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Changes in tumor necrosis factor-a and interleukin-1 beta production following liver surgery on cirrhotic patients
Background/Aims:
The purpose of this study is to investigate the possible participation of inflammatory cytokine release from macrophages/monocytes following liver surgery on cirrhotic patients in the pathogenesis of postoperative organ failures.
Materials And Methods:
Postoperative changes in tumor necrosis factor-a and interleukin-1 beta production in peripheral blood monocytes stimulated by lipopolysaccharide were examined in cirrhotic patients with hepatocellular carcinoma undergoing hepatic resections.
Results:
Monocytes separated from the blood in cirrhotic patients prior to operation showed a greater ability to produce tumor necrosis factor-a and interleukin-1 beta than those in healthy volunteers. Monocytes in postoperative cirrhotic patients showed a greater ability to produce tumor necrosis factor-a and interleukin-1 beta in the presence of lipopolysaccharide than healthy controls and preoperative cirrhotic patients. In the case of postoperative hepatic failure, tumor necrosis factor-a and interleukin-1 beta production in monocytes showed a remarkable rise along with progression toward hepatic failure.
Conclusion:
These results indicate that tumor necrosis factor-a and interleukin-1 beta play an important role in the pathogenesis of postoperative liver failures. When there are any stimuli to produce cytokines in monocytes, such as ischemia, significant tissue injury and/or endotoxin, organ failures could develop and progress subsequently.