Heparin-induced thrombocytopenia (HIT) is a prothrombotic adverse event of heparin therapy caused by anti-platelet factor 4/heparin IgG with platelet-activating properties (HIT antibodies). Antigen immunoassays are commonly used worldwide ; however, they do not detect the platelet-activating properties of HIT antibodies, leading to a low specificity for HIT diagnosis. The detection of platelet-activating antibodies using a functional assay is crucial for an accurate diagnosis.

　　The pathogenesis of HIT includes several clinical features atypical of immune-mediated diseases. Heparin-naïve patients can develop IgG antibodies as early as day 4, as in a secondary adoptive immune response, but evidence for an anamnestic response on heparin re-exposure is lacking. HIT antibodies are relatively short-lived, unlike those in a secondary immune response. This suggests that the mechanisms underlying HIT antibody formation are consistent with a non-T cell-dependent innate immune reaction.

　　These atypical clinical and serological features should be carefully considered while deciding therapy such as immediate administration of an alternative anticoagulant for preventing thromboembolic events. High-dose IVIg and plasma exchange may be promising for the treatment of severe HIT patients.

　　Several clinical studies suggested that severe trauma patients, especially those with infectious disease, have a relatively high risk of HIT.