Coagulation factor VIII plasma

USA rAHF-PFM antihemophilic Advate Recombinant human coagulation factor VIII produced by a plasma/albumin-free method Hemophilia... 

UF has also been used to concentrate antihemophilic coagulation factor VIII (AHF) with no measurable loss in activity it is particularly susceptible to thermal and shear denaturation. All of the other plasma proteins, including antithrombin III have been concentrated as well. 

Physical methods cryopredpitation is often used as the initial step for the production of Factor VIII and fibrinogen. It has no impact on the viral safety of such products. Subsequent purification techniques, such as precipitation by agents other than ethanol or chromatographic separation as well as procedures for viral inactivation are used to obtain the finished products. Cryoprecipitate-depleted plasma can be used for the separation of other coagulation factors or plasma protein solutions. 

Antihemophilic factor [9001-28-9] (AHF) is a protein found in normal plasma that is necessary for clot formation. It is needed for transformation of prothrombin to thrombin. Administration of AHF by injection or infusion can temporarily correct the coagulation defect present in patients with hemophilia. Antihemophilic factor VIII (Alpha Therapeutic) has been approved by the FDA as replacement therapy in patients with hemophilia B to prevent bleeding episodes, and also during surgery to correct defective hemostasis (178). 

Hemophilia A and B are coagulation disorders that result from defects in the genes encoding for plasma coagulation proteins. Hemophilia A (classic hemophilia) is caused by the deficiency of factor VIII, and hemophilia B (Christmas disease) is caused by the deficiency of factor IX. The incidences of hemophilia A and B are estimated at 1 in 5000 and 1 in 30,000 male births, respectively. Both types of hemophilia are evenly distributed across all ethnic and racial groups.1... 

Clinical pharmacology Activated factor IX in combination with activated factor VIII activates factor X. This results ultimately in the conversion of prothrombin to thrombin. Thrombin then converts fibrinogen to fibrin, and a clot can be formed. Factor IX is the specific clotting factor deficient in patients with hemophilia B and in patients with acquired factor IX deficiencies. The administration of Coagulation Factor IX (Recombinant) increases plasma levels of factor IX and can temporarily correct the coagulation defect in these patients. 

The effect of NaCS on all coagulation factors (I—XII) is at least the same as that of heparin. In fact NaCS inhibits the action of the anticoagulant factor VIII (anti-thermophilic globulin) much more effectively than heparin. Therefore, it may be concluded that NaCS acts mainly on factor VIII and partly on factor IX (plasma thromboplastic component) the latter was found to be suppressed by heparin. 

Before the screening of blood and plasma and before virus inactivation procedures were applied to coagulation factor products (for example factor VIII and factor IX), many hemophiliacs who were treated with substitution therapy were exposed to infection with HIV. In the USA about 70% of tested persons with hemophiha A (factor VIII deficiency) and 35% with hemophilia B (factor IX deficiency) were HIV-seropositive (177). 

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