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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 has been associated with Von Willebrand disease, Amegakaryocytic thrombocytopenia (low platelet count), prolonged activated partial thromboplastin time, combined coagulation defects. When present, these Noonan-syndrome accompanying disorders can be associated with a predisposition to bruise easily, or hemorrhage.
An eponymous disease is a disease, disorder, condition, or syndrome named after a person, usually the physician or other health care professional who first identified the disease; less commonly, a patient who had the disease; rarely, a literary character who exhibited signs of the disease or an actor or subject of an allusion, as characteristics associated with them were suggestive of symptoms ...
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.
Von Willebrand disease is the most common coagulopathy, and most women with von Willebrand disease have heavy menstrual bleeding. [23] Of women with heavy menstrual bleeding, up to 20% will have a bleeding disorder. [24]
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]
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 ]