The effect of the administration of recombinant activated factor VII (NovoSeven®) on perioperative blood loss in patients undergoing transabdominal retropubic prostatectomy: the PROSE study

Friederich, Philip W.; Geerdink, M; Spataro, Marco; Messelink, E.J.; Henny, C. P.; Büller, Harry R.; Levi, Marilyn E.

doi:10.1097/00001721-200004001-00024

Cited by 53 publications

(26 citation statements)

References 20 publications

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“…64 -66 Preliminary clinical trials indicate that rFVIIa also promotes hemostasis in patients with normal coagulation systems. 67 It is rapidly acting and has a relatively short half-life of 2.5 hours, 68 which corresponds well with the duration of high risk for continued bleeding in the acute stage of ICH.…”

Section: Hemostatic Agents: Therapeutic Optionsmentioning

confidence: 92%

Ultra-Early Hemostatic Therapy for Intracerebral Hemorrhage

Mayer

2003

Stroke

193

110

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Background— Intracerebral hemorrhage (ICH) causes higher morbidity and mortality than other forms of stroke and has no proven effective treatment. Hematoma volume is a powerful predictor of outcome after ICH. Summary of Review— Historically, ICH bleeding was considered to be a monophasic event that stopped quickly as a result of clotting and tamponade by surrounding brain tissue. More recently, prospective and retrospective CT-based studies have demonstrated that hematoma growth occurs in up to 38% of patients initially scanned within 3 hours of onset and in 16% scanned between 3 and 6 hours, even in the absence of coagulopathy. Progressive bleeding of this type has been associated with contrast extravasation on CT angiography and poor outcome after early (<4 hours) surgical clot evacuation. On the basis of these observations, it is plausible that ultra-early hemostatic therapy given in the emergency setting might reduce ICH volume in some patients and improve outcome. Among candidate agents for this indication, the most promising is recombinant activated factor VIIa, which promotes local hemostasis at sites of vascular injury in both coagulopathic and normal patients. Conclusions— Ultra-early hemostatic therapy, given within 3 to 4 hours of onset, may potentially arrest ongoing bleeding and minimize hematoma growth after ICH. Given the current lack of effective therapy for ICH, clinical trials testing this treatment approach are justified.

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Section: Hemostatic Agents: Therapeutic Optionsmentioning

confidence: 92%

Ultra-Early Hemostatic Therapy for Intracerebral Hemorrhage

Mayer

2003

Stroke

193

110

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“…5,6 rFVIIa was originally developed for the treatment of inhibitor-complicated hemophilia A and B. 7,8 Currently, novel indications for rFVIIa, including its use in patients with liver disease, 9,10 thrombocytopenia, 11 and platelet function defects, 6,12 and in patients without coagulation disorders who are bleeding as a result of extensive surgery or major trauma, 13,14 are explored in clinical trials. The use of rFVIIa in patients with GT appears to be safe and effective, although randomized controlled clinical trials have not been performed in this small patient group.…”

Section: Introductionmentioning

confidence: 99%

Recombinant factor VIIa enhances deposition of platelets with congenital or acquired αIIbβ3 deficiency to endothelial cell matrix and collagen under conditions of flow via tissue factor–independent thrombin generation

Lisman

Moschatsis

Adelmeijer

et al. 2003

Blood

106

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A novel approach to treat bleeding episodes in patients with Glanzmann thrombasthenia (GT) and perhaps also in patients receiving ␣ IIb ␤ 3 inhibitors is the administration of recombinant factor VIIa (rFVIIa). The mechanism of action of rFVIIa in these patients is, however, still unclear. We studied the effect of rFVIIamediated thrombin formation on adhesion of ␣ IIb ␤ 3 -deficient platelets under flow conditions. Adhesion of ␣ IIb ␤ 3 -deficient platelets to the extracellular matrix (ECM) of stimulated human umbilical vein endothelial cells or to collagen type III was studied using a model system with washed platelets and red cells. When ␣ IIb ␤ 3 -deficient platelets were perfused over the surface at arterial shear rate for 5 minutes, a low surface coverage was observed (GT platelets, mean ؎ SEM, 37.5% ؎ 5.0%; normal platelets preincubated with an RGD-containing peptide, 7.4% ؎ 2.1%). When rFVIIa, together with factors X and II, was added to the perfusate, platelet deposition significantly increased (GT platelets, mean ؎ SEM, 67.0% ؎ 4.3%; normal platelets preincubated with an RGD-containing peptide, 48.2% ؎ 2.9%). The same effect was observed when normal platelets were pretreated with the commercially available anti-␣ IIb ␤ 3 drugs abciximab, eptifibatide, or tirofiban. It was shown that tissue factor-independent thrombin generation (presumably induced by binding of rFVIIa to adhered platelets) was responsible for the increase in platelet deposition. In conclusion, defective adhesion of ␣ IIb ␤ 3 -deficient platelets to ECM can be restored by tissue factor-independent rFVIIa-mediated thrombin formation. The enhanced generation of platelet procoagulant surface facilitates fibrin formation, so that lack of platelet aggregate formation might be compensated

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“…There are encouraging data on achieving haemostasis in intractable bleeding [12], in diffuse bleeding during neurosurgical operations [11], in patients with massive obstetric haemorrhage (placenta previa accreta, rupture of the uterus, and pre-eclampsia with HELLP) [17], in patients with coagulation abnormalities caused by Wilson's disease during liver transplantation [10], or in case of transabdominal retropubic prostatectomy [4].…”

Section: Discussionmentioning

confidence: 99%