New Research Offers Insights Into Fatal Blood Clots After COVID Vaccination
New research has shed light on the serious blood clotting disorder that some individuals experience after receiving a COVID-19 vaccine.
Scientists from the University of Birmingham, UK, funded by the National Institute for Health and Care Research and the British Heart Foundation, have identified a new mechanism of platelet activation in vaccine-induced immune thrombocytopenia and thrombosis (VITT).
VITT is a clinical syndrome associated with COVID-19 vaccines, characterized by blood clots in uncommon sites and varying degrees of thrombocytopenia, a condition where blood platelet levels are dangerously low, leading to increased bleeding. VITT shares similarities with heparin-induced thrombocytopenia (HIT), but occurs even in the absence of prior exposure to the anticoagulant drug, heparin.
Richard Buka, co-lead author and clinical research fellow at the University of Birmingham Institute of Cardiovascular Sciences, highlighted the significance of the research, stating, “Although VITT only emerged recently, the research that it has triggered is teaching us a lot about how the body works and how it can go wrong.” He emphasized that their work on VITT has unveiled a previously unknown biological pathway, one that may have implications for various other research fields, including clotting disorders and bone marrow function in platelet production.
The study revealed that individuals with VITT or HIT produce antibodies against a small chemokine protein released by activated platelets, forming immune complexes. These large clusters of molecules activate both platelets and immune system cells, ultimately leading to clotting and inflammation.
While scientists knew that platelet factor 4 (PF4) played a crucial role in promoting blood coagulation and was involved in immune responses to infections, the exact nature of how PF4 contributed to this process remained unclear.
The study found that PF4 binds to a receptor called c-Mpl on the surface of platelets, triggering the activation of small cells known to cause clotting. Higher concentrations of PF4 led to robust platelet aggregation, while lower concentrations increased the likelihood of platelet activation through the same pathway.
Mr. Buka explained that their research uncovered the role of PF4 in platelet activation in VITT, challenging the previous belief that only antibodies were responsible for platelet activation. He added that understanding the role of PF4 could pave the way for improved treatments for VITT, suggesting the potential use of the drug ruxolitinib.
While Mr. Buka acknowledged that this drug might play a more minor role in platelet activation, he noted that there are other medications that could be explored to reduce platelet activation, offering promising avenues for treatment.
It is important to note that this study has some limitations, including a small sample size and variations in treatments received by participants prior to sample collection. Additionally, the study tested a limited number of conditions due to the availability of sera, and aggregation measurements were conducted over 10 minutes, rather than the standard 30 minutes for VITT cases.
Despite these limitations, Mr. Buka expressed gratitude to the patients and their families affected by VITT, highlighting the importance of their contributions in advancing our understanding of this condition.
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