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The researchers from the University of North Carolina (UNC) School of Medicine, US noted that the finding will lead to earlier diagnosis, appropriate and optimised treatment, and better outcomes in patients who develop this life-threatening disorder.
The study, published in the New England Journal of Medicine, sheds new light on the flu virus and its role in causing an anti-platelet factor 4 disorder.
It also opens a whole new door for research, as many questions remain as to how and why this condition occurs—and who is most likely to develop the disorder.
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In anti-PF4 disorders, the person’s immune system makes antibodies against platelet factor-4 (PF4), a protein that is released by platelets.
When an antibody forms against PF4 and binds to it, this can trigger the activation and rapid removal of platelets in the bloodstream, leading to blood clotting and low platelets, respectively.
Sometimes, the formation of anti-PF4 antibodies is triggered by a patient’s exposure to heparin, called heparin-induced thrombocytopenia (HIT), and sometimes it occurs as an autoimmune condition without heparin exposure, which is referred to as “spontaneous HIT.” The finding started when a young child, who had been diagnosed as an outpatient with adenovirus infection, had to be admitted to the hospital with an aggressive blood clot forming in his brain (called cerebral sinus vein thrombosis) and severe thrombocytopenia.
Doctors determined that they hadn’t been exposed to heparin or the adeno-vector COVID-19 vaccination, the classical triggers of HIT.
“The intensive care unit physicians, the neuro-intensivist, and hematology group were working around the clock to determine the next steps in the care for this young child,” said Jacquelyn Baskin-Miller from UNC.
“They weren’t responding to therapy and were progressing quickly. We had questioned whether it could have been linked to the adenovirus considering the vaccine data, but there was nothing in the literature at that time to suggest it,” Baskin-Miller added.