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Von Willebrand disease (VWD) is the most common hereditary blood-clotting disorder in humans. An acquired form can sometimes result from other medical conditions. [1] It arises from a deficiency in the quality or quantity of von Willebrand factor (VWF), a multimeric protein that is required for platelet adhesion.
Von Willebrand factor (VWF) (German: [fɔn ˈvɪləbʁant]) is a blood glycoprotein that promotes hemostasis, specifically, platelet adhesion. It is deficient and/or defective in von Willebrand disease and is involved in many other diseases, including thrombotic thrombocytopenic purpura , Heyde's syndrome , and possibly hemolytic–uremic ...
Numerous papers were subsequently published on the disease and it became eponymously known as von Willebrand disease between the late 1930s and the early 1940s. [5] [13] In 1957, it was discovered that von Willebrand disease is caused by a deficiency of a protein in blood plasma that enables hemostasis. [14]
The National Bleeding Disorders Foundation (NBDF) is a United States patient advocacy organization for the care and treatment of inheritable blood and bleeding disorders such as hemophilia and von Willebrand disease. Founded in 1948, NBDF, then known as the National Hemophilia Foundation, helps secure funding for treatment centers and develops ...
Von Willebrand disease in dogs is the most common inherited blood disorder our canine friends suffer with, and it also happens in humans and many other species.
Von Willebrand disease (which behaves more like a platelet disorder except in severe cases), is the most common hereditary bleeding disorder and is characterized as being inherited autosomal recessive or dominant. In this disease, there is a defect in von Willebrand factor (vWF), which mediates the binding of glycoprotein Ib (GPIb) to collagen.
In addition, desmopressin (DDAVP) is known to be effective in people with von Willebrand's disease, [17] [18] including people with valvular heart disease. [19] [20] Desmopressin stimulates release of von Willebrand factor from blood vessel endothelial cells by acting on the V2 receptor, which leads to decreased breakdown of Factor VIII.
Blood disorders (e.g., von Willebrand disease) Brachycephalic syndrome (respiratory issues in flat-faced breeds) Heart defects (e.g., mitral valve disease) Cushing’s disease.