Interleukin-6 mediates host defense responses induced by abdominal surgery.

Abstract

Cytokines have been implicated as pivotal mediators of the host defense reaction. In patients undergoing surgery we investigated the relationship between such mediators and postoperative host defense responses. Tumor necrosis factor (TNF) was determined with an immunoradiometric assay, interleukin (IL)-6 by a B9-cell bioassay, and endotoxin by a chromogenic limulus lysate assay. C-reactive protein, alpha 1-antitrypsin, and alpha 2-macroglobulin were quantified by nephelometric assay. In 19 consecutive patients undergoing pancreaticoduodenectomy, a large increase in portal, and a significantly lower increase in peripheral, IL-6 levels was observed. No significant increase in TNF levels was noted. Fever developed in 16 patients within 24 hours (84%). The highest peripheral IL-6 levels correlated logarithmically (R = 0.59; p = 0.0039) with the peak body temperatures. C-reactive protein levels correlated with IL-6 levels (R = 0.49; p = 0.020). Increased IL-6 levels were observed in all nine patients undergoing either hemihepatectomy, breast reduction, or extensive breast reconstruction; however, only patients undergoing hemihepatectomy had endotoxemia. We conclude that abdominal surgery causes acute release of IL-6, but not TNF, in the portal circulation. IL-6 seems to be a major endogenous mediator of fever and the acute-phase response. The presence of endotoxin might be synergistic but is not obligatory for the host defense response after surgical trauma.