Endothelial Cell Activation Enhances Thromboinflammation in Vitt

Dupuy, Alexander; Liu, Xiaoming; Tieng, Jessica; Johnston, Bede; Nasser, Arian; Coleman, Paul R.; Zhang, Yingqi; Ju, Lining Arnold; Tran, Huyen; Chen, Vivien; Gardiner, Elizabeth E.; Passam, Freda

doi:10.1182/blood-2022-168441

Cited by 2 publications

(3 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…75 Furthermore, published abstracts from two different groups implicate endothelial activation as a potential additional or even alternative driver to platelet activation for thrombus formation in VITT. 76,77 Interestingly, sera from patients that fit the clinical syndrome in which PF4 antibodies are not detectable appear to demonstrate endothelial-associated ex vivo thrombus formation. 77…”

Section: Endothelial Cellsmentioning

confidence: 99%

“…76,77 Interestingly, sera from patients that fit the clinical syndrome in which PF4 antibodies are not detectable appear to demonstrate endothelial-associated ex vivo thrombus formation. 77…”

Section: Endothelial Cellsmentioning

confidence: 99%

“…NETosis NETosis [84][85][86] Endothelium [75][76][77] Procoagulant platelets [95][96][97] Monocytes 59 Vaccine components 84 Abbreviations: HIT, heparin-induced thrombocytopenia; LMWH, low molecular weight heparin; NETosis, the formation of neutrophil extracellular traps; PF4, platelet factor 4; VITT, vaccine-induced immune thrombotic thrombocytopenia.…”

Section: Other Contributors To Thrombosismentioning

confidence: 99%

See 2 more Smart Citations

Mechanisms of Thrombosis in Heparin-Induced Thrombocytopenia and Vaccine-Induced Immune Thrombotic Thrombocytopenia

Selvadurai

Favaloro

Chen

2023

Semin Thromb Hemost

View full text Add to dashboard Cite

Heparin-induced thrombocytopenia (HIT) and vaccine-induced immune thrombotic thrombocytopenia (VITT) are rare, iatrogenic immune-mediated conditions with high rates of thrombosis-related morbidity and mortality. HIT is a long-recognized reaction to the administration of the common parenterally administered anticoagulant heparin (or its derivatives), while VITT is a new, distinct syndrome occurring in response to adenovirus-based vaccines against coronavirus disease 2019 and potentially other types of vaccines. A feature of both HIT and VITT is paradoxical thrombosis despite a characteristic low platelet count, mediated by the presence of platelet-activating antibodies to platelet factor 4. Several additional factors have also been suggested to contribute to clot formation in HIT and/or VITT, including monocytes, tissue factor, microparticles, endothelium, the formation of neutrophil extracellular traps, complement, procoagulant platelets, and vaccine components. In this review, we discuss the literature to date regarding mechanisms contributing to thrombosis in both HIT and VITT and explore the pathophysiological similarities and differences between the two conditions.

show abstract