Response to The challenges of diagnosing heparin‐induced thrombocytopenia in patients with COVID‐19

Riker, Richard R.; May, Teresa L.; Fraser, Gilles L.; Gagnon, David J.; Bandara, Mahesh; Zemrak, Wes; Seder, David B.

We thank May et al for their comments, expanding the number of reported cases of suspected and confirmed heparin‐induced thrombocytopenia (HIT) associated with COVID‐19, and reemphasizing the complexity of the prothrombotic state observed (1). We agree that false‐positive enzyme immunoassay (EIA) detection of anti‐platelet factor 4 (PF4)/heparin antibodies could explain the results we observed in patients #2 and #3 (2), and this has been the conventional interpretation when functional testing (such as the serotonin‐release assay [SRA]) returns negative. We suggested that a false negative SRA result could have explained our findings, as opposed to the contention by May et al that we concluded they were falsely positive, to broaden our discussion about SRA‐negative HIT, a relatively new and evolving clinical condition (3‐6).