Heparin-induced thrombocytopenia (HIT) is an immune reaction to heparin — driven by antibodies against platelet factor 4/heparin complexes — that paradoxically causes thrombocytopenia together with a high risk of thrombosis. Management, per the 2018 ASH guidelines, is to stop all heparin immediately and start a non-heparin anticoagulant (argatroban, bivalirudin, or fondaparinux). Increasingly, direct oral anticoagulants (rivaroxaban, apixaban) are used off-label, with contemporary series showing they prevent new or recurrent thrombosis in the large majority of patients with low bleeding rates, and meta-analyses suggesting little difference in outcomes between parenteral non-heparin agents and DOACs (albeit with low-certainty evidence).
A closely related disorder that emerged in 2021 is vaccine-induced immune thrombotic thrombocytopenia (VITT), which involves anti-PF4 antibodies arising without heparin exposure and is treated with intravenous immunoglobulin plus non-heparin anticoagulation. Emerging HIT-directed strategies — including agents targeting the underlying immune mechanism and IgG-degrading enzymes — remain investigational.
Further reading: ASH 2018 HIT guideline (Cuker et al., Blood Advances 2018); contemporary HIT management review (Ng et al., 2024); DOACs in HIT (Barlow et al., 2019).