Antithrombin Activity Unit Converter
Antithrombin Activity Unit Converter
Convert antithrombin activity between %, IU/mL and proportion — 1.00 IU/mL is by definition 100% of pooled normal plasma — and see why the result must not be measured during an acute thrombosis or on heparin.
Antithrombin Activity converter
% ⇄ IU/mLAntithrombin activity 95% on a functional (activity) assay
The conversion, and why 1.00 IU/mL is 100%
% = IU/mL × 100
because 1.00 IU/mL of antithrombin activity is defined as the activity present in 1 mL of pooled normal plasma, which is 100%
- % activity
- activity as a percentage of pooled normal plasma, which is how most UK laboratories report it. It is a relative measurement, not a concentration: there is no molecular weight in this conversion and no molar unit exists for it
- IU/mL = U/mL
- international units per millilitre, against a WHO plasma standard. Because one international unit is the activity in one millilitre of normal pooled plasma, 1.00 IU/mL and 100% are the same statement — so a report of 0.95 IU/mL and a report of 95% are identical results
- proportion
- the same number as a bare fraction: 0.95. Used by some reporting systems and by most of the literature on antithrombin concentrate dosing
- functional, not antigenic
- this is an activity assay, measuring how well the antithrombin present inhibits thrombin or factor Xa. The antigen assay measures how much protein is there. Type I deficiency reduces both; type II deficiency reduces function with normal antigen, so an antigen assay alone misses it. A thrombophilia screen should request the functional assay
Worked example
Antithrombin activity 95% on a functional (activity) assay
95% ÷ 100 = 0.95 IU/mL, and identically 0.95 U/mL
As a proportion that is 0.95 — the same number again
95% sits inside the adult interval of 80–120%
There is no molecular weight anywhere in this conversion. Antithrombin activity is measured against pooled normal plasma, so the units are relative by construction and the international unit is defined so that 1.00 IU/mL equals 100%
Now the part that decides whether the number means anything. If this sample was taken while the patient was on an unfractionated heparin infusion, during an acute pulmonary embolism, or in nephrotic syndrome, a low result would be expected and would say nothing about inherited deficiency
And in the other direction: a patient on warfarin or on a direct factor Xa inhibitor can return a normal antithrombin while genuinely being heterozygous for deficiency, because both drugs raise the measured activity
So the timing rule is the result. Test when the patient is well, not in the acute phase, and off anticoagulation — and repeat any abnormal value before it is given a name
The same activity in every unit
| % of normal | IU/mL = U/mL | Proportion | Reading |
|---|---|---|---|
| 120 | 1.20 | 1.20 | Conventional upper limit of the adult interval |
| 100 | 1.00 | 1.00 | By definition, the activity of pooled normal plasma |
| 95 | 0.95 | 0.95 | Mid-interval — the default on this page |
| 80 | 0.80 | 0.80 | Conventional lower limit of the adult interval |
| 60 | 0.60 | 0.60 | Typical of heterozygous inherited deficiency — but acquired causes look identical |
| 40 | 0.40 | 0.40 | Markedly reduced; expect clinically significant heparin resistance |
Why an antithrombin result is low — and why the timing rule exists
| Cause | Mechanism | What to do about the result |
|---|---|---|
| Unfractionated heparin therapy | Heparin accelerates antithrombin’s action and the complex is cleared, so plasma antithrombin falls during treatment | Uninterpretable for inherited deficiency. Retest off heparin |
| Acute thrombosis | Antithrombin is consumed forming thrombin–antithrombin complexes | Uninterpretable. Retest once the acute event has resolved |
| Disseminated intravascular coagulation | Widespread consumption | Treat the cause; the antithrombin is a severity marker, not a thrombophilia result |
| Nephrotic syndrome | Antithrombin is a 58 kDa protein and is lost in the urine | Explained by the proteinuria; part of why nephrotic syndrome is prothrombotic |
| Liver disease | Reduced synthesis — antithrombin is made in the liver | Explained; interpret with the rest of the liver’s synthetic output |
| Asparaginase, oestrogen, pregnancy, major surgery | Reduced synthesis or increased consumption | Retest away from the exposure |
| Inherited deficiency | Type I (reduced quantity) or type II (reduced function) — the strongest of the inherited thrombophilias | Only considered once every cause above is excluded, on a repeat sample, with family testing and a clinical genetics or haematology opinion |
Drugs and assays that move the result the wrong way
| Interference | Effect | Consequence |
|---|---|---|
| Unfractionated heparin in the sample or in the patient | Lowers measured activity | A false impression of deficiency |
| Warfarin | Can raise activity | May mask a heterozygous deficiency — a normal result on warfarin does not exclude it |
