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

• Published in: Research and Practice in Thrombosis and Haemostasis Vol. 4; no. 6; pp. 1068 - 1069
• Main Authors: Riker, Richard R., May, Teresa L., Fraser, Gilles L., Gagnon, David J., Bandara, Mahesh, Zemrak, Wes, Seder, David B.
• Format: Journal Article Web Resource
• Language: English
• Published: United States Elsevier Inc 01.08.2020; John Wiley & Sons, Inc; Elsevier Limited; John Wiley and Sons Inc; Elsevier
• Subjects: Antibodies; Coronaviruses; COVID-19; Letter to the Editor; Letters to the Editor; Severe acute respiratory syndrome; Severe acute respiratory syndrome coronavirus 2; Thrombocytopenia
• ISSN: 2475-0379; 2475-0379
• DOI: 10.1002/rth2.12417

Neither our patient 3 nor the seven patients presented by May et al met these definitions, and we did not perform any of the proposed adaptations of functional testing to confirm SRA‐negative HIT, so our contention remains possible, but not confirmed. Testing to confirm SRA‐negative HIT might include adding exogenous human PF4, 4 or using a flow cytometry PF4‐dependent P‐selectin expression assay. 6 May et al also cite the review by Connors and Levy, 7 which does not mention HIT as a potential contributor to the prothrombotic state associated with COVID‐19; we would highlight two additional concerns regarding this otherwise comprehensive review. Additionally, Connors and Levy propose empiric escalation of heparin to treatment levels when sudden respiratory decompensation, right ventricular strain, or peripheral thrombosis is noted and imaging to test for pulmonary embolism cannot be obtained. 7 If HIT is not considered and excluded in this situation, continuing heparin may have life‐threatening consequences.