Prevalence of hereditary antithrombin deficiency (hATd)

Image showing 8 out of 10 patients having a clot by age 50

More than 8 out of 10 patients with hereditary AT deficiency have at least one clot by age 5010

 
 
Image showing 6 out of 10 patients having recurrent blood clots

About 6 in 10 patients with hereditary AT deficiency have recurrent blood clots10

 

  • hATd affects 1 in every 500 to 5000 individuals9,14
    • This range suggests that approximately 65,000 to 650,000 people in the United States are affected15
  • Approximately 50% of individuals with hereditary AT deficiency will develop at least one clot in their lifetime (usually after adolescence).16
  • 85% of patients with hATd will have at least 1 thrombotic episode by age 507
  • ~70% of all patients with hATd will have a thrombotic event before the age of 357
  • Up to 70% of pregnant women with hATd may experience thromboembolic complications17
  • About 6 in 10 patients with hereditary AT deficiency have recurrent blood clots19
  • Inherited blood-clotting disorders are diagnosed with a test called a thrombophilia panel. This test can help to diagnose hereditary antithrombin deficiency or another inherited blood-clotting disorder, like factor V Leiden, or protein C or protein S deficiency
 

hATd has one of the highest thrombotic risks of all of the inherited thrombophilias18

  • hATd is a hereditary autosomal dominant disorder that typically reduces functional antithrombin levels to 40% to 60% of normal19
  • Patients with hereditary antithrombin deficiency are about 20 times more likely to have a VTE compared with the general population19
  • The risk of VTE is much higher in hereditary antithrombin-deficient patients than it is in patients with other thrombophilias like factor V Leiden or prothrombin gene mutation19
  • Risk increases progressively with lower antithrombin levels20, 21
  • Of the estimated 547,596 patients hospitalized for VTE each year in the United States, up to 3% (~16,500) of these patients may have hATd22
 

Learn more about:

THE RISKS OF LOW AT: See how THROMBATE III replaces missing AT

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CAUSES OF HEPARIN RESISTANCE: Hear Dr. Bader talk about inherited clotting disorders

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THROMBATE III REDUCES VTE RISK: Dr. Bader talks about surgery in patients with hATd

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IMPORTANT SAFETY INFORMATION


THROMBATE III® (antithrombin III [human]) is indicated in patients with hereditary antithrombin deficiency for treatment and prevention of thromboembolism and for prevention of perioperative and peripartum thromboembolism.

Hypersensitivity reactions may occur. Should evidence of an acute hypersensitivity reaction be observed, promptly interrupt the infusion and begin appropriate treatment.

Because THROMBATE III is made from human blood, it may carry a risk of transmitting infectious agents, eg, viruses, the variant Creutzfeldt-Jakob disease (vCJD) agent, and, theoretically, the Creutzfeldt-Jakob disease (CJD) agent. There is also the possibility that unknown infectious agents may be present in the product.

Perform coagulation tests to avoid excessive or insufficient anticoagulation and monitor for bleeding or thrombosis. Measure functional plasma AT levels with amidolytic or clotting assays; do not use immunoassays.

In clinical studies, the most common adverse reactions (≥ 5% of subjects) were dizziness, chest discomfort, nausea, dysgeusia, and pain (cramps).

The anticoagulant effect of heparin is enhanced by concurrent treatment with THROMBATE III in patients with hereditary AT deficiency. Thus, in order to avoid bleeding, the dosage of heparin (or low molecular weight heparin) may need to be reduced during treatment with THROMBATE III.

Please see full Prescribing Information for THROMBATE III.

You are encouraged to report negative side effects of prescription drugs to the FDA. Visit http://www.fda.gov/medwatch, or call 1-800-FDA-1088.

