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The Treatment of Sepsis with Interleukin-1 Receptor Antagonist

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Sepsis

Part of the book series: Update in Intensive Care and Emergency Medicine ((UICM,volume 18))

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Abstract

Compelling experimental evidence and considerable clinical experience indicate that the proinflammatory cytokines are central to the pathogenesis of septic shock [1, 2]. Interleukin-1 (IL-1) and tumor necrosis factor-α (TNF) play an essential protective role in the priming and initiation of the host innate and acquired immune response to localized infection and inflammatory stimuli. However, excess systemic activation of these monocyte/macrophage-derived cytokines is clearly detrimental to the host and participate in the diffuse endothelial injury and disordered hemodynamic sequelae of sepsis [3]. In addition to their own intrinsic inflammatory actions, IL-1 and TNF stimulate the synthesis of additional host-derived inflammatory mediators such as platelet activating factor, eicosanoid compounds, interleukin-8 (IL-8), and other mediators which act in concert to produce septic shock. It has now become evident that activation of the cytokine-dependent nitric oxide synthase system by IL-1 and TNF is primarily responsible for the hypotension observed in septic shock [4].

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© 1994 Springer-Verlag Berlin Heidelberg

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Opal, S.M., Fisher, C.J., Pribble, J. (1994). The Treatment of Sepsis with Interleukin-1 Receptor Antagonist. In: Reinhart, K., Eyrich, K., Sprung, C. (eds) Sepsis. Update in Intensive Care and Emergency Medicine, vol 18. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-85036-3_30

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  • DOI: https://doi.org/10.1007/978-3-642-85036-3_30

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-85038-7

  • Online ISBN: 978-3-642-85036-3

  • eBook Packages: Springer Book Archive

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