Key result
Spontaneous HIT syndrome triggers potent heparin-independent platelet activation linked to anti-PF4 antibodies in case reports.
Case Report (n=2)
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The existence of spontaneous heparin-induced thrombocytopenia (HIT) syndrome (or autoimmune HIT), defined as a transient prothrombotic thrombocytopenic disorder without proximate heparin exposure serologically indistinguishable from HIT, is controversial. We describe 2 new cases presenting with thrombotic stroke/thrombocytopenia: one following shoulder hemi-arthroplasty (performed without heparin) and the other presenting to the emergency room without prior hospitalization, heparin exposure, or preceding infection. Both patients tested strongly positive for anti-platelet factor 4 (PF4)/heparin immunoglobulin (Ig)G in 2 different immunoassays and in the platelet serotonin-release assay. Crucially, both patients' sera also caused strong (>80%) serotonin release in the absence of heparin, a serologic feature characteristic of delayed-onset HIT (ie, where heparin use precedes HIT but is not required for subsequent development or worsening of thrombocytopenia). We propose that a rigorous definition of spontaneous HIT syndrome should include otherwise unexplained thrombocytopenia/thrombosis without proximate heparin exposure and with anti-PF4/heparin IgG antibodies that cause strong in vitro platelet activation even in the absence of heparin.
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Warkentin et al. (2014) conducted a case report in Spontaneous heparin-induced thrombocytopenia (HIT) syndrome (n=2). Spontaneous anti-PF4/heparin IgG antibodies was evaluated on In vitro platelet serotonin release in the absence of heparin. Spontaneous HIT syndrome patients tested strongly positive for anti-PF4/heparin IgG and exhibited >80% platelet serotonin release in the absence of heparin in 2 of 2 cases (100%).
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