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Continued Disappointment or Reason for Hope?

Edward Abraham, MD; Thomas A. Raffin, MD

JAMA. 1994;271(23):1876-1878.

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

Solid experimental and clinical data place interleukin 1 (IL-1) directly in the midst of the cascade of mediators leading to organ system dysfunction and death in sepsis. For example, infusion of IL-1 into animals produces hypotension and organ system dysfunction, a pattern similar to that seen clinically in severe infection.¹ Increased circulating levels of IL-1 appear to signal a poor prognosis in patients with sepsis.² In several animal models of endotoxemia or bacteremia, survival is improved when the actions of IL-1 are blocked by infusion of the naturally occurring IL-1 receptor antagonist (IL-1ra).^3,4 Perhaps most important, an unblinded, placebo-controlled study of IL-1ra therapy in critically ill patients with sepsis demonstrated a reduction in 28-day all-cause mortality from 44% in the placebo group to 16% in patients receiving high-dose IL-1ra therapy.⁵

See also p 1836.

In this issue of THE JOURNAL, Fisher et al⁶ report the . . . [Full Text PDF of this Article]

Author Affiliations
From the Section of Critical Care Medicine, Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Health Sciences Center, Denver (Dr Abraham); and the Division of Pulmonary and Critical Care Medicine, Stanford (Calif) University Medical Center (Dr Raffin).

Footnotes
Dr Abraham participated in the IL-1ra studies as a site investigator. However, he had no involvement in data analysis or interpretation.

Reprint requests to Division of Pulmonary and Critical Care Medicine, Stanford University Medical Center, Room H3151, Stanford, CA 94305-5236 (Dr Raffin).

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