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Volume 187, Issue 3, Pages 372-377 (March 2004)


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Intraperitoneal cytokine response after major surgery: higher postoperative intraperitoneal versus systemic cytokine levels suggest the gastrointestinal tract as the major source of the postoperative inflammatory reaction

Kjell Jansson, M.D.aCorresponding Author Informationemail address, Britt Redler, R.N.a, Lennart Truedsson, M.D., Ph.D.b, Anders Magnuson, B.Sc.c, Peter Matthiessen, M.D.a, Magnus Andersson, M.D., Ph.D.a, Lars Norgren, M.D., Ph.D., F.R.C.S.a

Received 17 December 2002; received in revised form 29 May 2003

Abstract 

Background

Cytokine response is an important factor in the development of shock and organ failure. The aim of this study was to investigate intraperitoneal (peritoneal) and venous (systemic) postoperative cytokine release after major surgery.

Methods

Major abdominal surgery was performed in 19 patients. Preoperative systemic measurements and postoperative systemic and peritoneal measurements of C-reactive protein (CRP) and the cytokines tumor necrosis factor-alpha (TNF-α), interleukin (IL-6), and IL-10 were performed.

Results

Significantly higher TNF-α, IL-6, and IL-10 peritoneal values were recorded compared with systemic values, whereas peritoneal CRP was significantly decreased. CRP increased significantly over time, whereas postoperative values of IL-6, IL-10, and peritoneal TNF-α decreased. Systemic TNF-α was constant over time, but values after emergent abdominal surgery showed a more extensive response. An additional effect of surgery and emergent abdominal disease was seen in increased TNF-α and IL-10 levels.

Conclusions

Compared with systemic cytokines, peritoneal cytokines respond extensively after major surgery, indicating that measurement of peritoneal cytokines is a more sensible method to determine postoperative inflammatory reaction. A normal postoperative course is characterized by decreasing levels of peritoneal cytokines.

a Department of Surgery, Örebro University Hospital, S-701 85 Örebro, Sweden

b Clinical Microbiology and Immunology Laboratory, Lund, Sweden

c Centre of Clinical Research, University Hospital, Örebro, Sweden

Corresponding Author InformationCorresponding author. Tel.: +46-19-6021000; fax: +46-19-125439.

PII: S0002-9610(03)00597-X

doi:10.1016/j.amjsurg.2003.12.019


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