| Direct factor Xa inhibitors (apixaban, rivaroxaban, edoxaban) | Falsely raise the result of anti-Xa-based functional assays | A deficient patient can read normal. Use a thrombin-based assay or retest off the drug |
| Direct thrombin inhibitors (dabigatran, argatroban) | Falsely raise thrombin-based (anti-IIa) functional assays | The mirror-image problem — the assay method determines which drug interferes |
| Antigen assay used instead of activity | Normal in type II deficiency | Misses functional variants entirely; request the functional assay |
| Drawing from a heparinised line | Lowers activity | Avoid heparin-locked catheters; take a clean peripheral sample |
A definition rather than a conversion, a timing rule that decides everything, and heparin resistance
Antithrombin activity is reported as a percentage of pooled normal plasma or in international units per millilitre, and the relationship between the two is a definition rather than a measurement. One international unit of antithrombin activity is the activity contained in one millilitre of normal pooled plasma, so 1.00 IU/mL and 100% are two ways of writing the same thing, and a result of 0.95 IU/mL is identical to a result of 95%. Dividing the percentage by a hundred gives IU/mL; multiplying by a hundred goes back. There is no molecular weight in any of this, because an activity expressed against a standard plasma is a relative quantity and not a concentration — which is also why no molar unit for antithrombin activity exists. The protein was called antithrombin III for many years and older reports use that name for the same molecule.
Everything difficult about an antithrombin result is about when the sample was taken. A low activity has two very different explanations. Inherited deficiency — type I, where there is less of a normal protein, and type II, where there is a normal amount of a dysfunctional one — is the strongest of the inherited thrombophilias, carrying a considerably higher relative risk of venous thromboembolism than factor V Leiden. Acquired reduction is much commoner and every cause of it is reversible: unfractionated heparin therapy, because heparin drives antithrombin into complexes that are then cleared; an acute thrombosis, because antithrombin is consumed neutralising the thrombin being generated; disseminated intravascular coagulation for the same reason on a larger scale; nephrotic syndrome, because a 58 kilodalton protein is lost through a leaking glomerulus; liver disease, because the liver makes it; and asparaginase, oestrogen — the combined pill included — pregnancy and major surgery. A result taken during an acute thrombotic event or while a patient is receiving heparin is low for the wrong reason, and it cannot be used to diagnose anything. It must not be measured in those circumstances. Treat the event, wait, and test when the patient is well and off anticoagulation, and repeat any abnormal value before it is given a name.
The same discipline applies in reverse, and this part is newer and less widely appreciated. Warfarin raises antithrombin activity, sometimes enough to lift a genuine heterozygous deficiency into the normal range. Direct factor Xa inhibitors — apixaban, rivaroxaban, edoxaban — falsely raise the result of anti-Xa-based functional assays, and direct thrombin inhibitors do the same to thrombin-based ones, so which drug causes trouble depends on the reagent your laboratory happens to use. The practical consequence is that a normal antithrombin in a patient on a direct oral anticoagulant does not exclude deficiency. It is also worth being specific about which assay was requested: the functional or activity assay measures how well the antithrombin present works and detects both type I and type II deficiency, while an antigen assay measures only how much protein is there and is normal in type II. A thrombophilia screen should ask for the functional assay.
One clinical consequence deserves separating out from the diagnostic question, because it matters acutely. Heparin has almost no anticoagulant effect of its own — it works by accelerating antithrombin, by a factor of around a thousand. A patient with low antithrombin therefore shows heparin resistance: the activated partial thromboplastin time fails to prolong despite escalating doses of unfractionated heparin. Recognising that pattern matters, because the reflex of pushing the infusion rate higher and higher does not work, and the answers are different — measuring the anti-Xa level rather than the APTT ratio, replacing antithrombin where a concentrate is indicated, or using an anticoagulant that does not depend on antithrombin at all, such as argatroban or a direct oral agent. Suspected heparin resistance in a patient needing urgent anticoagulation is one of the few situations in which an antithrombin level is genuinely useful during an acute illness — not to diagnose a thrombophilia, which it cannot do then, but to explain why the heparin is not working.
