Gastro-intestinal complement activation during human liver transplantation: impact on postoperative liver function

Liver transplantation elicits a systemic inflammatory response and eventually a multiple organ failure syndrome. Gastro-intestinal inflammatory activation with release of proinflammatory cytokines and complement activation may occur. This study evaluates gastro-intestinal complement activation and the association with postoperative parenchymatous liver cell injury and liver dysfunction.

In 17 patients undergoing liver transplantation, blood samples were collected from radial artery and portal vein for analysis of complement SC5b-9 and endotoxin concentration. Portal venous-arterial SC5b-9 plasma concentration gradients at 30 min after reperfusion were calculated. Outcome parameters included postoperative organ failure and serum concentrations of aspartate aminotransferase, alanine aminotransferase, bilirubin and factor II-VII-X.

Patients with gastro-intestinal SC5b-9 release (n=7) had higher postoperative serum aspartate aminotransferase and alanine aminotransferase concentrations [49 (32-80) microkat/l vs 8 (6-14) microkat/l, P<0.01 and 33 (15-54) microkat/l vs 8 (4-23) microkat/l, P<0.04, respectively] and lower factor II-VII-X concentrations [46 (21-48)% vs 60 (47-69)%, P<0.02] compared to patients without gastro-intestinal SC5b-9 release (n=10). The ICU stay was prolonged in patients with gastro-intestinal complement release. There was no difference in number of organ failures and serum bilirubin concentration between the groups. The endotoxin concentration in arterial and portal vein blood was low and the association between endotoxaemia and complement activation was poor.

Gastro-intestinal complement activation may contribute to postoperative parenchymatous liver cell injury and liver dysfunction in patients undergoing liver transplantation.