Biochemical aspects of the pathogenesis of venous thrombosis.

In this review, an attempt has been made to present new data on the mechanisms that can be involved in DVT and to emphasize the role of the cell in these processes. It has been demonstrated that cells can mediate the relevant expression of tissue factor without cell disruption and that the fibrinolytic responses can also be modulated by the cells. It has also been demonstrated that the fibrinolytic system seems to be designed to work on the cell surface based upon (1) the existence of specific receptors, (2) the modulation of the expression of these receptors and (3) the comprehensive increase in plasmin generation by up-regulating, for example, the plasminogen receptors. It could also be worthwhile to attempt to explain some beneficial effects of drugs such as heparins by studying their action on these compartments. It is important to note that recently Rosenfeld et al. have described an increase in t-PA and u-PA binding to endothelium by pre-incubation of endothelial cells with unfractionated heparin. This work would be a first step in a very exciting and interesting new era in the prevention of venous thromboembolism.