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“Autoimmune HIT” antibodies in diagnostic samples are a potential artifact and not associated with more severe outcomes

Year: 2023

Type: article

Abstract: In recent years, there has been increasing use of the term autoimmune heparin-induced thrombocytopenia (aHIT) to describe patients whose blood samples activate platelets in the absence of exogenous heparin (ie, in the no-heparin/buffer-control serotonin release assay [SRA]).[1][2][3][4][5][6][7][8] This term has been proposed to include not only syndromes in which patients develop anti-PF4-mediated thrombotic thrombocytopenia without proximate heparin exposure, such as spontaneous HIT and vaccine-induced immune thrombotic thrombocytopenia, but also several clinically severe HIT subtypes that occur after heparin exposure.These additional entities include delayed-onset HIT, persistent HIT, heparin flushinduced HIT, and severe HIT with a platelet count <20 000/μL with associated disseminated intravascular coagulation.1,2 Although limited data appear to support the correlation between reactivity in no-heparin SRA and disease severity in patients with aHIT who were exposed to herapin, rigorous studies to confirm this association are lacking.2,9 It has also been proposed that the incidence of aHIT is underrecognized because most laboratories (including ours) do not perform SRA in the absence of heparin for diagnostic purposes.

Source: Blood Advances

DOI: 10.1182/bloodadvances.2023009811