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.