HIT continues to pose several enigmas including the fundamental issue of how heparin induces the formation of self-reactive antibodies to a native protein in such a high proportion of immunologically competent individuals (Visentin et al., 1996; Bauer et al., 1997). It also remains unclear why only a subset of patients with anti-PF4-heparin antibodies develops thrombocytopenia, and fewer still develop thrombosis. It is possible that characteristics of HIT antibodies, such as their subtype, specificity, and affinity for portions of the PF4 molecule, may provide some of the answers. However, it is also likely that part of the propensity for thrombosis, and the localization of clotting observed in HIT, relate to antigen expression and response to injury at the level of the vessel wall itself
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