References: 1. THROMBATE III [Prescribing Information]. Research Triangle Park, NC: Grifols Therapeutics LLC. 2. Maclean PS, Tait RC. Hereditary and acquired antithrombin deficiency: epidemiology, pathogenesis, and treatment options. Drugs. 2007;67(10):1429-1440. 3. Li W, Johnson DJ, Esmon CT, Huntington JA. Nat Struct Mol Biol. 2004;11(9):857-862. 4. James AH, Konkle BA, Bauer KA. Prevention and treatment of venous thromboembolism in pregnancy and patients with hereditary antithrombin deficiency. Int J Womens Health. 2013;5:233-241. 5. Wolberg AS. Blood Rev. 2007;21(3):131-142. 6. Davi G, Patrono C. N Engl J Med. 2007;357(24):2482-2494. 7. Kottke-Marchant K, Duncan A. Antithrombin deficiency: issues in laboratory diagnosis. Arch Pathol Lab Med. 2002;126(11):1326-1336. 8. Mitton BA, Steineck A. Antithrombin deficiency. eMedicine from WebMD. http://emedicine.medscape.com/article/198573-overview. Updated August 22, 2019. Accessed September 4, 2020. 9. Patnaik MM, Moll S. Inherited antithrombin deficiency: a review. Haemophilia. 2008;14(6):1229-1239.10. Pabinger I, Schneider B. Thrombotic risk in hereditary antithrombin III protein C, or protein S deficiency. Arteroscler Thromb Vasc Biol. 1996;16(6):742-748. 11. Ranucci M. Antithrombin III: key factor in extracorporeal circulation. Minerva Anestesiol. 2002;68(5):454-457. 12. Foy P, Moll S. Thrombophilia: 2009 update. Curr Treat Options Cardiovasc Med. 2009;11(2):114-128. 13. AABB, American Red Cross, America's Blood Centers, Armed Services Blood Program. Circular of information for the use of human blood and blood components. October 2017. http://www.aabb.org/tm/coi/Documents/coi1017.pdf. Accessed September 4, 2020. 14. Wells PS, Blajchman MA, Henderson P, et al. Am J Hematol. 1994;45:321-324. 15. US Census Bureau, Population Division. US and World Population Clock. http://www.census.gov/ popclock/. Accessed February 13, 2020. 16. Khawar H, Kelley W,Guzman N. Fresh frozen plasma. In: StatPearls. https://www.ncbi.nlm.nih.gov/books/NBK513347/. Updated October 7, 2019. Accessed February 10, 2020. 17. Hellgren M, Tengborn T, Abildgaard U. Pregnancy in women with congenital antithrombin III deficiency: experience of treatment with heparin and antithrombin. Gynecol Obstet Invest. 1982;14:127-141. 18. Franchini M, Veneri D, Salvagno GL, Manzato F, Lippi G. Inherited thrombophilia. Crit Rev Clin Lab Sci. 2006;43(3):249-290. 19. Rodgers GM. Role of antithrombin concentrate in hereditary antithrombin deficiency: an update. Thromb Haemost. 2009;101(5):806-812. 20. Di Minno MND, Dentali F, Lupoli R, Ageno W. Mild antithrombin deficiency and risk of recurrent venous thromboembolism. Circulation. 2014;129(4):497-503. 21. Bucciarelli P, Passamonti SM, Biguzzi E, et al. Low borderline plasma levels of antithrombin, protein C and protein S are risk factors for venous thromboembolism. J Thromb Haemost. 2012;10(9):1783-1791. 22. Centers for Disease Control and Prevention. Venous thromboembolism in adult hospitalizations – United States, 2007-2009. MMWR Morb Mortal Wkly Rep. 2012;61(22):401-404. 23. Finley A, Greenberg C. Review article: heparin sensitivity and resistance: management during cardiopulmonary bypass. Anesth Analg. 2013;116(6):1210-1222. 24. Kovács B, Bereczky Z, Oláh Z, et al. The superiority of anti-FXa assay over anti-FIIa assay in detecting heparin-binding site antithrombin deficiency. Am J Clin Pathol. 2013;140(5):675-679. 25. Olson E, Whitney M, Friedman B et al. In vivo fluorescence imaging of atherosclerotic plaques with activatable cell-penetrating peptides targeting thrombin activity, Integrative Biology, 2012;4(6):595–605. 26. Lloyd-Jones D, Adams RJ, Brown TM, et al; on behalf of the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation. 2010;121:e46-e215.