Blood coagulation & fibrinolysis : an international journal in haemostasis and thrombosis
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Blood Coagul. Fibrinolysis · Mar 1998
ReviewRecombinant activated factor VII as a universal haemostatic agent.
Haemostasis is initiated by the complex formed by tissue factor (TF) and activated factor VII (FVIIa) present in the blood [1% of the factor VII (FVII) protein]. Recombinant FVIIa (rFVIIa), enzymatically active only after complex formation with TF exposed following tissue damage, has been demonstrated to induce haemostasis in haemophilia patients with life- and limb-threatening bleedings with an efficacy rate of 76-84% in patients having failed on other treatment. rFVIIa has been successfully used in patients with congenital FVII deficiency and has been demonstrated to normalize the prolonged prothrombin time in patients with liver disease and in warfarin-treated individuals. ⋯ One patient with Glanzmann's thrombasthenia and three with Type III von Willebrand's disease were successfully treated with rFVIIa. By exploiting the binding capacity of FVIIa to platelets, rFVIIa, may also be used to enhance normal haemostasis in patients without coagulation defects but suffering from bleedings in organs or at sites with limited possibilities for mechanical haemostasis.
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Blood Coagul. Fibrinolysis · Mar 1998
Levels of prothrombin activation peptide F1+2 in patients with a bleeding tendency.
Numerous recent publications point to significant improvements in haemostasis in the bleeding patient suffering from haemophilia with inhibitors when a recombinant activated factor VII (rFVIIa) molecule is administered in high doses. In theory, activated factor VII (FVIIa) is believed to initiate haemostasis through its physiological interaction with tissue factor at sites of cellular injury, whereby factor X (FX) activation and, in consequence, thrombin formation is amplified. There has been speculation, however, whether high circulating FVII procoagulant (FVII:C) levels may induce systemic coagulation activation. ⋯ In FVII-deficient individuals, the mean rise in F1+2 was <0.10 nmol/l. In the control group, the mean elevation of F1+2 was 0.13 nmol/l (range -0.5 to 0.7 nmol/l). Hence, our results show that only discrete changes in F1+2 follow administration of rFVIIa.