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Blood. 2014 Jun 5;123(23):3651-4. doi: 10.1182/blood-2014-01-549741. Epub 2014 Mar 27.

Spontaneous heparin-induced thrombocytopenia syndrome: 2 new cases and a proposal for defining this disorder.

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Department of Pathology and Molecular Medicine, Michael G. DeGroote School of Medicine, McMaster University, Hamilton, ON, Canada;
Department of Medicine, and.
Division of Interventional Neuroradiology, Department of Neurosurgery, Weill Cornell Medical Center, New York, NY; and.
Ken and Ruth Davee Department of Neurology and Clinical Neurological Sciences, Feinberg School of Medicine of Northwestern University, Chicago, IL.


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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