The complicated relationships of heparin‐induced thrombocytopenia and platelet factor 4 antibodies with COVID‐19

Abstract

COVID‐19 (coronavirus disease 2019) represents a prothrombotic disorder, and there have been several reports of platelet factor 4/heparin antibodies being present in COVID‐19‐infected patients. This has thus been identified in some publications as representing a high incidence of heparin‐induced thrombocytopenia (HIT), whereas in others, findings have been tempered by general lack of functional reactivity using confirmation assays of serotonin release assay (SRA) or heparin‐induced platelet aggregation (HIPA). Moreover, in at least two publications, data are provided suggesting that antibodies can arise in heparin naïve patients or that platelet activation may not be heparin‐dependent. From this literature, we would conclude that platelet factor 4/heparin antibodies can be observed in COVID‐19‐infected patients, and they may occur at higher incidence than in historical non‐COVID‐19‐infected cohorts. However, the situation is complex, since not all platelet factor 4/heparin antibodies may lead to platelet activation, and not all identified antibodies are heparin‐dependent, such that they do not necessarily reflect “true” HIT. Most recently, a “HIT‐like” syndrome has reported in patients who have been vaccinated against COVID‐19. Accordingly, much more is yet to be learnt about the insidious disease that COVID‐19 represents, including autoimmune outcomes in affected patients.