Fibrinogen replacement therapy: a critical review of the literature.

Fibrinogen is a plasma glycoprotein with a molecular weight of 340 kDa; it is synthesised by the liver. The conversion of fibrinogen to fibrin is catalysed by thrombin and plays a key role in clot formation and stabilisation. In addition, fibrinogen induces platelet activation and aggregation by binding to the platelet fibrinogen receptor glycoprotein GPIIb/IIIa1. Fibrinogen replacement therapy is currently indicated as prophylaxis and therapy of haemorrhage in congenital and acquired fibrinogen deficiency, this latter being associated with liver failure, disseminated intravascular coagulation, massive transfusion and cardiac surgery)2,3. Hypofibrinogenaemia is defined by a decreased level of normal fibrinogen between 0.5 g/L and the lower limit of the normal range for the local laboratory (usually 1.5 g/L)4. Fibrinogen supplementation can be provided by transfusion of fresh-frozen plasma (FFP), cryoprecipitate and fibrinogen concentrate5,6. However, as FFP has several limitations including a low fibrinogen content, which means that large volumes must be given, and the risk of transfusion-related complications (e.g., transfusion-related acute lung injury [TRALI] and viral transmission), this critical analysis is focused on the role of cryoprecipitate and fibrinogen concentrate.