Von Willebrand disease (vWD) is an inherited trait where an individual’s bleeds excessively. It is very rare that the vWD is acquired later in life due to autoantibodies. The impairment of protein called von Willebrand factor which is an important component in blood–clotting process. The vWF gene is located on chromosome 12. Types 1 and 2 are inherited as autosomal dominant traits and type 3 is inherited as autosomal recessive. Occasionally type 2 also inherits recessively.
Disease statistics: In 1924, a 5-year-old girl who lived on the Åland Islands was brought to Deaconess Hospital in Helsinki, Finland, where she was seen by Dr. Erik von Willebrand. He ultimately assessed 66 members of her family and reported in 1926 that this was a previously undescribed bleeding disorder that differed from hemophilia.
Treatment: The two main treatment possibilities for patients with von Willebrand disease (vWD) are desmopressin (DDAVP) and von Willebrand factor/factor VIII (vWF/FVIII) concentrates. DDAVP is a synthetic analogue of the antidiuretic hormone vasopressin; it has enhanced antidiuretic activity and no pressor activity related to vasopressin. Purified plasma-derived concentrates of vWF/FVIII are used for treatment of bleeds and for surgical prophylaxis when DDAVP is ineffective or contraindicated.