A normal hemostatic response to vascular injury requires both factor VIII (FVIII) and von
Willebrand factor (VWF). In plasma, VWF and FVIII normally circulate as a noncovalent …

Factor VIII (FVIII) replacement therapy is the foundation of treatment in hemophilia A and is
effective unless a patient develops an alloantibody (inhibitor) against exogenous FVIII …

Background The development of neutralizing anti–factor VIII alloantibodies (inhibitors) in
patients with severe hemophilia A may depend on the concentrate used for replacement …

Background: Different rates of inhibitor development after either plasma‐derived (pdFVIII) or
recombinant (rFVIII) FVIII have been suggested. However, conflicting results are reported in …

Although immune tolerance induction (ITI) has been used for 30 years to eliminate inhibitors
and restore normal factor pharmacokinetics in patients with hemophilia, there is a paucity of …

The plasma glycoprotein von Willebrand factor (VWF) is exclusively synthesized in
endothelial cells (ECs) and megakaryocytes, the precursor cells of platelets. Its primary …

The interaction of factor VIII (FVIII) with von Willebrand Factor (VWF) is of direct clinical
significance in the diagnosis and treatment of patients with haemophilia A and von …

In the last few decades, the management of patients with haemophilia has witnessed
dramatic improvements, through the larger availability of safe plasma‐derived and …

Coagulation factor (F) VIII and von Willebrand factor (VWF) are known for their crucial roles
in hemostasis. The functional absence of either VWF or FVIII is associated with severe …

Abstract von Willebrand factor (vWF) was first identified as an adhesive glycoprotein
involved in hemostasis by Zimmermann in 1971. Since then, vWF has been shown to play a …