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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 .
The differential diagnosis for Bernard–Soulier syndrome includes both Glanzmann thrombasthenia and pediatric Von Willebrand disease. [5] BSS platelets do not aggregate to ristocetin , and this defect is not corrected by the addition of normal plasma, distinguishing it from von Willebrand disease. [ 4 ]
CCP-224, a short PEG-conjugated form of the cyclic peptide OS-1, binds to human GPIb alpha with high affinity and can prevents neutrophil-platelet aggregation in Sickle Cell Disease. [13] In vivo, platelet-mediated thrombus formation can be greatly reduced in arterioles of mice, injured by laser, following an infusion of the OS-1 peptide. [ 14 ]
Von Willebrand Disease (vWD) is an inherited blood clotting disorder, similar (but different to) hemophilia. It is known to affect dogs, humans, and many other species, but it’s not contagious ...
Gray platelet syndrome (GPS), or platelet alpha-granule deficiency, [1] is a rare congenital autosomal recessive bleeding disorder caused by a reduction or absence of alpha-granules in blood platelets, and the release of proteins normally contained in these granules into the marrow, causing myelofibrosis. [2]
In 1924, a Finnish physician Erik Adolf von Willebrand (1870–1949) was consulted about a young girl with a bleeding disorder. Von Willebrand described this disorder in 1926, distinguishing it from hemophilia. The disorder was named after him, becoming known as von Willebrand disease.
It is similar to the ristocetin cofactor assay but has the added benefit in that it helps in the diagnosis of type 2B/pseudo von Willebrand disease (vWD) and Bernard–Soulier syndrome because it uses patient's live endogenous platelets, whereas ristocetin cofactor assay tests the function of only the vWF and not the platelets. Ristocetin ...
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.
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