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Von Willebrand’s Disease

The adhesion of platelets to the collagen exposed on endothelial cell surfaces is mediated by von Willebrand factor (vWF). Inherited deficiencies of vWF cause von Willebrand disease (vWD). The function of vWF is to act as a bridge between specific glycoproteins present on the surface of thrombocytes and collagen fibrils. vWF also binds to and stabilizes Coagulation Factor VIII, which is required for the survival of Factor VIII in circulation.

Von Willebrand’s Disease (vWD) is the most common presenting coagulopathy present in dogs. This condition is particularly present in the Dobermans Pinscher breed and occurs rarely if ever, in cats, horses or cows. Von Willebrand Coagulation Factor is produced mainly in endothelial cells and is a critical factor in Platelet Aggregation at the site of injury or disruption. VWD exists in three forms and in multimer form.

Type I

Type I vWD is the most common type of the disease recognized. It is comprised of small multimer chains.

Type II

Type II vWD is virtually absent, or has significantly reduced numbers of multimers and is seen most prevalently in German Shorthaired Pointer.

Type III

Type III vWD is devoid of multimers and causes the animal to present with severe hemorrhage. Type III vWD is seen mostly in Scottish Terriers, Shetland Sheepdogs, Chesapeake Bay retreivers, and German Wirehaired Pointers⁴³.

vWF is found attached to circulating Factor VIII. With severe vWF deficiency, Factor VIII levels may decrease but not enough to cause a change in the PTT.

Uremia may decrease the ability of platelet to adhese and liver disease may indirectly impair platelet function through accumulation of FDPs, which causes the inhibition of fibrinogen attachment to thrombocytic receptors.