protein C

The anticoagulant pathway of protein C, as an appendage to TFPI (a tissue factor pathway inhibitor) and antithrombin, is another important inhibitor in the coagulation cascade. The basic composition includes protein C and its cofactor protein S, both of which are vitamin K-dependent hemostatic proteins that co-hydrolyze inactivated coagulation accelerators (factors Va and VIIIa). Protein C, protein S reduction or deficiency or inactivation of accelerator function loss (Factor V Leiden) increases the risk of thrombosis. Basic Information Specialist classification: cardiovascular examination classification: blood examination Applicable gender: whether men and women apply fasting: not fasting Tips: Keep a normal mindset. Normal value PC activity is 70% to 140%. The PC concentration is 70% to 140% (3 to 6 mg/L). Suspect factor V Leiden normal protein C activation rate ≤ 0.8. Clinical significance Deletion of the protein C pathway increases venous thrombosis, although there is speculation that there is a link between the high risk of thrombosis and acquired PC loss, but it remains to be confirmed. The physiological role of the protein C pathway is to inhibit the coagulation system, which has been reported to be associated with stimulation of fibrinolysis, but needs further confirmation. Protein S has an effect of accelerating the activation of protein C, and when the protein S is deficient, the anticoagulant effect disappears. Activated protein C inhibits factor V variation, but has a small effect. Therefore, this mutation causes the protein C anticoagulant pathway to be inhibited and the risk of thrombosis increases. The decrease in protein C and protein S activity is clinically relevant, and its genetic defects have two forms. Type I reduces both protein concentrations and activities due to reduced synthesis. Type II has a non-functional protein, ie, the concentration is normal and the activity is significantly reduced. There are other types in protein S: A decrease in the concentration of type III free protein S causes an increase in the concentration of the C4b binding protein, that is, the total concentration and activity of the protein S are normal and the concentration and activity of the free protein S antigen are decreased. Regarding the variation of Factor V Leiden, due to the autosomal dominant inheritance type, the heterozygous carrier is different from the homozygous type. Low results may be diseases: hemoglobin C disease, hereditary protein S deficiency, acute hemiplegia in children, idiopathic thrombocytopenic purpura in children, disseminated intravascular coagulation in children, thrombotic thrombocytopenic purpura in pregnancy, pediatric hemorrhage Disease, thrombotic thrombocytopenic purpura, pregnancy with thrombotic disease, pediatric antiphospholipid syndrome considerations Other reference values ​​have been reported in the commodity reagent box. Inspection process The protein C concentration measurement (immunochemistry) is different from the protein C activity measurement method (physiological hemostatic activity). Under certain conditions, such as the acute reaction period, the results of the two methods are inconsistent. (1) Enzyme immunoassay: The protein C antigen concentration was determined. (2) Coagulation method: In the coagulation method, the target is the anticoagulant activity of protein C, that is, the inactivation ability of factor VIIIa and factor Va. (3) Aminolysis method: This method uses a chromogenic substrate to determine protein C enzyme activity. Different from the coagulation method, the phospholipid binding site changes, such as oral anticoagulant therapy is more obvious, does not have any effect. Not suitable for the crowd Those without examination indications should not be tested. Adverse reactions and risks No complications.