[1][2] The disorder is characterized by large amounts of the fibrinolytic enzyme urokinase-type plasminogen activator (uPA) in platelets.

[6] In 2010, the genetic cause of QPD was determined as a mutation involving an extra copy of the gene encoding uPA.

[7] The mutation causes overproduction of uPA, an enzyme that accelerates blood clot breakdown.

[8] Bleeding episodes are treated using antifibrinolytic medication, particularly tranexamic acid, to prevent fibrinolysis.

[8] The discovery was made by a team of doctors at McMaster University led by Dr. Catherine Hayward, a hematologist.