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The complicated relationships of heparin-induced thrombocytopenia and platelet factor 4 antibodies with COVID-19
Emmanuel J Favaloro1,2, Brandon Michael Henry3, Giuseppe Lippi4
1Haematology, Sydney Centres for Thrombosis and Haemostasis, Institute of Clinical Pathology and Medical Research (ICPMR), NSW Health Pathology, Westmead Hospital, Westmead, NSW, Australia.
Insights
COVID-19 patients may develop platelet factor 4/heparin antibodies, but these do not always cause platelet activation or indicate true heparin-induced thrombocytopenia (HIT). Further research is needed on COVID-19
Area of Science:
- Hematology and Immunology
- Infectious Diseases
Background:
- COVID-19 is recognized as a prothrombotic disorder.
- Reports indicate the presence of platelet factor 4/heparin antibodies in COVID-19 patients, with some suggesting a high incidence of heparin-induced thrombocytopenia (HIT).
- Conflicting findings exist regarding the functional reactivity and heparin-dependency of these antibodies.
Purpose of the Study:
- To review and synthesize current literature on platelet factor 4/heparin antibodies in COVID-19.
- To clarify the relationship between these antibodies, platelet activation, and the diagnosis of HIT in the context of COVID-19.
- To discuss the implications of these findings for understanding COVID-19 as a complex disease with potential autoimmune outcomes.
Main Methods:
- Literature review of publications reporting on platelet factor 4/heparin antibodies in COVID-19 patients.
- Analysis of data from functional assays such as serotonin release assay (SRA) and heparin-induced platelet aggregation (HIPA).
- Examination of studies investigating antibody development in heparin-naïve patients and heparin-independent platelet activation.
Main Results:
- Platelet factor 4/heparin antibodies are observed in COVID-19 patients, potentially at a higher incidence than in non-COVID-19 cohorts.
- Not all detected antibodies lead to significant platelet activation or meet the criteria for true HIT.
- Antibodies may arise in heparin-naïve individuals, and platelet activation may not always be heparin-dependent.
- A 'HIT-like' syndrome has been reported post-COVID-19 vaccination.
Conclusions:
- The presence of platelet factor 4/heparin antibodies in COVID-19 is complex and does not always equate to HIT.
- The pathophysiology of antibody formation and platelet activation in COVID-19 requires further investigation.
- Understanding the autoimmune aspects and long-term outcomes of COVID-19 is crucial.
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.
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