Management of XXXX disorders by prohemostatic therapy.

@entity1 @entity82 @entity882 @entity548 @entity1423 @entity447 @entity5507 @entity117 @entity149 @entity3459 @entity2881 @entity376 @entity1351 @entity1031 @entity2880
Pro-hemostatic therapy aims at an improvement of hemostasis, which may be achieved by amelioration of primary hemostasis, stimulation of fibrin formation or inhibition of fibrinolysis. These treatment strategies may be applied to specifically correct a defect in one of the pathways of coagulation, but have in some situations also been shown to be effective in reducing @entity548 in @entity1 without a primary @entity3459 . Besides the transfusion of platelets in case of @entity882 or severe @entity1423 , a pharmacological improvement of primary hemostasis may be achieved by the administration of desmopressin. The administration of DDAVP results in a marked increase in the plasma concentration of @entity2881 ) and (also by yet unexplained additional mechanisms) a remarkable potentiation of primary hemostasis as a consequence. DDAVP is used for the prevention and treatment of @entity548 in @entity1 with @entity2880 or mild @entity447 , and further in @entity1 with an impaired function of primary hemostasis, such as in @entity1 with @entity5507 , liver @entity82 or in @entity1 with @entity117 -associated @entity548 . Based on the current insight that activation of coagulation in vivo predominantly proceeds by the tissue factor/factor VII(a) pathway, recombinant factor VIIa has been developed as a prohemostatic agent and has recently become available for clinical use. Indeed, in uncontrolled clinical studies this compound has been shown to exert a potent procoagulant activity and appeared to be highly effective in the prevention and treatment of @entity548 , although most experience so far has been obtained in @entity1 with severe and @entity149 . At present, a more general use of this agent for @entity548 @entity1 without an apparent @entity3459 is the subject of a number of ongoing clinical trials. Agents that exert anti-fibrinolytic activity are aprotinin and the group of @entity376 analogues. The pro-hemostatic effect of these agents proceeds not only by the inhibition of fibrinolysis (thereby shifting the procoagulant/anticoagulant balance towards a more procoagulant state), but also due to a protective effect on platelets, as has been demonstrated at least for aprotinin. The mechanism of this platelet-protective effect has, besides a potential prevention of @entity1351 -mediated loss of platelet receptors not been elucidated. Whether the pro-hemostatic effect of the anti-fibrinolytic agents will eventually result in a higher incidence of @entity1031 is still a matter of debate (see further), however, this has so far not been shown in straightforward clinical trials.
