Severe and persistent heparin‐induced thrombocytopenia despite fondaparinux treatment

Tvito, Ariella; Bakchoul, Tamam; Rowe, Jacob M.; Greinacher, Andreas; Ganzel, Chezi

doi:10.1002/ajh.23971

Cited by 60 publications

(82 citation statements)

References 23 publications

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“…Moreover, there was no cross-reactivity with fondaparinux. Thus, this patient had the serological features of delayed-onset HIT 39,40 (also called autoimmune HIT 41 ). However, this patient was unusual in another respect: both of his episodes of HIT (in 1998 and 2009) were characterized by the phenomenon of persisting HIT (ie, both HIT episodes lasted for more than 4 weeks before platelet count recovery, which is a rare but recognized course of HIT).…”

Section: Blood 21 July 2016 X Volume 128 Number 3 How I Treat Patiementioning

confidence: 93%

How I treat patients with a history of heparin-induced thrombocytopenia

Warkentin

Anderson

2016

Blood

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Heparin-induced thrombocytopenia (HIT) is a relatively common prothrombotic adverse drug reaction of unusual pathogenesis that features platelet-activating immunoglobulin G antibodies. The HIT immune response is remarkably transient, with heparin-dependent antibodies no longer detectable 40 to 100 days (median) after an episode of HIT, depending on the assay performed. Moreover, the minimum interval from an immunizing heparin exposure to the development of HIT is 5 days irrespective of the patient’s previous heparin exposure status or history of HIT. This means that short-term heparin reexposure can be safely performed if platelet-activating antibodies are no longer detectable at reexposure baseline and is recommended when heparin is the clear anticoagulant of choice, such as for cardiac or vascular surgery. The risk of recurrent HIT 1 to 2 weeks after heparin reexposure is ∼2% to 5% and is attributable to formation of delayed-onset (or autoimmune-like) HIT antibodies that activate platelets even in the absence of pharmacologic heparin. Some studies suggest that longer-term heparin reexposure (eg, for chronic hemodialysis) may also be reasonable. However, for other antithrombotic indications that involve patients with a history of HIT (eg, treatment of venous thromboembolism or acute coronary syndrome), preference should be given to non-heparin agents such as fondaparinux, danaparoid, argatroban, bivalirudin, or one of the new direct-acting oral anticoagulants as appropriate.

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Section: Blood 21 July 2016 X Volume 128 Number 3 How I Treat Patiementioning

confidence: 93%

How I treat patients with a history of heparin-induced thrombocytopenia

Warkentin

Anderson

2016

Blood

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“…Limited data suggest that this drug may be an option (along with anticoagulation) in patients at high risk for thrombosis and bleeding (e.g., those who are pregnant or have sinus-vein thrombosis complicating HIT) or in patients who have autoimmune HIT. 51 PF4 forms complexes with negatively charged nucleic acids and aptamers, 20 which cross-react with anti-PF4-heparin antibodies. Aptamers and other nucleic acid-based drugs are entering clinical application, and it is unclear whether they can induce HIT.…”

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confidence: 99%

Heparin-Induced Thrombocytopenia

2015

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“…Including the 6 Hamilton patients in group C (Table 1), we identified a total of 11 patients who received a DOAC after platelet count recovery from HIT (rivaroxaban, n 5 7; apixaban, n 5 3; edoxaban, n 5 0; dabigatran, n 5 1). 40,47 None of the patients developed a thrombotic problem. One patient had a major bleed secondary to known varices.…”

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confidence: 99%