Sepsis is a major cause of morbidity during the neonatal period. Endotoxins play an important role in the development of sepsis syndrome. In septic patients, level of circulating endotoxins is a prognostic marker for clinical outcome of septic syndrome (Brandtzaeg et al., 1989).
It has been reported that exposure to endotoxins induces a procoagulant state characterized by activation of the contact system of coagulation and alteration of fibrinolytic system with depletion of coagulation inhibitors (Van Deventer et al., 1990).
In patients with sepsis and septic shock, both coagulation and fibrinolysis are activated frequently, leading to the syndrome of diffuse intravascular coagulation (DIC). The coagulation and fibrinolytic systems appear to be influenced by the septic process; largely independently, leading to a procoagulant imbalance between these systems. The resulting effects may be an important mechanism contributing to multiple organ failure (Vervloet et al., 1998).
Thrombomodulin TM is an endothelial glycoprotein that is present on the endothelial cell surface and in plasma. It binds thrombin and catalyzes the protein C activation (Esmon and Owen, 1981).
Plasma soluble TM levels have been reported to reflect vascular endothelial damage in various clinical disorders in adults including disseminated intravascular coagulation (DIC) (Wada et al., 1993).
Scanty knowledge concerning plasma soluble TM levels in newborn infants exists, although various complications that may occur in the neonatal period that might possibly affect the endothelial cells (Nako et al., 1997a).
Aim of the work :
The aim of this study is to determine whether microcirculatory dysfunction and vascular endothelial damage, assessed by plasma concentration of soluble thrombomodulin, could occur in infants with neonatal sepsis, and their possible link to hemostatic alterations induced by the sepsis process. |
