The coagulation process that leads to haemostasis involves a complex set of reactions involving approximately 30 different proteins. These reactions convert fibrinogen to fibrin, which, together with platelets, forms a stable thrombus. It has long been known that the clotting cascade consists of two separate initial pathways (intrinsic and extrinsic) that ultimately converge into the ‘common pathway’. The intrinsic and extrinsic pathways essentially serve to activate the precursor protein prothrombin to the active enzyme thrombin, which in turns converts fibrinogen into fibrin. The intrinsic pathway includes the “contact” activation system. The way in which this pathway is activated is a matter of continued activation. It has long been known that artificial agents such as glass, clay, or ellagic acid are able to act as activators for this pathway, but only recently have real pathophysiologic activators been identified, including RNA, NETs and polyphosphate (PolyP). The biological function of the latter has long been unknown, but recent studies have begun to elucidate the roles of PolyP in regulatory and metabolic functions in humans.
(BELG J HEMATOL 2015;6(3):127–8)