Czynniki kontaktu w fizjologicznym krzepnięciu krwi oraz w zakrzepicy**

*Michał B. Ponczek, Michał Bijak

Summary
A unique mechanism of clot formation evolved in time of the emergence of vertebrates, probably more than 500 million years ago. In the classical cascade of blood clotting thrombin formation may be initiated by two overlapping coagulation pathways – extrinsic and intrinsic pathway. The common target for these alternative routes is the initiation of coagulation factors X and IX, and next, in both cases, the activation of thrombin, which converts soluble fibrinogen into insoluble fibrin. Extrinsic pathway appears to be evolutionarily older, because the basic elements such as factor VII, tissue factor, and duplicated ancestor, descendant of factor IX and X, along with thrombin and fibrinogen are already appearing in primitive vertebrates such as jawless lampreys. Intrinsic pathway, also known as activation by contact, is evolutionarily much younger and is formed only in the ancestor of placental mammals and marsupials. Activation of blood coagulation by the contact is an invention of mammalian evolution, and in the remaining groups of terrestrial vertebrates plasma kinin-kallikrein system has no connection with the hemostatic system. New experimental and clinical observations confirm the protective role of contact factor deficiencies in certain types of disorders associated with thromboembolic disorders. The increased activity of the contact system is accompanied by life-threatening states such as sepsis, congenital angioedema or allergic conditions. A new approach to prevent and treat thromboembolic disease should take into account the contact factors, especially factor XI, but also factor XII and plasma prekallikrein, as novel targets for antithrombotic therapy, giving the opportunity to develop methods minimizing the bleeding complications.

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