antithrombin III

(redirected from AT-III)


any naturally occurring or therapeutically administered substance that neutralizes the action of thrombin and thus limits or restricts blood coagulation.
antithrombin I fibrin, referring to the capacity of fibrin to adsorb thrombin and thus neutralize it.
antithrombin III a naturally occurring inhibitor of blood coagulation; it is an α2-globulin member of the serpin group, synthesized in the liver and found in the plasma and various extravascular sites. It inactivates thrombin as well as certain coagulation factors and kallikrein. Inherited deficiency of the protein, an autosomal dominant disorder, is associated with recurrent deep vein thrombosis and pulmonary emboli. Complications from the disorder are prevented and, in conjunction with heparin, treated with a preparation of antithrombin III from pooled human plasma, administered intravenously.

an·ti·throm·bin III

a plasma α2-globulin process that inhibits thrombin and has anticoagulant activities. Deficiency [MIM*107300] is commonly inherited as an autosomal dominant trait, caused by mutation in antithrombin III gene (AT3) or chromosome 1q; this is one of the few known mendelizing disorders from which thrombotic disease occurs.


A gene on chromosome 1q23-q25.1 that encodes antithrombin III, a member of the serine protease inhibitor (serpin) family that rapidly inhibits thrombin, as well as other activated serine proteases of the coagulation system, and regulates the coagulation cascade.

Molecular pathology
SERPINC1 mutations cause antithrombin-III deficiency.

antithrombin III

Hematology A 58 kD α2-glycoprotein with a single polypeptide chain that inactivates serine proteases–thrombin and other coagulation proteins including factor Xa, IXa, kallikrein and others by an irreversible heparin-dependent reaction Function AT III dissolves blood clots that normally form within the circulation; heparin's anticoagulant activity hinges on activation of AT-III; AT-III-deficient individuals do not benefit from heparin therapy; ↓ AT-III may be a congenital AD condition, or acquired, occurring in DIC–due to 'consumption' or in liver disease–due to ↓ AT-III production, resulting in an ↑ risk of coagulation; AT III is ↓ in congenital deficiency, liver transplant, DIC, nephrotic syndrome, cirrhosis, chonic liver disease, carcinoma, mid-menstrual cycle; AT III is defective in 0.14% to 0.5% of the general population. See Hereditary thrombophilia, Recombinant human antithrombin III.
References in periodicals archive ?
Decreases in circulating natural anticoagulants, protein C (2), (3), (4), (5), (6), protein S (3), ve AT-III (5) and an increase in fibrinogen (5) have been shown to occur following SCT, which cause a hypercoagulable state, a risk factor associated with thromboembolic events post transplantation.
It has been reported that presence of some types of autoantibodies are associated with Th1 cytokine profile; which among them are ANA in patients with Sjogren's syndrome (6), rheumatic diseases (7) and multiple sclerosis (8), anti-dsDNA in NZB/W F1 lupus-prone mice (9), APA in recurrent spontaneous abortions (10), TgAbs in Graves' disease (11), TPOAbs in Hashimoto's thyroiditis (12) and thyroid-associated ophthalmopathy (13) and AT-III Abs in spontaneous abortion (14).
The patients were screened by a battery of immunological tests including ANA, anti-dsDNA, LACAbs, APA, ACA, TgAbs, TPOAbs and AT-III Abs and cases with one or more positive results for these autoantibodies were categorized as the IRA group.
The inhibition of thrombin by AT-III is greatly accelerated by heparin.
Antithrombin III (AT-III) deficiency is the most commonly inherited anticoagulant deficiency, and MVT is a relatively common presentation of AT-III deficiency.
In the absence of mechanical or infectious causes for MVT, assays for AT-III, protein C, and protein S should be done as the findings have relevance for the health of the patient's offspring.