Liver manipulation causes hepatocyte injury and precedes systemic inflammation in patients undergoing liver resection

Marcel C. G. van de Poll, Joep P. M. Derikx, Wim A. Buurman, Wilbert H. M. Peters, Hennie M. J. Roelofs, Stephen J. Wigmore, Cornelis Hc Dejong

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Abstract

Background Liver failure following liver surgery is caused by an insufficient functioning remnant cell mass. This can be due to insufficient liver volume and can be aggravated by additional cell death during or after surgery. The aim of this study was to elucidate the causes of hepatocellular injury in patients undergoing liver resection. Methods Markers of hepatocyte injury (AST, GST alpha, and L-FABP) and inflammation (IL-6) were measured in plasma of patients undergoing liver resection with and without intermittent inflow occlusion. To study the separate involvement of the intestines and the liver in systemic L-FABP release, arteriovenous concentration differences for L-FABP were measured. Results During liver manipulation, liver injury markers increased significantly. Arterial plasma levels and transhepatic and transintestinal concentration gradients of L-FABP indicated that this increase was exclusively due to hepatic and not due to intestinal release. Intermittent hepatic inflow occlusion, anesthesia, and liver transection did not further enhance arterial L-FABP and GST alpha levels. Hepatocyte injury was followed by an inflammatory response. Conclusions This study shows that liver manipulation is a leading cause of hepatocyte injury during liver surgery. A potential causal relation between liver manipulation and systemic inflammation remains to be established; but since the inflammatory response is apparently initiated early during major abdominal surgery, interventions aimed at reducing postoperative inflammation and related complications should be started early during surgery or beforehand
Original languageEnglish
Pages (from-to)2033-2038
JournalWorld journal of surgery
Volume31
Issue number10
DOIs
Publication statusPublished - 2007
Externally publishedYes

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