Inflammatory cytokine production enhancement in the presence of lipopolysaccharide after hepatic resection in cirrhotic patients.

Postoperative infection is one of the main factors that affect mortality after hepatic resection, especially in patients with liver cirrhosis. In the pathogenesis of postoperative organ failures complicating endotoxemia or other surgical injuries, inflammatory cytokine has proved to play an important role. We herein report the changes in tumor necrosis factor-alpha, interleukin-1 beta, and granulocyte colony-stimulating factor in production from macrophages/monocytes stimulated with lipopolysaccharide (LPS) after hepatic resection of cirrhotic livers. Seven hepatocellular carcinoma patients with liver cirrhosis who were undergoing limited resection or segmental resection of the liver were examined. Peripheral blood monocytes were separated and incubated with 10 microg/ml LPS, and cytokine release was measured by ELISA before surgery as well as on Postoperative Days (PODs) 1, 3, 7, and 14. Preoperative cytokine production in cirrhotic patients was greater than cytokine production in noncirrhotic controls. Cytokine productivity increased after hepatic resection. TNF-alpha production was 1,846.6 +/- 882.6 pg/ml, 1,947.3 +/- 221.9 pg/ml, 2,486.9 +/- 519.7 pg/ml, and 1,640.2 +/- 416.0 pg/ml on PODs 1, 3, 7, and 14, respectively. The values on all PODs were significantly greater than the healthy control value, and the value on POD 7 was significantly greater than the preoperative value. Interleukin-1 beta and granulocyte colony-stimulating factor production values corroborated this result in general. In conclusion, macrophages/monocytes are primed in cirrhotic patients preoperatively, and they are supposed to carry greater cytokine producing abilities after hepatic resection. When endotoxin spills over in the blood or in the liver after hepatic resection, postoperative hepatic failure could develop as a result of hypercytokinemia.