Heparin-induced thrombocytopenia (HIT) is a potentially life-threatening drug reaction to heparin therapy characterized by a decrease in platelet count and hypercoagulability. HIT occurs in approximately 1%-5% of patients exposed to heparin products (including unfractionated heparin and low molecular weight heparin). Heparin normally functions by binding to platelet factor 4 (PF4), which is released by alpha granules in platelets. This binding inhibits PF4's procoagulant function, but, in some instances, this binding can trigger the production of immunoglobulin G (IgG) antibodies specific to the heparin-PF4 complex. These antibodies activate more platelets, which in turn form more complexes, leading to a hypercoagulable state in which either venous or arterial thromboses can occur. Macrophages consume the IgG-coated platelets, which are removed by the reticuloendothelial system, causing thrombocytopenia.

There are two types of HIT. Type 1 is the most common form and is a nonimmune-mediated reaction in which platelet count will drop soon after exposure to heparin (can be as early as the first day of treatment) but will return to normal once the heparin is discontinued. Type 2 is an immune- or antibody-mediated reaction that takes 5-14 days after the start of heparin treatment to manifest. If a patient has been exposed to heparin and developed antibodies in the past, however, type 2 HIT can develop in the first day of treatment. The patient can develop hypercoagulability with high morbidity (10%) and mortality (20%).