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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. It is known to affect several ...
In an unknown fashion, the antibiotic ristocetin causes von Willebrand factor to bind the platelet receptor glycoprotein Ib (GpIb), so when ristocetin is added to normal blood, it causes agglutination of fixed platelets or initiates the initial agglutination phase of aggregation of live platelets. [citation needed]
Aortic stenosis, gastrointestinal angiodysplasia, and acquired von Willebrand disorder. Causes: Deficiency of high-molecular-weight multimers of von Willebrand factor. Risk factors: Recurrent gastrointestinal bleeding and heart failure. Diagnostic method: CBC, coagulation studies, metabolic panel, and test for fecal occult blood. Differential ...
Type 1 von Willebrand Disease in dogs. Type 1 von Willebrand Disease is the most common type, and also the mildest. It occurs when dogs have a mild deficiency in all the proteins making up their ...
Von Willebrand factor (VWF) (German: [fɔn ˈvɪləbʁant]) is a blood glycoprotein that promotes primary 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 syndrome. [5]
ABO blood group antigens present on red blood cells and IgM antibodies present in the serum. The ABO blood group system is used to denote the presence of one, both, or neither of the A and B antigens on erythrocytes (red blood cells). [1]
The factor VIII protein has a half-life of 12 hours in the blood stream when stabilized by the von Willebrand factor. [20] No longer protected by vWF, activated FVIII is proteolytically inactivated in the process (most prominently by activated protein C and factor IXa) and quickly cleared from the blood stream.
In the case of type 2B vWD, the gain-of-function mutation involves von Willebrand's factor (VWF gene), and in platelet-type vWD, the receptor is the object of the mutation (GPIb). This increased binding causes vWD because the high-molecular weight multimers are removed from circulation in plasma since they remain attached to the patient's ...