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.
| Original language | English |
|---|---|
| Pages (from-to) | 658–660 |
| Journal | Journal of Pediatric Hematology/oncology |
| Volume | 38 |
| Issue number | 8 |
| DOIs | |
| Publication status | Published - Nov 2016 |
Keywords
- children
- antithrombin deficiency
- Budapest III
- heparin resistance
- rivaroxaban
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