria, GJM Alexander… - The Lancet, 1988 - Elsevier
Y Muto, A Meager, KT Nouri-Aria, GJM Alexander, ALWF Eddleston, R Williams
The Lancet, 1988Elsevier
Sepsis and endotoxaemia are common in fulminant hepatic failure (FHF) and may contribute
to multisystem disease in such patients. Tumour necrosis factor (TNF) is a probable mediator
of endotoxic shock and infusion of this monokine into animals causes multi-organ failure that
shares features with FHF. In patients with FHF, TNF production was increased and
correlated closely with activity of interleukin-1, another cytokine that is released by
monocytes/macrophages in response to infection and endotoxin and is produced in …
Abstract
Sepsis and endotoxaemia are common in fulminant hepatic failure (FHF) and may contribute to multisystem disease in such patients. Tumour necrosis factor (TNF) is a probable mediator of endotoxic shock and infusion of this monokine into animals causes multi-organ failure that shares features with FHF. In patients with FHF, TNF production was increased and correlated closely with activity of interleukin-1, another cytokine that is released by monocytes/macrophages in response to infection and endotoxin and is produced in increased quantities in FHF. Interleukin-2 activity was impaired in FHF and correlated negatively with TNF production.
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