Von Willebrand disease (VWD) is a genetic disorder caused by missing or defective von Willebrand factor (VWF), a clotting protein. VWF binds factor VIII, a key clotting protein, and platelets in blood vessel walls, which help form a platelet plug during the clotting process. The condition is named after Finnish physician Erik von Willebrand, who first described it in the 1920s.

VWD is the most common bleeding disorder. It is carried on chromosome 12 and occurs equally in men and women.
There are three main types of VWD based on qualitative or quantitative defects in VWF. A fourth type, acquired VWD, is not hereditary.

Type 1 VWD is found in 60%-80% of patients. People with type 1 VWD have a quantitative deficiency of VWF. Levels of VWF in the blood range from 20%-50% of normal. The symptoms are usually mild.
Type 2 VWD is found in 15%-30% of patients. People with type 2 VWD have a qualitative deficiency in their VWF. Type 2 is broken down into four subtypes: type 2A, type 2B, type 2M and type 2N, depending on the presence and behavior of multimers, molecular chains of VWF. Symptoms are mild to moderate.
Type 3 VWD is found in 5%-10% of patients. People with type 3 VWD have a quantitative deficiency of VWF. Symptoms are typically severe, and include spontaneous bleeding episodes, often into their joints and muscles.    

Decreased VWF antigen may be seen in:
* Acquired VWD. This type of VWD in adults' results after a diagnosis of an autoimmune disease, such as lupus, or from heart disease or some types of cancer. It can also occur after taking certain medications and  may be associated with monoclonal gammopathies, lymphoproliferative disorders, autoimmune disorders, and hypothyroidism.
* Congenital von Willebrand disease.

Increased VWF antigen may be seen in association with:
-Pregnancy and/or estrogen use.
-Inflammation (acute-phase reactant).
-Exercise or stress.
-Liver disease.
-Vasculitis.
-Thrombotic thrombocytopenic purpura/hemolytic uremic syndrome.