**17. Sepsis**

Initiation of coagulation takes place when TF is exposed, such as by fibroblasts, when there is tissue damage or by cytokine-stimulated monocytes and endothelial cells216, as in sepsis. While TF is the major initiator of coagulation, endotoxin, foreign bodies, and negatively charged particles may initiate coagulation via contact system activation. TF binds to factor

Risk Factors of Deep Vein Thrombosis 19

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VIIa, and this complex (TF:VIIa) may then activate factor X and factor IX217. Factor Xa, associated with factor Va, forms the prothrombinase complex, which subsequently turns prothrombin into thrombin.

The relationship between coagulation and inflammation is complex and, as yet, not completely understood. It is known that blood clotting not only leads to fibrin deposition and platelet activation, but it also results in vascular cell activation, which contributes to leukocyte activation218. On the other hand, inflammation can induce TF expression in monocytes, via nuclear factor kappa-B (NF-kB) activation, thus initiating coagulation216.

Examples of this interaction are readily seen. First, leukocytes are found at relatively high concentrations in venous thrombi, and leukocytes and activated platelets can form rosettes mediated by P-selectin expression on the surface of the activated platelet 219,220.

These microscopic observations are probably elicited from the actions of thrombin, which can activate platelets and endothelium, increasing the surface expression of P-selectin221,222. P- electin is the primary initial mediator of leukocyte-endothelial cell rolling and is critical for leukocyte adhesion. Second, TF:VIIa and factor Xa have been shown to activate cells and generate responses similar to those mediated by thrombin218. Third, GAG and TM expression on cell surfaces are inhibited by inflammatory cytokines 223,224,225,226 and lipopolysaccharide (LPS)227, thus blocking the augmentation of AT action by GAG, and APC formation by TM.
