Protein C Antigen

Hormone/ Element

Report in 72Hrs

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No Fasting Required

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Anticoagulant protein assay.

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Protein C Antigen Test Information Guide

Why is it done?
- Measures the quantity of Protein C, a natural anticoagulant produced by the liver that helps prevent blood clots by inactivating clotting factors V and VIII
- Evaluates personal or family history of blood clots (thrombosis) to assess inherited or acquired bleeding disorders
- Investigates recurrent or unprovoked venous thromboembolism (DVT or pulmonary embolism)
- Screens for Protein C deficiency in patients with purpura fulminans or neonatal thrombosis
- Monitors anticoagulation therapy, particularly warfarin treatment where Protein C levels may be affected
- Evaluates liver disease or disseminated intravascular coagulation (DIC) where Protein C synthesis may be impaired
Normal Range
- Normal Range: 70-130% or 70-140% depending on laboratory standards
- Units of Measurement: Percentage (%) of normal activity or antigen concentration in micrograms per milliliter (μg/mL)
- Normal Result: 70-130% indicates adequate Protein C levels for normal anticoagulation function and suggests low risk for thrombotic events
- Low Result (Less than 60%): Suggests Protein C deficiency, which may be congenital or acquired, increasing thrombotic risk
- Borderline Low (60-70%): Requires careful clinical interpretation and may warrant repeat testing or additional coagulation studies
- High Result (Greater than 130%): Less clinically significant but may indicate acute phase response or laboratory variation
Interpretation
- Type I Protein C Deficiency: Both antigen and activity levels are low (typically 50-60% of normal); represents true quantitative deficiency and carries significant thrombotic risk
- Type II Protein C Deficiency: Antigen levels are normal or near-normal but activity levels are reduced; indicates dysfunctional Protein C molecule with variable thrombotic risk
- Inherited Deficiency: Autosomal dominant inheritance pattern; heterozygous individuals have 50% activity levels; homozygous deficiency is rare but severe
- Acquired Deficiency: Secondary to vitamin K deficiency, liver disease, warfarin therapy, DIC, or malignancy; may develop during acute illness or pregnancy
- Factors Affecting Results: Recent anticoagulation therapy (heparin, warfarin), acute inflammatory states, recent thrombotic events, pregnancy, estrogen use, and specimen handling or timing can influence values
- Clinical Significance: Levels below 60% are associated with increased thrombotic risk; first thrombotic event typically occurs in third decade of life; arterial thrombosis is less common than venous events
- Interaction with Other Conditions: Combined with other thrombophilic conditions (Factor V Leiden, prothrombin mutation) significantly increases thrombotic risk; warfarin-induced skin necrosis may occur due to Protein C depletion
Associated Organs
- Primary Organ Systems: Liver (site of Protein C synthesis), vascular system (blood vessels where coagulation occurs), and coagulation system (intrinsic and extrinsic pathways)
- Liver Disease: Cirrhosis, hepatitis, and liver failure impair Protein C synthesis, leading to acquired deficiency and increased bleeding/clotting risk
- Venous Thromboembolic Disease: Deep vein thrombosis (DVT) in legs, pelvis, or upper extremities; pulmonary embolism (PE) with potential for sudden death; mesenteric vein thrombosis
- Arterial Thrombotic Complications: Stroke, myocardial infarction, and peripheral arterial occlusion (less common but possible with Protein C deficiency)
- Skin and Subcutaneous Tissue: Warfarin-induced skin necrosis, particularly in areas of high adiposity (breast, buttocks, abdomen, thighs) due to rapid Protein C depletion
- Neonatal Manifestations: Purpura fulminans with disseminated intravascular coagulation, microvascular thrombosis, and tissue necrosis in homozygous or severe deficiency cases
- Associated Medical Conditions: Disseminated intravascular coagulation (DIC), sepsis, malignancy, antiphospholipid syndrome, and nephrotic syndrome may reduce Protein C levels
Follow-up Tests
- Protein C Activity Test: Functional assay that measures anticoagulant activity; essential to differentiate Type I (low antigen and activity) from Type II (normal antigen, low activity) deficiency
- Protein S Antigen and Activity: Protein S is a cofactor for Protein C; deficiency often accompanies Protein C deficiency and increases thrombotic risk
- Factor V Leiden Testing: Genetic mutation testing for resistance to Protein C; important to identify combined thrombophilic defects that dramatically increase clotting risk
- Prothrombin Gene Mutation (G20210A): Genetic variant that increases prothrombin levels; commonly tested alongside Protein C deficiency in thrombophilia workup
- Comprehensive Coagulation Panel: Prothrombin time (PT), activated partial thromboplastin time (aPTT), thrombin time, and fibrinogen to assess overall hemostatic function
- Antithrombin III and Thrombin-Antithrombin Complex: Additional thrombophilia markers; evaluate for combined inherited or acquired anticoagulant deficiencies
- Liver Function Tests: Bilirubin, albumin, liver enzymes; assess hepatic synthetic function if acquired Protein C deficiency is suspected
- D-Dimer and Fibrinogen: Markers of thrombin generation and fibrin formation; elevated in acute thrombotic events or DIC
- Imaging Studies: Compression ultrasound for DVT assessment, CT pulmonary angiography for PE evaluation, venography if deep venous thrombosis is suspected
- Genetic Testing: DNA sequencing for Protein C gene mutations (PROC gene) in confirmed deficiency to differentiate inherited from acquired deficiency
- Monitoring Frequency: For inherited deficiency with anticoagulation therapy, retest after 3-6 months once stabilized; annually for asymptomatic carriers; more frequently if on warfarin or during acute illness
Fasting Required?
- Fasting Required: No
- Food and Beverage Restrictions: No fasting period required; patient may eat and drink normally before the test
- Medication Management: Continue regular medications unless specifically instructed otherwise by healthcare provider; do not discontinue anticoagulant therapy without medical approval
- Warfarin and Heparin: Do not alter anticoagulation dosing before testing; stable therapeutic levels provide most accurate baseline values for comparison
- Estrogen-Containing Medications: Continue regular use (oral contraceptives, hormone replacement therapy); note that estrogen increases Protein C levels, affecting baseline interpretation
- Specimen Collection Timing: Collect blood sample in morning preferably when possible; avoid collection within 48 hours of acute thrombotic event as inflammatory markers may affect results
- Patient Positioning: Sit quietly for 5 minutes before blood draw; patient should be relaxed and not have recently exercised or experienced extreme stress which can alter results
- Specimen Type: Citrated plasma (3.2% sodium citrate); blood collection tube ratio is critical (usually 1 part citrate to 9 parts whole blood); must be filled to the correct line to ensure proper anticoagulant concentration
- Specimen Transport: Keep blood sample at room temperature in the collection tube; deliver to laboratory within 4 hours of collection for accurate results; do not refrigerate or freeze unless instructed
- Additional Preparation: Inform healthcare provider of all current medications, supplements, and herbal products; report recent illness, surgery, or thrombotic events; disclose any family history of clotting disorders

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