A B C D E F G H I J K L M N O P Q R S T U V W X Y Z # |
Protein C Antigen : 1000745
MessageThe aliquot must remain frozen. Freeze thaw cycle will adversely affect specimen integrity. CRITICAL FROZEN: Separate specimens must be submitted when multiple tests are ordered.
Test Code
PRTC or 1000745
Alias/See Also
Protein C Immunologic
CPT Codes
85302
Instructions
Blue top tube, 3.2% sodium citrate.
• Obtain venous blood by clean venipuncture. Avoid slow-flowing draws and/or traumatic venipunctures as either of these may result in an activated or clotted specimen. Do not use needles smaller than 23 gauge. Do not leave the tourniquet on for an extended length of time before drawing the sample.
• A pilot tube (non-additive or light blue tube) before drawing coagulation specimens in light blue vacuum tubes is only necessary when using a butterfly blood collection set as this will cause reduced draw volume in the first tube. Discard the pilot tube.
• Fill light blue tubes as far as vacuum will allow and mix by gentle inversion. Exact ratio of nine parts blood to one part anticoagulant must be maintained. Inadequate filling of the sample tube will alter this ratio and may lead to inaccurate results. Patients who have hematocrit values above 55 percent should have the anticoagulant adjusted to maintain the 9:1 ratio. Use the following formula to determine the amount of anticoagulant to use: [(100 – Hct) / (595 – Hct) ]* total volume = amount of anticoagulant required.
• After collecting the blood, examine the tube to ensure that it is filled to within 90% of the fill line.
• Note: Specimens containing heparin should not be used for coagulation studies. If possible, stop heparin therapy before the draw to avoid contamination. Heparin interferes with most clotting assays. If heparinized line must be used to obtain the sample, flush line with 5mL saline and discard the first 5 mL of blood drawn into a syringe, or 6 “dead space” volumes of the line.
• Obtain venous blood by clean venipuncture. Avoid slow-flowing draws and/or traumatic venipunctures as either of these may result in an activated or clotted specimen. Do not use needles smaller than 23 gauge. Do not leave the tourniquet on for an extended length of time before drawing the sample.
• A pilot tube (non-additive or light blue tube) before drawing coagulation specimens in light blue vacuum tubes is only necessary when using a butterfly blood collection set as this will cause reduced draw volume in the first tube. Discard the pilot tube.
• Fill light blue tubes as far as vacuum will allow and mix by gentle inversion. Exact ratio of nine parts blood to one part anticoagulant must be maintained. Inadequate filling of the sample tube will alter this ratio and may lead to inaccurate results. Patients who have hematocrit values above 55 percent should have the anticoagulant adjusted to maintain the 9:1 ratio. Use the following formula to determine the amount of anticoagulant to use: [(100 – Hct) / (595 – Hct) ]* total volume = amount of anticoagulant required.
• After collecting the blood, examine the tube to ensure that it is filled to within 90% of the fill line.
• Note: Specimens containing heparin should not be used for coagulation studies. If possible, stop heparin therapy before the draw to avoid contamination. Heparin interferes with most clotting assays. If heparinized line must be used to obtain the sample, flush line with 5mL saline and discard the first 5 mL of blood drawn into a syringe, or 6 “dead space” volumes of the line.
Transport Container
Blood collected in 3.2% sodium citrate (light blue top tube). Proper blood to anticoagulant ratio is required. The tubes must be at a 100 ± 10% fill volume to maintain the correct ratio. Centrifuge light blue-top tube at 1500 g for no less than 15 minutes or speed/time to consistently yield platelet-poor plasma (<10,000/µL). Using a plastic pipette, remove plasma, taking care to avoid the WBC/platelet buffy layer, and place into a plastic transport tube (Min. 0.5 mL). Immediately freeze the aliquot and ship on dry ice.
Transport Temperature
Frozen.
