Anti Thrombin III Activity

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No Fasting Required

Details

Measures activity of antithrombin III (natural anticoagulant).

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Anti Thrombin III Activity

Why is it done?
- Measures the functional activity of antithrombin III (AT III), a natural anticoagulant protein that inhibits blood clotting factors and prevents excessive blood clot formation
- Evaluates patients with unexplained thrombosis (blood clots) or recurrent clotting episodes
- Diagnoses antithrombin III deficiency, which can be hereditary or acquired and increase thrombotic risk
- Investigates poor response to heparin therapy, as AT III is essential for heparin's anticoagulant effect
- Screens patients with family history of thrombotic disorders or pulmonary embolism
- Monitors patients with disseminated intravascular coagulation (DIC), severe liver disease, or nephrotic syndrome
- Evaluates abnormal coagulation study results as part of a thrombophilia workup
Normal Range
- Normal AT III Activity Range: 80-120%
- Some laboratories report ranges as: 82-126%
- Alternative expression: 0.80-1.20 IU/mL (International Units per milliliter)
- Units of Measurement: Percentage (%) or IU/mL - measured via functional activity assay
- Normal Result Interpretation: AT III levels are adequate for normal clotting regulation and heparin response
- Low Result (<70-80%): Indicates AT III deficiency with increased thrombotic risk
- Elevated Result (>130%): Unusual; may occur in certain disease states or be a laboratory variation
- Borderline Values (70-80%): Requires clinical correlation and may warrant repeat testing or additional investigations
Interpretation
- Decreased AT III Activity (below 70-80%): Suggests hereditary or acquired AT III deficiency with significantly increased risk of thrombotic events including DVT, PE, and arterial thrombosis
- Hereditary Deficiency: Type I (85% of cases) shows reduced AT III concentration and activity; Type II (15% of cases) shows normal concentration but reduced activity due to dysfunctional protein
- Acquired Deficiency: Occurs with liver disease (decreased synthesis), nephrotic syndrome (urinary loss), DIC (consumption), active thrombosis, heparin therapy (heparin binding), or L-asparaginase chemotherapy
- Heparin Resistance: Low AT III activity explains poor response to heparin therapy, as AT III is a mandatory cofactor for heparin's anticoagulant function
- Normal AT III Activity with Thrombosis: Suggests alternative thrombophilia such as Factor V Leiden, prothrombin G20210A mutation, or antiphospholipid syndrome
- Factors Affecting Results: Acute illness, stress, oral contraceptives (can lower AT III by 20%), pregnancy, recent thrombotic events, L-asparaginase therapy, estrogen therapy, and specimen handling errors
- Clinical Significance: AT III deficiency carries a 5-10 fold increased risk of thrombosis; diagnosis is essential for therapeutic decisions, anticoagulation strategies, and family screening
- Specimen Considerations: Citrated plasma (blue-top tube); improper collection ratio or prolonged storage may affect results; testing should be repeated if initial results are abnormal
Associated Organs
- Primary Systems Involved:
  - Hematologic system (blood and clotting cascade)
  - Liver (primary synthesis organ for AT III)
  - Kidneys (urinary loss in nephrotic syndrome)
  - Vascular system (site of thrombotic complications)
- Diseases and Conditions Associated with Abnormal AT III:
  - Hereditary AT III deficiency (autosomal dominant inheritance)
  - Cirrhosis and severe liver disease
  - Nephrotic syndrome (proteinuria with AT III loss)
  - Disseminated intravascular coagulation (DIC) with AT III consumption
  - Acute thrombotic events (DVT, PE, myocardial infarction, stroke)
  - Sepsis and critical illness
  - Malignancy with increased thrombotic tendency
  - L-asparaginase chemotherapy effects
  - Estrogen or oral contraceptive use
  - Antiphospholipid syndrome
- Potential Complications Associated with Low AT III:
  - Deep vein thrombosis (DVT) with risk of embolization
  - Pulmonary embolism (PE) causing acute respiratory compromise
  - Arterial thrombosis with stroke or myocardial infarction risk
  - Mesenteric thrombosis
  - Heparin resistance requiring alternative anticoagulation strategies
  - Pregnancy complications including miscarriage and placental infarction
Follow-up Tests
- Confirmation and Repeat Testing:
  - Repeat AT III activity testing if initial results are low (confirm abnormality and exclude laboratory error)
  - AT III antigen (immunologic assay) to differentiate Type I from Type II deficiency
- Additional Thrombophilia Workup:
  - Factor V Leiden and prothrombin G20210A mutations
  - Protein C and Protein S activity levels
  - Antiphospholipid antibodies (lupus anticoagulant, anticardiolipin, β2-glycoprotein-I)
  - Homocysteine level (elevated homocysteine is a thrombotic risk factor)
  - Lipoprotein(a) [Lp(a)] if arterial thrombosis is present
- Baseline Coagulation Studies:
  - Prothrombin time (PT) and international normalized ratio (INR)
  - Partial thromboplastin time (aPTT)
  - Platelet count and fibrinogen level
  - Thrombin time if DIC is suspected
- Liver and Kidney Function Assessment:
  - Liver function tests (AST, ALT, bilirubin, albumin) if acquired deficiency suspected
  - Serum creatinine, BUN, urinalysis, and urine protein to detect nephrotic syndrome
- Imaging Studies:
  - Lower extremity ultrasound to detect DVT
  - CT pulmonary angiography (CTPA) or ventilation-perfusion scan to evaluate for PE
- Monitoring Frequency:
  - Hereditary deficiency: One-time confirmatory testing; monitor AT III levels before major surgery or during acute illness
  - Acquired deficiency: Monitor at baseline and every 3-6 months to assess response to treatment of underlying condition
  - Heparin therapy monitoring: Assess AT III levels if patient develops heparin resistance
- Family Screening:
  - First-degree relatives should be tested for AT III deficiency (autosomal dominant inheritance with 50% transmission risk)
  - Presymptomatic carriers may benefit from prophylactic anticoagulation during high-risk periods
Fasting Required?
- Fasting Status: No - Fasting is NOT required for this test
- Specimen Requirements:
  - Venipuncture with collection in blue-top tube (sodium citrate) for plasma preparation
  - Proper blood-to-citrate ratio (usually 9:1) is critical for accurate results
  - Specimen should be gently mixed and processed within 2-4 hours of collection
- Medications to Avoid/Review:
  - Heparin therapy: Notify laboratory if patient is receiving heparin (can artificially lower AT III levels)
  - Oral contraceptives: Can lower AT III levels by approximately 15-20%; report to clinician
  - Hormone replacement therapy: May decrease AT III activity slightly
  - Warfarin/anticoagulants: No direct effect on AT III but report all anticoagulation to laboratory
  - L-asparaginase: Known to reduce AT III levels during cancer therapy
- Patient Preparation:
  - No special fasting or dietary restrictions required
  - Patient can eat and drink normally before the test
  - Inform laboratory of any recent acute illness, thrombotic events, or hospitalizations
  - Report all current medications to phlebotomist and laboratory
  - Avoid strenuous physical activity or stress immediately before testing
  - For hereditary deficiency testing, optimal specimen collection should avoid acute illness or thrombotic events (allow 2-4 weeks after acute thrombosis)
- Timing Considerations:
  - Testing should ideally be performed when patient is stable and not acutely ill or immediately post-thrombotic event
  - For suspected hereditary deficiency, repeat testing after 2-4 weeks if initial values are low
  - Avoid testing during or immediately after heparin treatment initiation

How our test process works!