Persistent heparin-induced thrombocytopenia: danaparoid cross-reactivity or delayed-onset heparin-induced

Geoffrey Horlait1, Valentine Minet, François Mullier

  • 1aUniversité Catholique de Louvain, CHU UCL Namur, Intensive Care Unit bUniversity of Namur, Namur Thrombosis and Hemostasis Centre (NTHC), Namur Research Institute for LIfe Sciences (NARILIS), Department of Pharmacy cUniversité Catholique de Louvain, CHU UCL Namur, Namur Thrombosis and Hemostasis Center (NTHC), Namur Research Institute for LIfe Sciences (NARILIS), Hematology Laboratory, Belgium.

Clinical suspicion of immune heparin-induced thrombocytopenia (HIT) requires cessation of heparin and initiation of an alternative anticoagulant. The platelet count will subsequently recover. This case report describes the clinical course of a patient after a cardiovascular surgery. HIT was clinically and biologically confirmed. Unexpectedly, the platelet count did not recover despite the arrest of heparin. Danaparoid was initiated, and thrombocytopenia persisted. Danaparoid cross-reactivity was suspected, and laboratory assay was performed. Results were misinterpreted because no comparative buffer control was performed to ensure that the platelet aggregation was caused by danaparoid. Moreover, plasma/serum must be diluted to demonstrate this effect. Danaparoid cross-reactivity was incorrectly concluded, and the patient was switched to bivalirudin. The severe thrombocytopenia persisted. Plasmapheresis was started, and platelet count finally increased. The clinical course suggested a delayed-onset HIT. This case report illustrates the need for appropriate testing to differentiate drug cross-reactivity from delayed-onset HIT.

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