Specimen Stability
After separation from cells: Ambient: Unacceptable; Refrigerated: Unacceptable; Frozen: 30 days
Methodology
Enzyme-Linked Immunosorbent Assay (ELISA)
Setup Schedule
Tuesday & Thursday
Report Available
1-6 days
Reference Range
72-160 %
Clinical Significance
Protein C is a vitamin K-dependent protein synthesized primarily by hepatocytes in the liver and plays an important physiologic role in the Protein C Anticoagulant System. Protein C, through complex interactions with thrombin from blood clots, endothelial cells, and other factors of the coagulation cascade, contributes to the maintenance of normal hemostatic mechanisms by down-regulating clot formation and promoting fibrinolysis. The Protein C Anticoagulant System is activated by the binding of thrombin to thrombomodulin, a transmembrane protein receptor on endothelial cells. The thrombin-thrombomodulin binding on endothelial cell membranes activates circulating Protein C. Activated Protein C binds to Protein S on the membrane of endothelial cells or platelets. In this Protein C-Protein S complex, activated Protein C is now capable of inactivating the coagulation cascade factors Va and VIIIa, down-regulating clot formation.
Protein C deficiency, either congenital or acquired, may lead to serious thrombotic events such as thrombophlebitis, deep vein thrombosis, or pulmonary embolism. Patients with a congenital heterozygous deficiency may present with venous thrombosis (purpura fulminans) during the neonatal period. The prevalence of Protein C deficiency in the general population has been estimated at 1 in 300. In younger patients (<40-45 years) with recurrent venous thrombosis, the frequency of Protein C deficiencies may be as high as 10-15%. Acquired Protein C deficiency may be seen in liver diseases, extensive thrombotic episodes, surgery, oral anticoagulation, antiphospholipid syndrome, etc. A decreased Protein C activity in plasma may be the result of low concentrations and function (Type I) or only low function (Type II).
The laboratory diagnosis of Protein C deficiency may require both quantitative and qualitative (functional) determinations. Quantitative determinations of Protein C Antigen are based on immunologic procedures such as Enzyme-Linked Immunosorbent Assay (ELISA).
LIMITATIONS:
The Protein C Antigen concentration values obtained from this assay are an aid to diagnosis only. Each physician must interpret these results in light of the patient’s history, physical findings, and other diagnostic procedures. Patients with congenital homozygous deficiency of Protein C may have undetectable levels of Protein C, while those with heterozygous deficiency typically have levels between 30 to 60%. Acquired Protein C deficiency may be seen with numerous clinical conditions: neonates show 20-50% lower levels than adults, severe liver diseases, oral anticoagulants, post-operative period, disseminated intravascular coagulation (DIC), anti-phospholipid syndrome, etc. Increased levels of Protein C may be seen in patients with renal disease. Plasma samples could be inadvertently depleted of Protein C or degradation could occur by improper collection or laboratory processing.
Protein C deficiency, either congenital or acquired, may lead to serious thrombotic events such as thrombophlebitis, deep vein thrombosis, or pulmonary embolism. Patients with a congenital heterozygous deficiency may present with venous thrombosis (purpura fulminans) during the neonatal period. The prevalence of Protein C deficiency in the general population has been estimated at 1 in 300. In younger patients (<40-45 years) with recurrent venous thrombosis, the frequency of Protein C deficiencies may be as high as 10-15%. Acquired Protein C deficiency may be seen in liver diseases, extensive thrombotic episodes, surgery, oral anticoagulation, antiphospholipid syndrome, etc. A decreased Protein C activity in plasma may be the result of low concentrations and function (Type I) or only low function (Type II).
The laboratory diagnosis of Protein C deficiency may require both quantitative and qualitative (functional) determinations. Quantitative determinations of Protein C Antigen are based on immunologic procedures such as Enzyme-Linked Immunosorbent Assay (ELISA).
LIMITATIONS:
The Protein C Antigen concentration values obtained from this assay are an aid to diagnosis only. Each physician must interpret these results in light of the patient’s history, physical findings, and other diagnostic procedures. Patients with congenital homozygous deficiency of Protein C may have undetectable levels of Protein C, while those with heterozygous deficiency typically have levels between 30 to 60%. Acquired Protein C deficiency may be seen with numerous clinical conditions: neonates show 20-50% lower levels than adults, severe liver diseases, oral anticoagulants, post-operative period, disseminated intravascular coagulation (DIC), anti-phospholipid syndrome, etc. Increased levels of Protein C may be seen in patients with renal disease. Plasma samples could be inadvertently depleted of Protein C or degradation could occur by improper collection or laboratory processing.
Performing Laboratory
med fusion