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.