[SIRS and the coagulation of normality].
Systemic inflammatory response syndrome(SIRS) is a pathologic condition associated with infection and tissue injury and it frequently leads to multiple organ dysfunction syndrome and disseminated intravascular coagulation(DIC). Pathologic events observed in SIRS can be attributable to the actions of cytokines such as tumor necrosis factor-alpha(TNF-alpha) and interleukin-1 beta. These cytokines activate monocytes and endothelial cells to induce the expression of tissue factor on their cell surfaces. Tissue factor then activates the extrinsic pathway of the coagulation system to induce microthrombus formation. These cytokines also contribute to microthrombus formation by decreasing the endothelial expression of thrombomodulin and glycosaminoglycans that regulate the coagulation system. Consequently, these cytokines induce DIC. These cytokines can activate neutrophils to release various inflammatory mediators which are capable of damaging the endothelial cell. The resultant endothelial cell injury, together with the microthrombus formation, may lead to microcirculatory disturbance which plays a role in ischemic organ dysfunction. Although physiological anticoagulants such as antithrombin and activated protein C can prevent endothelial cell injury by inhibiting leukocyte activation, heparin does not. Thus, these anticoagulants except for heparin may be effective in treating DIC associated with SIRS.
Okajima
K
K
Department of Laboratory Medicine, Kumamoto University School of Medicine.
D000991:Antithrombins / Q000627:therapeutic use; D004211:Disseminated Intravascular Coagulation / Q000188:drug therapy / Q000209:etiology*; D004730:Endothelium, Vascular / Q000378:metabolism; D006025:Glycosaminoglycans / Q000378:metabolism; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D007375:Interleukin-1 / Q000502:physiology; D009504:Neutrophils / Q000378:metabolism; D011486:Protein C / Q000627:therapeutic use; D018746:Systemic Inflammatory Response Syndrome / Q000150:complications*; D018180:Thrombomodulin / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
D000991:Antithrombins; D006025:Glycosaminoglycans; D018836:Inflammation Mediators; D007375:Interleukin-1; D011486:Protein C; D018180:Thrombomodulin; D014409:Tumor Necrosis Factor-alpha