What this test measures
Antithrombin (historically AT III) is a serine protease inhibitor that neutralises thrombin, factor Xa, and several other activated clotting factors. It is the cornerstone of the body's natural anticoagulant system. The functional assay measures the percentage of normal antithrombin activity (reference 80–120%).
Deficiency can be inherited (autosomal dominant, type I quantitative or type II qualitative) or acquired (severe liver disease, nephrotic syndrome with urinary loss, disseminated intravascular coagulation, prolonged heparin therapy, oestrogen use, sepsis). Hereditary deficiency raises lifetime venous thromboembolism risk by 10–20×. Importantly, antithrombin is the molecule heparin works through — severe deficiency causes heparin resistance, an important consideration in the ICU.
Why it matters
Antithrombin testing is part of the thrombophilia workup in young patients with unprovoked deep vein thrombosis, pulmonary embolism, recurrent miscarriage (especially mid-trimester), or a strong family history of clotting. It is also tested in ICU patients on heparin who are not achieving therapeutic anticoagulation despite escalating doses — heparin resistance can mean acquired AT III deficiency.
For Indian patients, thrombophilia testing is increasingly available and antithrombin is one of five standard components (along with Protein C, Protein S, Factor V Leiden, prothrombin gene mutation). Cost is moderate; the test is best ordered after at least 2 weeks off any anticoagulation, away from the acute thrombotic episode, and preferably with haematology guidance.
How to prepare
No fasting required. Ideally tested at least 2 weeks after stopping warfarin, 24 hours after stopping heparin/LMWH, and at least 6 weeks after an acute thrombotic event. Disclose pregnancy, oestrogen (OCP, HRT) use, liver or kidney disease.
Markers & reference ranges
Reference ranges below are typical adult values. Your lab's reported range may differ slightly based on the assay platform and patient demographics — always read your report against the range printed on it.
| Marker | Normal range | If low | If high |
|---|---|---|---|
| Antithrombin III Activity (%)[1][2] | 80–120% | Reduced activity (<80%). Causes: hereditary AT deficiency (~50% of normal), severe liver disease, nephrotic syndrome (urinary loss), DIC, sepsis, prolonged heparin therapy, oestrogen use (OCP, HRT, pregnancy). Severe deficiency (<50%) significantly raises VTE risk and causes heparin resistance. | High AT III is generally not clinically significant. May be seen with warfarin therapy (warfarin paradoxically raises AT III). |
Antithrombin III patterns
| Activity (%) | Interpretation | Action |
|---|---|---|
| 80 – 120 | Normal | — |
| 50 – 80 | Mild reduction | Consider acquired causes (liver, nephrotic, OCP, heparin); repeat in stable state |
| < 50 | Significant deficiency | Hereditary deficiency likely; family testing + thromboprophylaxis decisions |
| Failure to anticoagulate on heparin | Heparin resistance | Suspect AT III deficiency; consider AT III concentrate or switch to direct anticoagulant |
Frequently asked questions
When is antithrombin tested?
In the workup of unexplained venous thrombosis (DVT, PE), recurrent miscarriage, family history of clotting, or heparin resistance.
Do I need to fast?
No.
Can my medications affect the result?
Yes. Heparin and LMWH lower AT III through ongoing consumption. Warfarin paradoxically raises it. Stop heparin 24 hours before testing, and ideally do thrombophilia workup 2 weeks off warfarin. Also disclose oral contraceptives (lower AT III) and pregnancy.
My AT III is 60% — what does that mean?
60% is reduced. The cause matters — acquired (liver disease, nephrotic syndrome, sepsis, OCP) needs treatment of the underlying condition; hereditary deficiency needs genetic counselling and consideration of long-term anticoagulation after a thrombosis. Haematology referral is warranted.
Is hereditary AT III deficiency common in India?
Rare — about 1 in 2,000 in general population. Among unselected DVT/PE patients, ~1–2% have AT III deficiency. Family screening is offered when a hereditary case is identified.
What is heparin resistance?
Failure to reach therapeutic anticoagulation (e.g. aPTT target) despite high heparin doses. Acquired AT III deficiency (DIC, sepsis, post-cardiopulmonary bypass) is a common cause. Treatment includes AT III concentrate or switching to a direct thrombin inhibitor.
Does pregnancy affect AT III?
Pregnancy and oestrogen-containing contraceptives modestly reduce AT III. Test results from these states should be interpreted with caution.
How long does the report take?
Most NABL labs report AT III activity within 24–48 hours.
Related Coagulation tests
Tests commonly ordered alongside ANTITHROMBIN III, or that help interpret an unexpected result.
Sources & references
- NCBI StatPearls — Antithrombin III Deficiency · accessed 2026-05-30T00:00:00.000Z
- ISTH — Antithrombin Deficiency · accessed 2026-05-30T00:00:00.000Z
- BSH — Thrombophilia Testing · accessed 2026-05-30T00:00:00.000Z
- NIH MedlinePlus — Antithrombin Test · accessed 2026-05-30T00:00:00.000Z
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