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HelpTest ID CFX Protein C Activity, Plasma
Useful For
As an initial test for evaluating patients suspected of having congenital protein C deficiency, including those with personal or family histories of thrombotic events
Because coagulation testing and its interpretation is complex, Mayo Medical Laboratories suggests ordering THRMP / Thrombophilia Profile.
Detecting and confirming congenital Type I and Type II protein C deficiencies, detecting and confirming congenital homozygous protein C deficiency, and identifying decreased functional protein C of acquired origin (eg, due to oral anticoagulant effect, vitamin K deficiency, liver disease, intravascular coagulation and fibrinolysis/disseminated intravascular coagulation.)
Special Instructions
Method Name
Amidolysis of Chromogenic Substrate
Reporting Name
Protein C Activity, PSpecimen Type
Plasma Na CitSee Coagulation Studies in Special Instructions.
Specimen Type: Platelet-poor plasma
Collection Container/Tube: Light-blue top (citrate)
Submission Container/Tube: Plastic vial
Specimen Volume: 1 mL
Collection Instructions:
1. Fasting
2. Spin down, remove plasma, and spin plasma again.
3. Freeze specimen immediately at ≤-40° C, if possible.
Additional Information:
1. Double-centrifuged specimen is critical for accurate results as platelet contamination may cause spurious results.
2. Each coagulation assay requested should have its own vial.
3. If the patient is being treated with Coumadin, this should be noted. Coumadin will lower protein C.
4. Heparin ≥4 U/mL may interfere with this assay.
5. Lipemic specimen may be rejected.
6. Coagulation testing is highly complex, often requiring the performance of multiple assays and correlation with clinical information. For that reason, we suggest ordering THRMP / Thrombophilia Profile.
Forms: If not ordering electronically, complete, print, and send a Coagulation Test Request Form (T753) with the specimen (http://www.mayomedicallaboratories.com/it-mmfiles/coagulation-test-request-form.pdf)
Specimen Minimum Volume
0.5 mL
Specimen Stability Information
| Specimen Type | Temperature | Time |
|---|---|---|
| Plasma Na Cit | Frozen | 14 days |
Clinical Information
Physiology:
Protein C is a vitamin K-dependent anticoagulant proenzyme. It is synthesized in the liver and circulates in the plasma. The biological half-life of plasma protein C is approximately 6 to 10 hours, similar to the relatively short half-life of coagulation factor VII.
Protein C is activated by thrombin, in the presence of an endothelial cell cofactor (thrombomodulin), to form the active enzyme activated protein C (APC). APC functions as an anticoagulant by proteolytically inactivating the activated forms of coagulation factors V and VIII (factors Va and VIIIa). APC also enhances fibrinolysis by inactivating plasminogen activator inhibitor (PAI-1).
Expression of the anticoagulant activity of APC is enhanced by a cofactor, protein S, another vitamin K-dependent plasma protein.
Pathophysiology:
Congenital homozygous protein C deficiency results in a severe thrombotic diathesis, evident in the neonatal period and resembling purpura fulminans.
Congenital heterozygous protein C deficiency may predispose to thrombotic events, primarily venous thromboembolism; arterial thrombosis (stroke, myocardial infarction, etc.) may occur. Some individuals with hereditary heterozygous protein C deficiency may have no personal or family history of thrombosis and may or may not be at increased risk. Congenital heterozygous protein C may predispose to development of coumarin-associated skin necrosis. Skin necrosis has occurred during the initiation of oral anticoagulant therapy.
Two types of hereditary heterozygous protein C deficiency are recognized:
-Type I (concordantly decreased protein C function and antigen)
-Type II (decreased protein C function with normal antigen level)
Acquired deficiencies of protein C may occur in association with:
-Vitamin K deficiency
-Oral anticoagulation with coumarin compounds
-Liver disease
-Intravascular coagulation and fibrinolysis/disseminated intravascular coagulation (ICF/DIC)
The clinical hemostatic significance of acquired protein C deficiency is uncertain.
Assay of protein C functional activity is recommended for the initial laboratory evaluation of patients suspected of having congenital protein C deficiency (personal or family history of thrombotic diathesis), rather than assay of protein C antigen (PCAG / Protein C Antigen, Plasma).
Reference Values
Adults: 70%-150%
Normal, full-term newborn infants or healthy premature infants may have decreased levels of protein C activity (15%-50%), which may not reach adult levels until later in childhood or early adolescence.*
*See Pediatric Hemostasis References in Coagulation Studies in Special Instructions.
Cautions
Protein C Activity result may be affected by:
-Heparin (Unfractionated) >4 U/mL
-Heparin (low-molecular-weight) >2 U/mL
-Hemoglobin >500 mg/dL
-Bilirubin >21 mg/dL
-Triglycerides >890 mg/dL
Heparin therapy may temporarily decrease plasma protein C activity into the abnormal range.
Lipemia may interfere with functional protein C assay. Blood specimens for protein C functional assay should be drawn in the fasting state, if possible.
Protein C functional assay using a venom activator and a chromogenic peptide substrate has the potential of not detecting certain congenital protein C variants that might be detectable using clot-based assay of protein C function.
Day(s) Performed
Monday through Friday
Report Available
1 dayPerforming Laboratory
Mayo Medical Laboratories in Rochester
Test Classification
This test has been cleared or approved by the U.S. Food and Drug Administration and is used per manufacturer's instructions. Performance characteristics were verified by Mayo Clinic in a manner consistent with CLIA requirements.CPT Code Information
85303