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Abstract Sepsis is a major cause of morbidity and mortality among hospitalized patients. Sepsis is defined as a life-threatening organ dysfunction caused by a dysregulated host response to infection. Early diagnosis of sepsis is vital because rapid and appropriate therapy is associated with improved outcomes. Regardless of the inciting pathogen, endothelial activation and inflammation are found to be key in the initiation and continuation of host response, which primarily determine clinical outcomes within septic patients. Endothelial expression of tissue factor induced by a myriad of pro-inflammatory cytokines leads to subsequent systemic pro-coagulant response and activation of the anti-fibrinolytic pathway. With the coagulation cascade inadequately contained by natural anti-coagulant reaction, the shift toward procoagulant state results in excessive thrombin generation, microvascular fibrin deposition, and consumption of clotting factors, a process termed disseminated intravascular coagulation, contributing to significant morbidity and mortality secondary to associated MOF and coagulopathy. plasminogen activator and plasminogen activator inhibitor-1. They play crucial roles in the development of clot formation and disseminated intravascular coagulation that leads to fatal organ dysfunction. Basically, fibrinolysis is a simple system compared to the complex coagulation cascade. Plasmin is the only factor that regulates fibrinolysis, and this enzyme is modulated by several |