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Apoptosis in the Resolution of Systemic Inflammation

  • J. C. Marshall
  • R. W. G. Watson
Conference paper
Part of the Yearbook of Intensive Care and Emergency Medicine book series (YEARBOOK, volume 1997)

Abstract

Admission to a contemporary ICU is precipitated by a heterogeneous group of disease processes, yet the final common pathway to death is strikingly similar [1]. Fully 80% of all ICU deaths occur in association with the multiple organ dysfunction syndrome (MODS) [2], a poorly understood process characterized by the development of progressive physiologic dysfunction in organ systems initially unaffected by the primary disease process. Activation of a host inflammatory response by infection, injury, or ischemia, invariably proceeds the development of MODS [3]. The proximate causes of organ injury are not bacterial products, but the same endogenous host-derived mediators of inflammation that are responsible for containing an infectious challenge and initiating the process of tissue repair. MODS can be conceptualized as the consequence of an overly activated or inappropriately prolonged systemic inflammatory response, therefore an understanding of the mechanisms underlying the resolution of inflammation is important to the development of clinical strategies to prevent the syndrome.

Keywords

Systemic Inflammatory Response Syndrome Tumor Necrosis Factor Receptor Multiple Organ Dysfunction Syndrome Staphylococcal Enterotoxin Neutrophil Apoptosis 
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

© Springer-Verlag Berlin Heidelberg 1997

Authors and Affiliations

  • J. C. Marshall
  • R. W. G. Watson

There are no affiliations available

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