Fondaparinux sodium/heparin
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Heparin induced thrombocytopenia and thrombosis in the form of paradoxical reaction and cross reactivity: case report A 70-year-old woman developed heparin induced thrombocytopenia (HIT) and thrombosis in the form of paradoxical reaction during treatment with heparin as thromboprophylaxis. Additionally, she developed crossreactivity with fondaparinux. The woman, who was diagnosed with glioblastoma, started receiving treatment with heparin [unfractionated heparin] prior to tumour resection. Thereafter, craniotomy was performed and treatment with heparin was resumed. Nine days following the initiation of heparin (on postoperative day 4), the platelet count decreased to 124 from 207 and on day 12 after the initiation heparin it reached to 25 × 109/L (nadir). On the same day, due to the left lower limb swelling venous ultrasound was performed, which revealed acute occlusive left popliteal vein thrombosis. She was treated with SC fondaparinux sodium [fondaparinux] 7.5mg daily for presumed HIT. Laboratory investigation showed decreased fibrinogen and greatly increased fibrin D-dimer level. After three days, she developed right upper-extremity deep vein thrombosis associated with symptomatic percutaneously inserted central catheter. Evidence of fondaparinux sodium cross-reactivity in HIT was noted due to persistent thrombocytopenia and hypofibrinogenaemia. Based on strong-positive polyspecific PF4/polyvinyl sulfonate EIA and (in-house) IgG-specific PF4/heparin EIA, as well as by strong positive serotonin-release assay (SRA) with approximately 90% serotonin release, HIT in the form of paradoxical reaction was confirmed. The woman was treated with immunoglobulin and as a result, minor initial platelet count increase was noted. Due to fondaparinux sodium cross-reactivity, her treatment was switched to rivaroxaban. Her platelet count continued to recover and on the 41th day it reached a normal level. Fibrinogen and fibrin D-dimer levels started to normalise. Her HIT antibodies (day 11 sample obtained prior to the initiation of fondaparinux sodium) showed strong in vitro crossreactivity with fondaparinux. Despite the EIA cross-reactivity remained strongly positive on the day 21 sample (postimmunoglobulin treatment), the SRA was negative, which were consistent with inhibition of platelet activation after immunoglobulin treatment. After 21 days, the dose of rivaroxaban was changed, and she successfully completed a 12 week total course of rivaroxaban without complications. Author comment: "Our case illustrates [fondaparinux sodium] cross-reactivity in HIT manifesting as persisting thrombocytopenia". "HIT antibodies cause strong platelet activation, hypercoagulability and high thrombotic risk, resulting in the paradoxical clinical presentation of thrombocytopenia and thrombosis." Manji F, et al. Fondaparinux cross-reactivity in heparin-induced thrombocytopenia successfully treated with high-dose intravenous immunoglobulin and rivaroxaban. Platelets 31: 124-127, No. 1, 2020. Available from: URL: http:// 803443615 doi.org/10.1
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