Enhanced tumour necrosis factor and interleukin-1 in fulminant hepatic failure.
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.
D000293:Adolescent; D000328:Adult; D005260:Female; D006525:Hepatitis, Viral, Human / Q000378:metabolism; D006801:Humans; D007375:Interleukin-1 / Q000096:biosynthesis* / Q000302:isolation & purification; D007376:Interleukin-2 / Q000302:isolation & purification / Q000378:metabolism; D008107:Liver Diseases / Q000209:etiology / Q000378:metabolism* / Q000401:mortality; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000378:metabolism; D011863:Radioimmunoassay; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis* / Q000302:isolation & purification
D007375:Interleukin-1; D007376:Interleukin-2; D014409:Tumor Necrosis Factor-alpha