A cDNA for coagulation factor XII has been used to investigate the presence of gene lesions and restriction fragment length polymorphisms in two brothers with Hageman trait and their family. A TaqI polymorphic fragment has been found in the two propositi and in 11 members of the paternal lineage. This polymorphism, absent in the normal population, is correlated with the reduction of factor XII ...

The differential diagnosis of a long APTT with a normal prothrombin time can be due to either a clotting factor deficiency or the presence of an inhibitor, which can be distinguished by using a plasma-mixing study. The various clotting factor deficiency states are reviewed. Clinical bleeding following cardiac bypass surgery due to acquired factor V and thrombin antibodies is also reviewed.

Coagulation factor V (FV), present in plasma and platelets, is indispensable to thrombin formation, yet patients with undetectable plasma FV seldom experience major bleeding. We used thrombin generation assays to explore the role of platelet FV in 4 patients with severe congenital FV deficiency (3 with plasma FV clotting activity [FV:C] < 1%). When triggered with tissue factor (TF) concentratio...

In his original description of a patient with parahemophilia and his studies on the nature of the defect, Owren (1) proposed that the missing factor, proaccelerin (Factor V), was converted, in the presence of calcium, into a prothrombinconverting substance ("prothrombinase," Factor VI) by the action of tissue thromboplastin. Other investigators, notably Ware and Seegers (2) in a series of studi...

Objective To provide evidence to support updated guidelines for the management of pregnant women with hereditary thrombophilia in order to reduce the risk of a first venous thromboembolism (VTE) in pregnancy.Design Systematic review and bayesian meta-analysis.Data sources Embase, Medline, Web of Science, Cochrane Library, and Google Scholar from inception through 14 November 2016.Review methods...

Thromb Haemost 2006; 95: 896–7 The clotting factor now known as factorV (FV) was first described in 1908 (1), and a deficiency of this factor was first described by Owren as parahaemophilia in 1947 (2). FV is predominantly produced in the liver and to a lesser degree by the megakaryocytes. Circa 80% of FV circulates in the plasma while 20% is stored in platelets. Following α-granule release upo...