作者: U. Hedner
DOI: 10.1097/00001721-200004001-00020
关键词:
摘要: Initiation of haemostasis involves the formation a complex between tissue factor (TF) and activated VII (FVIIa) following injury. TF is found in deeper layers vessel wall, atherosclerotic plaques some types tumour cell only exposed to circulating blood after damage. Likewise, FVII enzymatically active when complexed with (TF/FVIIa). It has recently been shown that administration recombinant (rFVIIa) high doses (approximately 100 microg/kg) can induce absence FVIII FIX. In addition, from in-vitro studies it appears rFVIIa bind low affinity platelet surface and, independently TF, thrombin burst needed for haemostasis. The ability compensate FVIII/FIX deficiency proven clinically haemophilia patients life- limb-threatening bleeds. congenital have successfully treated bleeds rFVIIa. Recombinant FVIIa used disorders; five Glanzmann's thrombasthenia one Bernard-Soulier's had bleeding episodes managed effectively. also normalize prothrombin time liver disease warfarin-treated individuals.