Frequently asked questions
Is 1 IU/mL of antithrombin the same as 100%?
Yes, by definition. One international unit of antithrombin activity is defined as the activity present in one millilitre of pooled normal plasma, so 1.00 IU/mL and 100% are the same statement and a result of 0.95 IU/mL is identical to 95%. Divide the percentage by 100 to get IU/mL and multiply by 100 to go back. Because the measurement is relative to a standard plasma, no molecular weight and no molar unit are involved.
What is a normal antithrombin level?
Roughly 80–120% — equivalently 0.80–1.20 IU/mL — for adults over 16 on a functional activity assay. The interval is age-dependent: activity is physiologically low in newborns and rises through infancy and childhood, with 96–126% quoted for 11–16 year olds. It is also assay-specific, so use the interval printed on your own report.
Why should antithrombin not be measured during an acute thrombosis or on heparin?
Because both lower it, so the result will be low for a reason that has nothing to do with inherited deficiency. An acute thrombosis consumes antithrombin in thrombin–antithrombin complexes, and heparin therapy accelerates that consumption and clearance. A low result in either setting is uninterpretable as a thrombophilia test. Treat the event, wait until the patient is well and off heparin, then test — and repeat any abnormal result before giving it a name.
What causes a low antithrombin apart from inherited deficiency?
Heparin therapy, an acute thrombosis, disseminated intravascular coagulation, nephrotic syndrome (antithrombin is lost in the urine), liver disease (it is synthesised in the liver), asparaginase, oestrogen therapy including the combined oral contraceptive, pregnancy and major surgery. All of these are commoner than inherited deficiency and all are reversible, which is why every one has to be excluded before an inherited diagnosis is considered.
Why does antithrombin deficiency cause heparin resistance?
Because heparin acts through antithrombin. Heparin has very little anticoagulant activity of its own; it binds antithrombin and accelerates its inhibition of thrombin and factor Xa roughly a thousandfold. With little antithrombin available there is little for heparin to work through, so the APTT fails to prolong despite escalating doses of unfractionated heparin. The management is not simply more heparin: measure anti-Xa levels, consider antithrombin replacement where indicated, or use an anticoagulant that does not depend on antithrombin.
Can a direct oral anticoagulant affect an antithrombin result?
Yes, and in the dangerous direction. Direct factor Xa inhibitors such as apixaban, rivaroxaban and edoxaban falsely raise the result of anti-Xa-based functional antithrombin assays, and direct thrombin inhibitors do the same to thrombin-based assays, so a genuinely deficient patient can be reported as normal. Warfarin can also raise activity enough to mask a heterozygous deficiency. Test off anticoagulation where that is clinically safe, and always state the current drugs on the request form.
Related calculators
References
- Labcorp. Antithrombin (AT) Activity, test 015040. Reference interval 80–120% for adults over 16 years and 96–126% at 11–16 years; testing should not be performed on patients receiving unfractionated heparin, warfarin can artificially elevate results in heterozygous deficiency, and direct factor Xa inhibitors may falsely elevate results.
- Khor B, Van Cott EM. Laboratory tests for antithrombin deficiency. Am J Hematol. 2010;85(12):947–950.
- Patnaik MM, Moll S. Inherited antithrombin deficiency: a review. Haemophilia. 2008;14(6):1229–1239.
- Van Cott EM, Orlando C, Moore GW, et al. Recommendations for clinical laboratory testing for antithrombin deficiency; Communication from the SSC of the ISTH. J Thromb Haemost. 2020;18(1):17–22.
- Levy JH, Sniecinski RM, Maier CL, et al. Antithrombin: anti-inflammatory properties and clinical applications. Thromb Haemost. 2016;116(4):612–622.
- Di Minno MND, Ambrosino P, Ageno W, et al. Natural anticoagulants deficiency and the risk of venous thromboembolism: a meta-analysis of observational studies. Thromb Res. 2015;135(5):923–932.
Medical Disclaimer: The tools and content provided here are for educational and reference purposes only. They are not intended to substitute for professional medical advice, diagnosis, or treatment. Clinical decisions should always be based on the comprehensive assessment of a qualified healthcare professional.