Factor Xa and Prothrombin:  Mechanism of Action of FEIBA

Turecek, Peter L.; Váradi, Katalin; Gritsch, Herbert; Auer, Wilfried; Pichler, Ludwig; Eder, Gerald; Schwarz, Hans

doi:10.1159/000056722

Cited by 60 publications

(56 citation statements)

References 22 publications

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“…The mechanism of action is multifactorial, though prothrombin and factor X are thought to be critical components. 41 rfVIIa and FEIBA VH have similar efficacy and rates of thrombosis; however, in a prospective randomized comparison of rfVIIa and FEIBA VH, approximately 30% of subjects responded more favorably to one product or the other 6 and 12 hours after treatment. 42 To better tailor treatment in individual patients some have looked to thromboelastography and endogenous thrombin potential.…”

Section: Treatment Of Acute Bleedingmentioning

confidence: 91%

How we treat a hemophilia A patient with a factor VIII inhibitor

Kempton

White

2009

Blood

146

144

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The most significant complication of treatment in patients with hemophilia A is the development of alloantibodies that inhibit factor VIII activity. In the presence of inhibitory antibodies, replacement of the missing clotting factor by infusion of factor VIII becomes less effective. Once replacement therapy is ineffective, acute management of bleeding requires agents that bypass factor VIII activity. Long-term management consists of eradicating the inhibitor through immune tolerance. Despite success in the treatment of acute bleeding and inhibitor eradication, there remains an inability to predict or prevent inhibitor formation. Ideally, prediction and ultimately prevention will come with an improved understanding of how patientspecific and treatment-related factors work together to influence anti-factor VIII antibody production. (Blood. 2009;113: 11-17)

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Section: Treatment Of Acute Bleedingmentioning

confidence: 91%

How we treat a hemophilia A patient with a factor VIII inhibitor

Kempton

White

2009

Blood

146

144

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“…Activated PCCs contain more active components than PCCs and were developed specifically for use in inhibitor patients. Although their precise mechanism of action is unknown, a recent study has shown that a complex consisting of highly purified activated factor X and prothrombin was able to achieve equivalent coagulant properties to an aPCC in in vitro testing as well as in an animal model [23].…”

Section: Control Of Acute Bleeding: Bypassing Therapymentioning

confidence: 99%

Prevention of bleeds in hemophilia patients with inhibitors: Emerging data and clinical direction

Leissinger

2004

American J Hematol

103

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In patients with hemophilia, the development of high-responding inhibitors to factor VIII prevents adequate replacement therapy and results in increased risk of serious bleeding episodes, poor control of joint bleeding, and progressive, debilitating joint disease. Immune tolerance therapy can eradicate inhibitors, but it is not uniformly successful. Emerging data suggest that prophylaxis using activated prothrombin complex concentrates may be effective and safe in reducing the incidence of joint bleeding during immune tolerance therapy and for patients in whom immune tolerance induction fails. However, only controlled clinical trials will ultimately demonstrate whether prophylaxis can prevent joint bleeding and damage, and improve quality of life in patients with inhibitors. Am.

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“…It triggers the formation of the prothrombinase complex, which leads to thrombin generation (TG). Feedback reactions mediated by thrombin and activated FX are thereby potentiated [7,8]. In addition FVIIa-dependent FX activation similar to one of the active principles of pure FVIIa cannot be excluded.…”

Section: Introductionmentioning

confidence: 99%

Factor VIII Inhibitor-Bypassing Agents Act by Inducing Thrombin Generation and Can Be Monitored by a Thrombin Generation Assay

Turecek

Váradi

Keil

et al. 2003

Pathophysiol Haemos Thromb

111

110

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Factor VIII (FVIII)-bypassing agents have complex modes of action but all control bleeding in inhibitor patients by triggering the generation of thrombin. No routine test is available for monitoring this therapy in patients with inhibitors against FVIII. We present an assay that records FEIBA- or FVIIa-mediated changes in thrombin generation (TG) in FVIII inhibitor plasma samples. In plasma samples spiked with FEIBA TG was normalized above 0.4 U/ml, while for recombinant FVIIa (rFVIIa) more than 12.5 µg/ml were required to induce TG in the absence of tissue factor (TF). Addition of TF increased the TG potential of rFVIIa in vitro. This assay seems suitable for monitoring the pharmacokinetics of inhibitor bypassing agents during treatment and possibly for predicting responses to treatment.

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Factor Xa and Prothrombin: Mechanism of Action of FEIBA

Cited by 60 publications

References 22 publications

How we treat a hemophilia A patient with a factor VIII inhibitor

How we treat a hemophilia A patient with a factor VIII inhibitor

Prevention of bleeds in hemophilia patients with inhibitors: Emerging data and clinical direction

Factor VIII Inhibitor-Bypassing Agents Act by Inducing Thrombin Generation and Can Be Monitored by a Thrombin Generation Assay

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