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Protein S Antigen, Free
MessagePerforming Lab: Regions
Test Code
5349
Alias/See Also
Sunquest: FPSAG ;Free Protein S Antigen
CPT Codes
85306
Preferred Specimen
2.7 mL (in 3 mL tube) 3.2% Sodium Citrate Plasma (light blue-top) tube filled to fill line on the tube
Minimum Volume
1.0 mL plasma aliquot per test
Other Acceptable Specimens
1.0 mL platelet poor plasma (frozen)
Instructions
Processing: Freeze an aliquot of platelet poor plasma at -20C if not performed within 4 hours of collection
Centrifuge light blue-top tube for 15 minutes at approximately 1500 g within 60 minutes of collection. Using a plastic pipette, remove plasma, taking care to avoid the WBC/platelet buffy layer and place into a plastic vial. Centrifuge a second time and transfer platelet poor plasma into a new plastic vial. Plasma must be free of platelets (<10,000/mcl). Freeze immediately and ship on dry ice.
Centrifuge light blue-top tube for 15 minutes at approximately 1500 g within 60 minutes of collection. Using a plastic pipette, remove plasma, taking care to avoid the WBC/platelet buffy layer and place into a plastic vial. Centrifuge a second time and transfer platelet poor plasma into a new plastic vial. Plasma must be free of platelets (<10,000/mcl). Freeze immediately and ship on dry ice.
Transport Container
Transport processed samples frozen on Dry Ice
Transport Temperature
Frozen if > 4 hours old
Specimen Stability
Room Temperature: 4 hours Refrigerated: 4 hours Frozen 72 hours at -20C or 2 weeks at -80C
Reject Criteria (Eg, hemolysis? Lipemia? Thaw/Other?)
Refrigerated or Room temperature >4 hours, hemolysis, underfilled tubes, clotted
Methodology
Immuno-turbidimetric
Setup Schedule
Monday, Wednesday, Friday
Report Available
3 business days
Limitations
The presence of rheumatoid factor may lead to an over-estimation of the Free Protein S level.
Reference Range
55 - 142% Activity
Clinical Significance
Protein S has an essential anticoagulant function. It acts as the cofactor of activated protein C, with which it appears to form a stoichiometric complex. This complex binds strongly to phospholipid surfaces and thus regulates the coagulation process, inhibiting thrombin-stimulated factors V and VIII. Protein S greatly enhances the anticoagulant function of activated Protein C, probably by increasing Protein C affinity for phospholipid membranes.
Congenital protein S deficiency is an autosomal dominant disorder that is present in 2% to 6% of patients with venous thrombosis. Patients with protein S deficiency have an approximately 10-fold increased risk of venous thrombosis. In addition they may also experience recurrent miscarriage, complications of pregnancy (preeclampsia, abruptio placentae, intrauterine growth restriction, and stillbirth) and possibly arterial thrombosis.
Three types of protein S deficiency have been described according to the levels of total protein S antigen, free protein S antigen, and protein S activity in plasma. Types I and III protein S deficiency are much more common than type II (dysfunctional) protein S deficiency. Type III protein S deficiency appears to be partly due to mutations within the protein S binding region for C4bBP-beta.
Homozygous protein S deficiency is rare, but can present as neonatal purpura fulminans, reflecting severe disseminated intravascular coagulation/intravascular coagulation and fibrinolysis (DIC/ICF) caused by the absence of plasma protein S.
Acquired deficiency of protein S has causes that are generally of unknown haemostatic significance (ie, uncertain thrombosis risk), and is much more common than hereditary protein S deficiency. Acquired protein S deficiency can present through vitamin K deficiency, oral anticoagulant therapy, liver disease, DIC/ICF, thrombotic thrombocytopenia purpura, pregnancy or estrogen therapy, nephritic syndrome, and sickle cell anemia. As an acute-phase reactant, plasma C4bBP levels increase with acute illness and may cause acquired free protein S deficiency
Congenital protein S deficiency is an autosomal dominant disorder that is present in 2% to 6% of patients with venous thrombosis. Patients with protein S deficiency have an approximately 10-fold increased risk of venous thrombosis. In addition they may also experience recurrent miscarriage, complications of pregnancy (preeclampsia, abruptio placentae, intrauterine growth restriction, and stillbirth) and possibly arterial thrombosis.
Three types of protein S deficiency have been described according to the levels of total protein S antigen, free protein S antigen, and protein S activity in plasma. Types I and III protein S deficiency are much more common than type II (dysfunctional) protein S deficiency. Type III protein S deficiency appears to be partly due to mutations within the protein S binding region for C4bBP-beta.
Homozygous protein S deficiency is rare, but can present as neonatal purpura fulminans, reflecting severe disseminated intravascular coagulation/intravascular coagulation and fibrinolysis (DIC/ICF) caused by the absence of plasma protein S.
Acquired deficiency of protein S has causes that are generally of unknown haemostatic significance (ie, uncertain thrombosis risk), and is much more common than hereditary protein S deficiency. Acquired protein S deficiency can present through vitamin K deficiency, oral anticoagulant therapy, liver disease, DIC/ICF, thrombotic thrombocytopenia purpura, pregnancy or estrogen therapy, nephritic syndrome, and sickle cell anemia. As an acute-phase reactant, plasma C4bBP levels increase with acute illness and may cause acquired free protein S deficiency