Plasma Protein C (protein C, PC)
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Normal Values
PC: A chromogenic substrate method: (100. 24±13. 18) %.PC: Ag immunoelectrophoresis method: (102. 5±20. 1) %.>>>>
Influencing Factors
1. It is best to use siliconized or plastic syringes; glass tubes need to be siliconized, as glass can activate the coagulation response.2. The ideal anticoagulant should be sodium citrate.3. Establishing normal reference values during testing is crucial. Due to the significant fluctuation in PC activity, each laboratory must establish its own reference range, and the preparation of normal mixed plasma should be standardized. It is recommended to use mixed plasma from over 100 individuals, ensuring a balanced age and gender distribution.>>>>
Clinical Interpretation
PC is a vitamin K-dependent proenzyme whose main function is to activate and subsequently inactivate factor VIIIa in conjunction with factor Va, inhibiting blood coagulation.1. Decreased levels are seen in congenital PC structural abnormalities or production disorders (Type I: both PC: Ag and PC: A are decreased; Type II: PC: Ag is normal, PC: A is decreased) or acquired PC deficiencies, such as deep vein thrombosis, pulmonary embolism, DIC, severe liver disease, post-surgery, and skin purpura induced by oral anticoagulants like coumarin.2. Increased levels are observed in coronary heart disease, diabetes, nephrotic syndrome, late pregnancy, and during the acute phase of inflammation and other diseases.Activated Protein C Resistance Test (resistance to activated protein C test, APC-R)>>>>
Normal Values
Chromogenic substrate method: APC-R ratio > 1.96 (95% range, average ratio 2.36).>>>>
Influencing Factors
1. It is best to use siliconized or plastic syringes; glass tubes need to be siliconized, as glass can activate the coagulation process.2. The ideal anticoagulant should be sodium citrate.>>>>
Clinical Interpretation
1. APC-R is a recently discovered risk factor for hereditary thrombosis with a higher incidence, occurring in 2% to 10% of the normal population. One of the main causes is a mutation in the factor V gene that resists the degradation effect of activated protein C (APC). The rate in thrombosis patients can be as high as 15%, and in cases with a family history, it can rise to about 30%.2. APC-R is associated with various thrombotic diseases, such as venous thrombosis, stroke, myocardial infarction, and arrhythmias; additionally, the incidence in pregnant women is 60%.3. APC resistance may manifest in familial or early-onset thrombotic lesions, deep vein thrombosis, and may indicate a higher chance of arterial thrombosis compared to individuals without APC resistance.4. Clinically, the APC-R test can be applied to various patients suspected of venous thrombosis, pulmonary embolism, shortened APTT, those on oral contraceptives, pre-surgical patients, and those with familial thrombotic diseases for cause and risk factor analysis. If plasma levels of AT-III, PC, and PS are also checked, it can better determine the cause of thrombosis and provide accurate treatment guidance for APC-R positive patients.Plasma Protein S (protein S, PS)>>>>
Normal Values
Immunoelectrophoresis method:Total PS (TPS): (96. 6±9. 8) %.Free PS (FPS): 72%~130% (100. 9±11. 6) %.>>>>
Influencing Factors
1. It is best to use siliconized or plastic syringes; glass tubes need to be siliconized, as glass can activate the coagulation response.2. The ideal anticoagulant should be sodium citrate.3. Establishing normal reference values during testing is crucial. Due to the significant fluctuation in PS activity, each laboratory must establish its own reference range, and the preparation of normal mixed plasma should be standardized. It is recommended to use mixed plasma from over 100 individuals, ensuring a balanced age and gender distribution.>>>>
Clinical Interpretation
PS is also a vitamin K-dependent proenzyme. It can cooperate with activated protein C (APC) to eliminate the protective effect of factor Xa on factors Va, IXa, and VIIIa, leading to their hydrolysis. Decreased levels are seen in congenital PS deficiencies, where patients often develop severe deep vein thrombosis. Acquired PS reductions are seen in liver disease, skin necrotizing venous inflammation, pregnancy, SLE, nephrotic syndrome, and after oral anticoagulants like coumarin.This article is sourced from: Journal of Laboratory Medicine and Clinical Medicine. The views expressed in this article do not represent the platform’s views and are for public welfare promotion. If there is any infringement, please contact for deletion!