作者: Charles A Dinarello , Jeffrey A Gelfand , Sheldon M Wolff
DOI: 10.1001/JAMA.1993.03500140081040
关键词:
摘要: The systemic inflammatory response syndrome (SIRS) is an acute illness characterized by generalized activation of the endothelium. most severe form found in patients with shock due to gram-negative sepsis. We examined both animal and limited human data for contribution cytokines this syndrome. Cytokines are endogenously produced proteins small molecular weight multiple biological effects. interleukin 1 (IL-1) tumor necrosis factor (TNF), as well interferon-γ 8, discussed. Laboratory investigations suggest that these play a critical role SIRS promoting biochemical clinical characteristics SIRS. changes induced TNF IL-1 include increased synthesis nitric oxide, prostaglandins, platelet-activating factor, endothelial cell adhesion molecules. Specific blockade using neutralizing antibodies or soluble receptors models reduces mortality severity disease. Similar results have been observed blocking receptor antagonists. Preliminary studies may be useful treating various strategies presented; addition, their mechanism(s) action safety humans conclude based on preliminary trials, block benefit syndrome, although thorough trials not completed. ( JAMA . 1993;269:1829-1835)