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Mark A. Crowther, MD,MSc,FRCPC; John C. Marshall, MD,FRCSC

JAMA. 2001;286:1894-1896.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

The cardinal clinical manifestations of sepsis are prompted by infection, but are not due directly to the infecting microorganism. Rather, the hypotension, coagulopathy, and multisystem organ dysfunction that characterize severe sepsis are due in part to dysregulated expression of host-derived mediators of inflammation. The link between the clinical manifestations of sepsis and the host inflammatory response has led to a variety of experimental approaches to abrogate this response in animal models. Thus, blockade of proinflammatory cytokines, such as interleukin 1 (IL-1)¹ or tumor necrosis factor ,² administration of counterinflammatory mediators,³ such as IL-10 or granulocyte colony-stimulating factor, and inhibition of coagulation or support of endogenous anticoagulant mechanisms⁴ can all protect a variety of animals against endotoxin or even live bacteria.

Extrapolating the results of animal models to the clinical setting, however, has proved more challenging. Nearly 70 trials of a variety of . . . [Full Text of this Article]

Author Affiliations: Department of Medicine, St Joseph's Hospital, Hamilton, Ontario (Dr Crowther) and Toronto General Hospital, University Health Network, Toronto, Ontario (Dr Marshall).

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