Heparin-resistant Thrombosis Due to Homozygous Antithrombin Deficiency Treated With Rivaroxaban: A Case Report

Publication date

2016-11

Authors

Van Bruwaene, Lore
Huisman, AlbertORCID 0000-0002-2291-2487ISNI 0000000390318604
Urbanus, Rolf T.ORCID 0000-0002-1601-9393ISNI 0000000396557403
Versluijs, Anne BirgittaISNI 000000039689555X

Editors

Advisors

Supervisors

Document Type

Article

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License

taverne

Abstract

BACKGROUND: Heparin fulfills its anticoagulant action through activation of antithrombin (AT), and thus thrombosis secondary to AT deficiency can be associated with heparin resistance. OBSERVATION: A 12-year-old girl with severe venous thrombosis was referred to us because of undetectable anti-Xa levels despite low-molecular-weight heparin therapy. Laboratory investigations revealed a homozygous AT mutation in the heparin binding site (AT Budapest III). She was subsequently treated with rivaroxaban successfully. CONCLUSIONS: Heparin resistance warrants evaluation for AT deficiency. Rivaroxaban may be considered a valid anticoagulant alternative to low-molecular-weight heparin in these patients.

Keywords

children, antithrombin deficiency, Budapest III, heparin resistance, rivaroxaban, Taverne, Journal Article, Case Reports

Citation

Van Bruwaene, L, Huisman, A, Urbanus, R T & Versluys, B 2016, 'Heparin-resistant Thrombosis Due to Homozygous Antithrombin Deficiency Treated With Rivaroxaban : A Case Report', Journal of Pediatric Hematology/oncology, vol. 38, no. 8, pp. 658–660. https://doi.org/10.1097/MPH.0000000000000608