Since protein S binds and helps protein C to activate in reducing the clotting of the coagulation factors Va and Villa, a protein S deficiency predisposes those affected for venous thrombosis.

Since protein S binds and helps protein C to activate in reducing the clotting of the coagulation factors Va and Villa, a protein S deficiency predisposes those affected for venous thrombosis.

(See also Thrombotic diseases at a glance.) Since protein S binds and helps protein C to activate in reducing the clotting of the coagulation factors Va and Villa, a protein S deficiency predisposes those affected for venous thrombosis. Protein S as a vitamin K-dependent protein is a cofactor for activated protein C-mediated cleavage of the factors Va and VIIIa. A heterozygous protein S deficiency increases the risk of venous thrombosis. A heterozygous protein S deficiency resembles the heterozygous protein C deficiency in terms of genetic transmission, prevalence, laboratory testing, treatment and precautions. The homozygous protein S deficiency can also lead to purpura fulminans the newborn and is clinically indistinguishable from occurring in the homozygous protein C deficiency form. The acquired deficiency of protein C (and, thereafter ald, Protein S) occurs during disseminated intravascular coagulation (DIC) or warfarin therapy. The diagnosis is made over a the entire antigen test or freely present in the plasma protein S (free protein S is the form which is not bound to the protein-S-bearing molecule C4-binding protein). Anticoagulation therapy, the treatment of the protein S deficiency with venous thrombosis is identical with one exception to the treatment of Protein C deficiency. Because there is no purified protein S concentrates for transfusion, regular plasma is used to replace protein S during a thrombotic emergency. It is not known if the newer oral anticoagulants, either thrombin (dabigatran) or factor Xa (z. B. rivaroxaban, apixaban) inhibit can be used for this disorder instead of other anticoagulants.

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