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Novel genotype-phenotype interaction in HIT: THROMBOSIS AND HEMOSTASIS - Blood

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  • Novel genotype-phenotype interaction in HIT: THROMBOSIS AND HEMOSTASIS - Blood

    JULY 21, 2022

    Blood (2022) 140 (3): 168–169.

    Through genome-wide association studies (GWAS) and fine-mapping, Karnes et al,1 in this issue of Blood, have shown that having platelet factor 4 (PF4)/heparin antibodies in the presence of type O blood predisposes one to heparin-induced thrombocytopenia (HIT).

    Unfractionated heparin (UFH) was first isolated in 1916 and entered clinical practice after its structure was determined in the 1930s. It remains one of the oldest drugs still in widespread clinical use.2 Of all the anticoagulants, heparin’s unique pharmacological properties will ensure its continued therapeutic use. However, HIT, first described in 1958, remains a significant iatrogenic complication of heparin use.3

    HIT is a pathological prothrombotic syndrome caused by an immunoglobulin G (IgG)-mediated immune response to complexes of PF4 bound to heparin. HIT antibodies can activate platelets, resulting in procoagulant platelet membrane changes that enhance thrombin generation.4 HIT occurs in ∼2.4% of patients receiving UFH and low-molecular-weight heparin.1 The mortality rate of HIT is high, and the prevalence of thromboembolic complications in these patients has been put at 60%.5 Currently, it is impossible to know before administration of heparin which patients will develop HIT.6 Furthermore, HIT has similarities to adenoviral vector SARS-CoV-2 vaccine-induced thrombotic thrombocytopenia (VITT); thus, discoveries related to HIT could aid in management of VITT (see figure). ...