Sign in →

Epic Test Code LAB489 Protein C Activity, Plasma

Important Note

Outpatient Use Only

 

Patient Instructions for Fasting Laboratory Testing

Additional Codes

MML Code: CFX

 

NY State Approved

Yes

Performing Laboratory

Mayo Clinic Laboratories in Rochester

Reporting Name

Protein C Activity, P

Method Name

Chromogenic

Specimen Stability Information

Specimen Type Temperature Time Special Container
Plasma Na Cit Frozen 14 days


Ordering Guidance


Coagulation testing is highly complex, often requiring the performance of multiple assays and correlation with clinical information. For that reason, consider ordering AATHR / Thrombophilia Profile, Plasma and Whole Blood.



Necessary Information


1. If the patient is being treated with Coumadin, this should be noted. Coumadin will lower protein C.

2. Heparin (unfractionated or low molecular weight) 2 U/mL or more may interfere with this assay.



Specimen Required


Specimen Type: Platelet-poor plasma

Patient Preparation: Fasting

Collection Container/Tube: Light-blue top (3.2% sodium citrate)

Submission Container/Tube: Plastic vial

Specimen Volume: 1 mL

Collection Instructions:

1. For complete instructions, see Coagulation Guidelines for Specimen Handling and Processing.

2. Centrifuge, transfer all plasma into a plastic vial, and centrifuge plasma again.

3. Aliquot plasma into a plastic vial leaving 0.25 mL in the bottom of centrifuged vial.

4. Freeze plasma immediately (no longer than 4 hours after collection) at -20° C or, ideally, at -40° C or below.

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.


Specimen Type

Plasma Na Cit

Specimen Minimum Volume

0.5 mL

Reference Values

70-150%

Report Available

1 to 3 days

Day(s) Performed

Monday through Friday

CPT Code Information

85303

Reject Due To

Gross hemolysis Reject
Gross lipemia Reject
Gross icterus Reject

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

 

Detecting and confirming congenital type I and type II protein C deficiencies

 

Detecting and confirming congenital homozygous protein C deficiency

 

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)

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.

 

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.

Interpretation

Values below 60% to 70% may represent a congenital deficiency state, if acquired deficiencies can be excluded.

 

Protein C activity (and antigen) is generally undetectable in individuals with severe, homozygous protein C deficiency.

 

Oral anticoagulant therapy (warfarin, Coumadin) decreases protein C activity, compromising the ability to distinguish between congenital and acquired protein C deficiency. Concomitant measurement of the activity of coagulation factor VII (or factor X) may aid in differentiating congenital deficiency state from acquired protein C deficiency due to oral anticoagulant effect, but the ratio of the activities of protein C:factor VII (or factor X) has not been demonstrated to provide certainty about  this distinction.

 

The clinical significance of acquired protein C deficiency and of increased protein C is unknown.

Cautions

Protein C activity result may be affected by:

-Heparin (unfractionated) ≥2 U/mL

-Heparin (low molecular weight) >2 U/mL

-Hemoglobin >500 mg/dL

-Bilirubin >21 mg/dL

-Triglycerides >890 mg/dL

 

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.

Specimen Retention Time

7 days