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The Liver as Modulator of the Host-Defense Response: Host-Defense Failure Disease as a Manifestation of Hepatic Decompensation

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Shock, Sepsis, and Organ Failure

Abstract

In this conference we are focusing on the relationship of the liver and the gut in the evolution of the post-injury septic process. However, I would like to refocus your attention on the liver as a critical organ modulating the entire host-defense response to trauma and to sepsis. Since the original studies of Tillet and Francis (1) which initiated our awareness of the presence of the process which we now call the acute phase response, we have become aware that the higher animal’s reaction to a localized but severe injury, or to its invasion by a bacterial or viral organism initiates an organized systemic host-defense response. When this host-defense response is appropriate to the stimulus, we see the initiation of a process which serves to control the initial disequilibrium introduced by the foreign stimulus and which acts to combat and eliminate invasive sepsis and to prevent septic decompensation. However, when this response process becomes disordered, we find ourselves dealing with what is truly a systemic disease of the acute phase response continued into a chronic decompensatory state, which we presently know as the Multiple Organ Failure Syndrome.

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Siegel, J.H. (1991). The Liver as Modulator of the Host-Defense Response: Host-Defense Failure Disease as a Manifestation of Hepatic Decompensation. In: Schlag, G., Redl, H., Siegel, J.H., Traber, D.L. (eds) Shock, Sepsis, and Organ Failure. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-76511-7_7

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