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June 15, 1994

Sepsis Therapy TrialsContinued Disappointment or Reason for Hope?

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).

JAMA. 1994;271(23):1876-1878. doi:10.1001/jama.1994.03510470080040

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

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