Q. I’m confused about DDAVP. Why do you use it in von Willebrand disease? I read that it raises VIII and VWF, but that doesn’t really make sense since the factor VIII is already there, there is no need to make more of it? Right? The issue isn’t lack of factor VIII but lack of vWF, which carries the factor VIII.
A. DDAVP (1-deamino 8-d-arginine vasopressin, or desmopressin acetate) increases the level of both von Willebrand factor and factor VIII, by mechanisms which are not completely understood. So it can be useful in both von Willebrand disease and hemophilia A.
You’re right: in von Willebrand disease the decreased level of factor VIII (if present) is due to the decreased level of vWF, which is the carrier for factor VIII. So really, the main usefulness of DDAVP in vWF lies in its ability to increase vWF. It doesn’t hurt to increase the level of factor VIII, while you’re at it, but really, you could just increase vWF and the factor VIII level would come up on its own.
Image credit: Leo Reynolds
You’re right: in von Willebrand disease the decreased level of factor VIII (if present) is due to the decreased level of vWF, which is the carrier for factor VIII. So really, the main usefulness of DDAVP in vWF lies in its ability to increase vWF. It doesn’t hurt to increase the level of factor VIII, while you’re at it, but really, you could just increase vWF and the factor VIII level would come up on its own.
Image credit: Leo Reynolds
VWF in sufficient dose serves to stabilize factor VIII, which is otherwise volatile. In deficiency its term life is greatly shortened, and for reasons not understood, DDAVP acts as such a stabilizer (so it doesn’t really increase factor VIII, it simply renders it effective longer as if vWF were present).
DDAVP stimulates release of vWF stored in weibel Palade bodies in endothelial cells. See http://www.nhlbi.nih.gov/guidelines/vwd/4_managementofvwd.htm for more detailed info.