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Cytokine Measurements in Septic Shock

Charles A. Dinarello, MD; and Joseph G. Cannon, PhD
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Tufts University and New England Medical Center, Boston, MA 02111. Requests for Reprints: Charles A. Dinarello, MD, Division of Geographic Medicine and Infectious Diseases, New England Medical Center Hospitals, 750 Washington Street, Box 68, Boston, MA 02111. Grant Support: In part by NIH grants AI15614, AI33414, and AR39595.

Copyright 2004 by the American College of Physicians

Ann Intern Med. 1993;119(8):853-854. doi:10.7326/0003-4819-119-8-199310150-00013
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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.

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