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Monoclonal Antibodies in the Pathogenesis of Heparin-Induced Thrombocytopenia

This NEJM study challenges the long-held view that heparin-induced thrombocytopenia (HIT) is a polyclonal antibody disorder. Using mass spectrometry and immunofixation, the investigators found that all 9 patients with HIT had monoclonal, platelet-activating anti–PF4–heparin antibodies, with 67% showing a detectable M-protein by immunofixation. Functional assays confirmed that only the monoclonal fraction was pathogenic. It looks like HIT is driven by a single rogue antibody clone, which could have big implications for diagnostics and targeted therapy—this would be a paradigm shift for how we think about this disease.

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