NovoSeven® as a universal haemostatic agent

Initiation of haemostasis involves the formation of a complex between tissue factor (TF) and activated factor VII (FVIIa) following injury TF is found in the deeper layers of the vessel wall, in atherosclerotic plaques and in some types of tumour cell and is only exposed to circulating blood after tissue damage. Likewise, MI is only enzymatically active when complexed with TF (TF/FVIIa). It has recently been shown that the administration of recombinant activated FVII (rFVIIa) in high doses (similar to 100 mu g/kg) can induce haemostasis in the absence of FVIII and FIX. In addition, from in-vitro studies it appears that rFVIIa can bind with low affinity to the activated platelet surface and, independently of TF, induce the thrombin burst needed for haemostasis. The ability of rFVIIa to compensate for FVIII/FIX deficiency has been proven clinically in haemophilia patients with life- and limb-threatening bleeds. In addition, patients with congenital FVII deficiency have been successfully treated for bleeds with rFVIIa. Recombinant FVIIa has been used in patients with platelet disorders; five patients with Glanzmann's thrombasthenia and one with Bernard-Soulier's thrombasthenia have had bleeding episodes managed effectively. Recombinant FVIIa has also been shown to normalize prothrombin time in patients with liver disease and in warfarin-treated individuals. Blood Coagul Fibrinolysis 11 (suppl 1):S107-S111 (C) 2000 Lippincott Williams & Wilkins.