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Sepsis

, Volume 3, Issue 1, pp 65–73 | Cite as

IL-6 as a Marker of Excessive TNF-α Activity in Sepsis

  • Edward A. Panacek
  • Martin Kaul
Article

Abstract

The proinflammatory response triggered by infection and injury is initially protective and mediated by a number of host factors including tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and IL-8. In excess, these factors may cause severe tissue damage and life-threatening physiologic perturbations. If patients with a hyperinflammatory response can be identified early, they may benefit from treatment aimed at attenuating this response. In experimental models of sepsis, proinflammatory cytokines appear in the circulation in a relatively ordered manner but clinical sepsis is not as predictable. Compromised response mechanisms, interfering physiologic disturbances and therapeutic agents, and a variable temporal relationship to the onset of infection probably all contribute to the wide variability in both frequency and magnitude of their appearance seen in different studies. Although TNF-α is a proximal mediator of sepsis, circulating TNF-α concentrations at the time of diagnosis do not consistently correlate with disease severity. IL-6 is induced by TNF, appears in the circulation after the initial TNF response, often remains elevated, and is more consistently measurable. These properties may make it a good surrogate measure of localized TNF-α activity. In numerous studies, IL-6 was consistently shown to be elevated in septic patients, and serum concentrations correlated well with measures of disease severity and mortality. Assessing circulating IL-6 at the time of sepsis diagnosis may enable treatment decisions that are more directed to the individual patient's inflammatory response.

Keywords

Tumor Necrosis Factor Septic Patient Proinflammatory Response Include Tumor Necrosis Severe Tissue 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Kluwer Academic Publishers 1999

Authors and Affiliations

  • Edward A. Panacek
    • 1
  • Martin Kaul
    • 2
  1. 1.University of California Davis Medical CenterSacramento
  2. 2.Knoll AGLudwigshafenGermany

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