Heparin-induced thrombocytopenia (HIT) is a life and limb-threatening thrombotic complication of heparin,
which is the result of platelet activation by anti-PF4/heparin antibodies. With lepirudin and danaparoid no longer available
in the US, treatment options are limited to argatroban, fondaparinux (off-label use) and bivalirudin (for patients undergoing
percutaneous coronary intervention). Both argatroban and bivalirudin are parenteral drugs and require close monitoring
and hospitalization. Fondaparinux is contraindicated in patients with significant renal impairment and is associated with a
small risk of HIT. Anticoagulants approved for thromboprophylaxis and management of thromboembolic conditions such
as rivaroxaban, dabigatran, and apixaban have fixed oral dose, rapid onset of action and does not require monitoring.
These novel agents do not interact with anti-PF4/heparin antibody and offer attractive therapy options for HIT. Their
utility in HIT has been supported by a few clinical reports, however, larger studies are needed before they can be utilized
in clinical practice. Therapeutic plasma exchange has been utilized with some success in patients with HIT, who need
heparin reexposure for cardiac surgery but their safety and efficacy needs further exploration. 2-O, 3-O desulfated
heparin, which lacks any anticoagulant effect, has been shown to reduce the development of HIT in murine models.
Finally, novel targets based on the molecular pathogenesis of HIT are being studied for therapeutic drug development.
We hope that the availability of novel therapies in the future will expand the options available for the management of HIT.