The Effect of In Vitro Recombinant Factor VIIA on Coagulation Parameters for Blood Taken During Liver Transplantation

2005 ◽  
Vol 37 (10) ◽  
pp. 4367-4369 ◽  
Author(s):  
B. Gali ◽  
S.R. Rettke ◽  
D.J. Plevak ◽  
G.A. Nuttall ◽  
P.J. Santrach ◽  
...  
2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Lisa M. Baumann Kreuziger ◽  
Joseph C. Keenan ◽  
Colleen T. Morton ◽  
David J. Dries

Ease of dosing and simplicity of monitoring make new oral anticoagulants an attractive therapy in a growing range of clinical conditions. However, newer oral anticoagulants interact with the coagulation cascade in different ways than traditional warfarin therapy. Replacement of clotting factors will not reverse the effects of dabigatran, rivaroxaban, or apixaban. Currently, antidotes for these drugs are not widely available. Fortunately, withholding the anticoagulant and dialysis are freqnently effective treatments, particularly with rivaroxaban and dabigatran. Emergent bleeding, however, requires utilization of Prothrombin Complex Concentrates (PCCs). PCCs, in addition to recombinant factor VIIa, are used to activate the clotting system to reverse the effects of the new oral anticoagulants. In cases of refractory or emergent bleeding, the recommended factor concentrate in our protocols differs between the new oral anticoagulants. In patients taking dabigatran, we administer an activated PCC (aPCC) [FELBA] due to reported benefit in human in vitro studies. Based on human clinical trial evidence, the 4-factor PCC (Kcentra) is suggested for patients with refractory rivaroxaban- or apixaban-associated hemorrhage. If bleeding continues, recombinant factor VIIa may be employed. With all of these new procoagulant agents, the risk of thrombosis associated with administration of factor concentrates must be weighed against the relative risk of hemorrhage.


2007 ◽  
Vol 27 (3) ◽  
pp. 683-689 ◽  
Author(s):  
Geoffrey A. Allen ◽  
Egon Persson ◽  
Robert A. Campbell ◽  
Mirella Ezban ◽  
Ulla Hedner ◽  
...  

2005 ◽  
Vol 11 (8) ◽  
pp. 895-900 ◽  
Author(s):  
Raymond M. Planinsic ◽  
Jan van der Meer ◽  
Giuliano Testa ◽  
Luis Grande ◽  
Angel Candela ◽  
...  

2005 ◽  
Vol 11 (8) ◽  
pp. 973-979 ◽  
Author(s):  
J. Peter A. Lodge ◽  
Sven Jonas ◽  
Robert M. Jones ◽  
Michael Olausson ◽  
José Mir-Pallardo ◽  
...  

Blood ◽  
2002 ◽  
Vol 99 (1) ◽  
pp. 175-179 ◽  
Author(s):  
Ton Lisman ◽  
Laurent O. Mosnier ◽  
Thierry Lambert ◽  
Evelien P. Mauser-Bunschoten ◽  
Joost C. M. Meijers ◽  
...  

Recombinant factor VIIa (rFVIIa) is a novel prohemostatic drug for patients with hemophilia who have developed inhibitory antibodies. The postulation has been made that hemophilia is not only a disorder of coagulation, but that hyperfibrinolysis due to a defective activation of thrombin activatable fibrinolysis inhibitor (TAFI) might also play a role. In this in vitro study, the potential of rFVIIa to down-regulate fibrinolysis via activation of TAFI was investigated. rFVIIa was able to prolong clot lysis time in plasmas from 17 patients with severe hemophilia A. The prolongation of clot lysis time by rFVIIa was completely abolished by addition of an inhibitor of activated TAFI. The concentration of rFVIIa required for half maximal prolongation of clot lysis time (Clys½-VIIa) varied widely between patients (median, 73.0 U/mL; range, 10.8-250 U/mL). The concentration of rFVIIa required for half maximal reduction of clotting time (Cclot½-VIIa) was approximately 10-fold lower than the Clys½-VIIa value (median, 8.4 U/mL; range, 1.7-22.5 U/mL). Inhibition of TFPI with a polyclonal antibody significantly decreased Clys½-VIIa values (median, 2.6 U/mL; range, 0-86.9 U/mL), whereas Cclot½-VIIa values did not change (median, 7.2 U/mL; range, 2.2-22.5 U/mL). On addition of 100 ng/mL recombinant full-length TFPI, a nonsignificant increase of Clys½-VIIa values was observed (median, 119.2 U/mL; range, 12.3-375.0 U/mL), whereas Cclot½-VIIa values did not change (median, 8.8 U/mL; range, 2.6-34.6 U/mL). In conclusion, this study shows that rFVIIa both accelerates clot formation and inhibits fibrinolysis by activation of TAFI in factor VIII-deficient plasma. However, a large variability in antifibrinolytic potential of rFVIIa exists between patients.


2016 ◽  
Vol 178 (3) ◽  
pp. 482-486 ◽  
Author(s):  
Anne Marieke Schut ◽  
Marc Kirschbaum ◽  
Jelle Adelmeijer ◽  
Philip G. de Groot ◽  
Ton Lisman

2001 ◽  
Vol 71 (3) ◽  
pp. 402-405 ◽  
Author(s):  
Herman G.D. Hendriks ◽  
Karina Meijer ◽  
Joost Th.M. de Wolf ◽  
Ids J. Klompmaker ◽  
Robert J. Porte ◽  
...  

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