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Successful Treatment of Diffuse Alveolar Hemorrhage with Activated Factor VII

David Henke, MD, MPH; Ronald J. Falk, MD; and Don A. Gabriel, MD, PhD
[+] Article and Author Information

From University of North Carolina at Chapel Hill, Chapel Hill, NC 27599.


Acknowledgments: The authors thank Dr. Harold Roberts for help with the Discussion section and Jean Brown and Melissa Lawrence for editorial and secretarial assistance. They also thank the clinical teams who cared for the patients.


Ann Intern Med. 2004;140(6):493-494. doi:10.7326/0003-4819-140-6-200403160-00033
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Figure.
Formation of the tenase complex and the prothrombinase complex.

Infused recombinant-activated human factor VII (rFVIIa) may initiate hemostasis by a tissue factor (TF)–dependent mechanism or by a TF-independent mechanism. Classically, TF expressed at an injury site activates factor VIIa (FVIIa). Then, FVIIa/TF activates both factor IX (FIX) and factor X (FX). Factor IXa (FIXa) and factor Xa (FXa) lead to stable thrombin formation by the assembly of the tenase complex (factor VIIIa [FVIIIa]/FIXa/FX) and the prothrombinase complex (factor Va [FVa]/FXa/factor II [FII]) on the surface of activated platelets. Infused rFVIIa may also initiate hemostasis by directly interacting with FIX on activated platelet surfaces. FIIa = factor IIa; FXIa = factor XIa.

Grahic Jump Location

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