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עמוד בית
Mon, 26.02.24

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December 2013
Nir Samuel, Anat K. Politansky, Ron Hoffman, Shlomit Itzkovich and Hanna Mandel
October 2009
T. Strauss, G. Kenet, I. Schushan-Eisen, R. Mazkereth and J. Kuint
February 2008
M. Chanimov, I. Ben-Shlomo, B. Chayen, V. Gurovich, M. Friedland, M.L. Cohen and M. Bahar
July 2003
R. Satran and Y. Almog

Sepsis is an infection-induced inflammatory syndrome that results in a complex network of adaptive and maladaptive alterations in homeostatic mechanisms. Severe sepsis, defined as sepsis associated with acute organ failure, is a serious disease with a mortality rate of 30–50%. The coagulation system, through complex interactions, has an important role in the final outcome of the sepsis-induced inflammatory cascade. A fine and delicate balance that normally exists between anticoagulant mechanisms and the procoagulant response is altered in sepsis. Activated protein C, an endogenous vitamin K-dependent anticoagulant, plays a major role in the down-regulation of the procoagulant arm. It also possesses anti-inflammatory properties. Endothelial damage during sepsis impairs the endothelium-dependent activation of protein C, thus shifting the balance towards thrombosis. This shift may contribute to the development of sepsis-related multi-organ failure. Evidence suggesting that activation of the coagulation system may contribute to sepsis-related morbidity and mortality has led to extensive research attempting to correct the hemostatic defects seen in septic patients. Indeed, a recent randomized controlled trial demonstrated a reduction in overall mortality in patients with severe sepsis treated with APC[1]. In this review we discuss the pathogenesis of the coagulopathy of sepsis, as well as the new therapeutic approaches aimed at correcting the defects in the coagulation system.






[1] APC = activated protein C


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