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. 2018 Nov 6;19(18):1413–1422. doi: 10.2217/pgs-2018-0147

Figure 1. . The pathogenesis of heparin-induced thrombocytopenia is characterized by gaps in our knowledge.

Figure 1. 

Genomic biomarkers have the potential to answer critical questions at every stage of HIT pathogenesis, including the predisposing immunogen, the cellular source of antibodies, the identification of pathogenic IgG antibodies and the mechanisms of thrombosis. Similarly, the clinical progression of patient who will eventually develop HIT is characterized by various unmet clinical needs. Genomic biomarkers have the potential to meet many of the unmet clinical needs for HIT, including limitations in the clinical utility of platelet count monitoring, PF4/heparin antibody testing, functional assay testing and limited treatment options.

APC: Antigen-presenting cell; FcγRIIA: Platelet FcγRIIa receptor; HIPA: Heparin-induced platelet aggregation; HIT: Heparin-induced thrombocytopenia; IVIG: Intravenous immunoglobulin; NOAC: New oral anticoagulant; PF4: Platelet factor 4; SRA: Serotonin release assay.