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Protein S Antigen Rocket Eid Kit Cat No 5359

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Last Updated: 02 July 2021

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General | Latest Info

Protein S is a vitamin K-dependent glycoprotein present in platelets and synthesize within liver and endothelial cells. Protein S works as part of the natural anticoagulant system by acting as cofactor to activate protein C in proteolytic inactivation of procoagulant factors Va and VIIIa. In addition, protein S has direct APC-independent anticoagulant activity by inhibiting formation of prothrombin and tenase complexes, possibly due to its high affinity for anionic phospholipid membranes. In human plasma, protein S forms a complex with compliment regulatory protein, C4b-binding protein. Of total plasma protein S, approximately 60 % circulates bound to C4bBP while the remaining 40 % circulates as free protein S. Only free protein S has anticoagulant function. C4bBP is composed of 6 or 7 alpha-chains and 1 or no beta-chain. Different C4bBP isoforms are present in plasma, but only C4bBP-beta binds to protein S. 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 and possibly arterial thrombosis. Three types of protein S deficiency have been described according to 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 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 disseminate intravascular coagulation / intravascular coagulation and fibrinolysis caused by absence of plasma protein S. Acquire deficiency of protein S has causes that are generally of unknown haemostatic significance, and is much more common than hereditary protein S deficiency. Acquire 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 acquire free protein S deficiency. Measurement of plasma free protein S antigen is performed as initial testing for protein S deficiency. When free protein S antigen level is below the age-and sex-adjust normal range, reflexive testing will be performed for total plasma protein S antigen.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Interpretation

Protein S is a vitamin K-dependent Plasma glycoprotein that synthesize predominantly within the liver. Protein S is also synthesize in endothelial cells and is present in platelets. As part of the Plasma anticoagulant system, Protein S acts as a necessary cofactor to activate Protein C in proteolytic inactivation of procoagulant factors Va and VIIIa. About 60 % of total Plasma Protein S antigen circulates bound to C4b binding Protein, while the remainder circulates as free Protein S. Only free Protein S has anticoagulant activity. Congenital Protein S deficiency is an autosomal codominant disorder that is present in 1 % to 3 % of patients with venous thromboembolism. Heterozygous Protein S deficiency carriers have an approximately 10-fold increased risk of venous thromboembolism. Other phenotypic expressions of heterozygous congenital Protein S deficiency include recurrent miscarriage, complications of pregnancy and possibly arterial thrombosis. Three types of heterozygous congenital Protein S deficiency have been described according to levels of total Protein S antigen, free Protein S antigen, and Protein S Activity in Plasma. Type I and III Protein S deficiency are much more common than Type II Protein S deficiency. Type III Protein S deficiency appears to be partly due to mutations within the Protein S binding region for C4b-BP. Homozygous Protein S deficiency is rare, but can present as neonatal purpura fulminans, reflecting severe intravascular coagulation and fibrinolysis / disseminate intravascular coagulation caused by absence or near absence of Plasma Protein S. Acquire deficiency of Protein S is much more common than hereditary Protein S deficiency and is generally of unknown hemostatic significance. Among many causes of acquire Protein S deficiency are:-acute illness

