Desmopressin and hemostasis

Since it has been synthetized in 1967, desmopressin (Minirin) R or DDAVP (1-desamino-8-Darginine vasopressin) was initially used for its antidiuretic properties [1]. Its capacity to induce an increase in plasma level of procoagulant factor VIII C (FVIII C), von Willebrand factor (vWF) and plasminogen activator was recognized in the following years [2,3]. In 1977, its efficiency as hemostatic agent was reported in hemophilia A and in von Willebrand disease [4]. Ever since DDAVP has been extensively used for the prevention and treatment of bleeding from several origins. This period has also been marked by a better approach to the disorders of hemostasis and an increase need for transfused blood products entailing a dramatic risk of viral contamination. DDAVP is one of the alternatives developped in response to these challenges. The originality of DDAVP is to insure hemostasis, at least in responding patients, by recruiting their own endogenous factors without any risk ofimmunogenicity. Unlike other hemostatic drugs like epsilon aminocaproic acid, tranexamic acid or aprotinin (a broad spectrum proteinase inhibitor), DDAVP does not inhibit fibrinolysis.