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(Circulation. 2005;111:2-4.)
© 2005 American Heart Association, Inc.

Editorial

Resolution for Sepsis?

Derek W. Gilroy, PhD; Patrick Vallance, MD

From the Medical Research Council Sepsis Co-operative, BHF Laboratories, Division of Medicine, University College London, Rayne Institute, London, United Kingdom.

Correspondence to Derek W. Gilroy, Medical Research Council Sepsis Co-operative, BHF Laboratories, Division of Medicine, University College London, Rayne Institute, 5 University St, London WC1 6JJ, UK. E-mail d.gilroy@ucl.ac.uk

Key Words: Editorials • sepsis • inflammation

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Charged with protecting the host from invading organisms, distinguishing self from nonself, and the repair of tissue injury, inflammation is no trivial event: Life depends on it. However, there are times when this most primordial of events fails to protect the host and, paradoxically, goes into disarray. This is abundantly evident in rheumatoid arthritis, asthma, and psoriasis, for example, in which a perfectly well-meaning innate immune response somehow fails to resolve and instead progresses, irreversibly, toward chronic inflammation. However, neither the complex activation of the adaptive immune system nor the characteristic mayhem of chronic inflammation is necessarily required to bring about Virchow’s 5th cardinal sign of inflammation: Loss of organ function.¹ This can happen in a much more immediate manner with innate immunity and its response to tissue injury or infection in the form of sepsis. During sepsis, there is a rapid activation of the innate immune response and the release of soluble factors, including glucocorticoids, catecholamines, and proinflammatory cytokines (including tumor necrosis factor- [TNF-], interleukin-1ß, and interleukin-6). Exaggerated cytokine production, along with that of inducible nitric oxide synthase (NOS)–derived nitric oxide, platelet activation factor, and eicosanoids, has been implicated in the endothelial cell dysfunction, hypotension, inadequate organ perfusion, and necrotic cell death associated with multiple organ failure.²

See p 97

Conventional treatment for septic shock has focused on source control, antimicrobials, vasopressors, and fluid resuscitation.³ Despite effective antibiotics, septic shock remains the most common cause of death in the intensive care unit, incurring a mortality rate of 30% . . . [Full Text of this Article]

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