Researchers at McMaster University are recommending a pair of treatments to fight Vaccine-induced thrombotic thrombocytopenia (VITT), identified in a small number of COVID-19 vaccine recipients.
A group from the McMaster Platelet Immunology Laboratory (MPIL), building off of previous investigations into a condition that prevents blood clotting, are suggesting that a combination of anti-clotting drugs with high doses of intravenous immunoglobulin — an antibody solution — may be effective against VITT.
VITT has been associated with but not definitively linked to the viral vector shots from Oxford-AstraZeneca and Johnson & Johnson.
A look at what we know about VITT, the rare blood clotting disorder
The McMaster experts say the disorder occurs when antibodies attack a blood protein, called platelet factor 4 (PF4), which results in the activation of platelets in the blood, causing them to clump together and form clots.
The study on the McMaster treatment, published in the New England Journal of Medicine, surrounded three Canadian patients who received the AstraZeneca vaccine and subsequently developed VITT. Two suffered clotting in their legs and the third had clots blocking arteries and veins inside the brain.
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Blood samples taken from the patients after treatment showed reduced antibody activation in all cases.
“If you were a patient with VITT, I’d be telling you we know of a treatment approach. We can diagnose it accurately with our tests, treat it and we know exactly how the treatment works,” said Ishac Nazy, scientific director of the lab and associate professor of medicine.
The lab’s scientists devised an effective test and treatment building on previous investigations into another condition, Heparin-Induced Thrombocytopaenia (HIT), which uncovered that a standard antibody test can detect VITT through false negative results.
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Modifications to the HIT test detected VITT-specific antibodies found in rare cases involving a COVID-19 vaccine.
The researchers say subsequent lab tests on the patient blood samples showed how high doses of the antibody solution coupled with blood-thinner medications shut down platelet activation and stopped the formation of clots.
“We now understand the mechanism that leads to platelet activation and clotting,” Nazy said.
External funding for the McMaster study was provided by the Canadian Institutes for Health Research.
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