Lore Van Bruwaene1, Albert Huisman, Rolf T Urbanus, Birgitta Versluys. 1. Departments of *Pediatric Hematology Wilhelmina Children's Hospital ‡Clinical Chemistry and Hematology, University Medical Center Utrecht, Utrecht, The Netherlands †Department of Pediatrics, Hospital Gasthuisberg, University Hospital Leuven, Leuven, Belgium.
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.
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.
Authors: Ján Mikler; Matej Samoš; Tomáš Bolek; Ingrid Škorňová; Lucia Stančiaková; Ján Staško; Marián Mokáň Journal: Pediatr Cardiol Date: 2019-07-20 Impact factor: 1.655