ABSTRACT
Heparin-induced thrombocytopenia (HIT) is a unique immune-mediated disorder. HIT is common, occurring in as many as 5% of certain patient populations. Affected patients can develop a paradoxical thrombotic episode, rather than bleeding, despite having thrombocytopenia. One possible reason for the unique clinical profile is the central role of platelet Fcg receptor (FcgR) IIa in mediating platelet activation in HIT. Indirect evidence suggests a crucial role for platelet activation in the pathogenesis of HIT since thrombocytopenia and the presence of HIT antibodies are strongly associated with thrombosis, whereas formation of antibodies without thrombocytopenia is not (Warkentin et al., 1995). Notwithstanding the role that platelet FcgRs play in platelet activation, leukocyte FcgRs could also contribute to the pathogenesis of HIT.
