Charles A. Dinarello, MD; Joseph G. Cannon, PhD
Dinarello C., Cannon J.; Cytokine Measurements in Septic Shock. Ann Intern Med. 1993;119:853-854. doi: 10.7326/0003-4819-119-8-199310150-00013
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Published: Ann Intern Med. 1993;119(8):853-854.
The cytokines interleukin-1 (IL-1) and tumor necrosis factor (TNF) affect nearly every cell type by increasing the production of substances that promote local and systemic inflammatory processes. These include the up-regulation of the genes for cyclooxygenase and nitric oxide synthases, the release of platelet-activating factor, and the synthesis of endothelial adhesion molecules. Vasodilation, reduced tissue oxidation, and leukocyte-mediated necrosis are thought to contribute to organ failure and death in patients with septic shock. Although IL-1 and TNF are capable of inducing shock individually, of greater biological relevance is the synergistic action of these two cytokines.
In animal models of disease, the roles of IL-1 and TNF have been defined by specifically inhibiting each cytokine. The anticytokine strategies for treatment of septic shock follow the same approach. Interleukin-1 can be blocked by reducing its synthesis ; infusing IL-1-receptor antagonist [2-4]; or administering soluble (extracellular) IL-1 receptors . Blocking TNF can be accomplished by reducing its synthesis, infusing neutralizing antibodies, or administering TNF-binding proteins that are the soluble forms of p55 or p75 TNF receptors [6, 7]. These agents are now being assessed in clinical trials.
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Infectious Disease, Pulmonary/Critical Care, Multi-Organ Failure and Sepsis.
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Print ISSN: 0003-4819 | Online ISSN: 1539-3704
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