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Method

Initially, methods were developed which use undiluted test plasma. However, this approach turned out to be inadequate due to the great influence of prothrombin levels, with increasing amounts of prothrombin resulting in decreasing clotting times. Later methods all utilize excess of protein S deficient plasma, thereby keeping the amount of prothrombin essentially constant. Activate partial thromboplastin time method variants, using either addition of exogenous APC or addition of Protac C for activation of protein C present in test plasma and in protein S deficient plasma. In these methods, cofactor activity of protein S in APC-dependent degradation of both factor Va and factor VIIIa is analyse. By adding factor Va, greater sensitivity is obtain, which allows for use of more diluted test plasma and seemingly improves specificity. Depending on actual assay system use, resolution of 15-60 seconds is obtain between 0 and 100 % protein S. Prothrombin time method. Cofactor activity of protein S is confined to APC-dependent degradation of factor Va. Originally, method was developed for characterization of purified protein S which was later followed by functional test for determination of protein S in plasma. In the latter method, Protac C is used for activation of protein C contained in protein S deficient plasma prior to addition of diluted test plasma. This method was designed for easy application on automated analyzers. It shows the schematic design of this method. Resolution of 40-50 seconds is obtain between 0 and 100 % protein S. Factor Xa-base methods. In these methods, coagulation is triggered by factor Xa in the presence of calcium ions and phospholipids. Originally, undiluted plasma was used. Due to the drawback mentioned above, this was later replaced by more sensitive methods allowing dilution of test plasma and providing close to 100 seconds resolution between 0 and 100 % protein S. In one variant of method, free protein S in test plasma is first adsorb on insolubilized monoclonal protein S antibody. Factor Xa has also been used as a trigger in systems utilizing purified components. It should also be mentioned that although preliminary and promising results have been presented with chromogenic protein S methods, no such methods are currently used in routine settings.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Protein S

Table

Antithrombin deficiency>79
Protein C deficiency>160
Protein S deficiency> 140
APC resistance1
Prothrombin1

Blood coagulation can somewhat simplified be described as a cascade system of proteolytic reactions initiated in response to tissue damage. In each reaction, inactive zymogen is converted to its active enzyme counterpart, which then participates in the subsequent step of coagulation cascade. The Protein C anticoagulant pathway is a key system for down regulation of blood coagulation. Here, Protein S serves as cofactor to APC in inactivation of coagulation factors VIIIa and Va. In addition to its cofactor activity to APC, Protein S also has anticoagulant activity that is independent of APC. Coagulation is down-regulate by the Protein C anticoagulant pathway, in which activate Protein C degrades activate factors VIII and V through specific proteolytic cleavage. Protein S is cofactor to APC in these events. Protein S also seems to have anticoagulant activities which are independent of APC. Already form fibrin is later degraded by plasmin, key enzyme in the fibrinolytic system. The Importance of Protein C anticoagulant pathway has been amply demonstrated through serious thrombotic events which occur in connection with severe deficiency of Protein C and Protein S. It has also been demonstrated by a 7-fold increase in thrombotic risk which is associated with one commonly ocurring single point mutation in factor V gene. This mutation results in impaired degradation of factor Va at one of three APC cleavage sites, condition denoted as APC resistance. One intriguing fact regarding Protein S is that it circulates in plasma partly in a complex with C4b-binding Protein; extensive research has clearly shown that only Free Protein S has anticoagulant activity. It must be emphasized that it is not yet known which anticoagulant activity of Protein S is most important in vivo, and its detailed mechanism of action awaits clarification. Due to difficulties in determination of Protein S antigen and activity, there is so far no firm knowledge of Protein S deficiency among the general population; and hence, increased risk connected with Protein S deficiency is not easily assess. Available data indicate, along with other anticoagulant components, that clinically important risk connected with fairly mild Protein S deficiency is primarily found in connection with other inherited or acquired thrombotic risk factors.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

Table2

Antithrombin 50%FV:Q506 20%AT + FV:Q506 91%H.H. van Boven et al, Thromb Haemost 75, 417 - 21 (1996)
Protein C 31%FV:Q506 13%Pr C + FV:Q506 73%B.P.C. Koeleman et al, Blood 84, 1031 - 35 (1994)
Protein S 19%FV:Q506 19%Pr S + FV:Q506 72%B. Zoller et al, Blood 85, 3518 - 23 (1995)

Table3

Classification SSC 1992Classification Comp 1990Protein S antigen, totalProtein S antigen, freeProtein S activity
Type IType ILowLowLow
Type IIType IIbNormalNormalLow
Type IIIType IIaNormalLowLow
* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Sources

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

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