The Clot Thickens: COVID Clot Clues Point to Autoimmune Antibody Culprit

People who get severe versions of COVID-19 tend to end up with blood clots in the arteries and veins of their lungs and other organs. Now, scientists from the Michigan Medicine Frankel Cardiovascular Center have figured out a reason why. A certain autoimmune antibody in the blood attacks cells, triggering clot formation. This antibody also shows up in people with the autoimmune disease antiphospholipid syndrome.

In an earlier study, the same research team found that roughly half of the patients with severe COVID-19 had both high levels of the antibodies and high levels of superactivated neutrophils, which can destroy white blood cells.  When they looked into how the destructive neutrophils and the COVID-19 antibodies interacted in mice with COVID-19 infections, they noticed that the mice developed severe levels of clotting, according to study coauthor Dr. Yogen Kanthi, an assistant professor at the Michigan Medicine Frankel Cardiovascular Center.

Study coauthor and rheumatologist Dr. Jason Knight of Michigan Medicine, also an associate professor, said that in the present study, the researchers were surprised to find that half of the hospitalized COVID-19 patients were “positive for at least one” autoantibody.

Explained Dr. Kanthi:

“In patients with COVID-19, we continue to see a relentless, self-amplifying cycle of inflammation and clotting in the body. Now we’re learning that autoantibodies could be a culprit in this loop of clotting and inflammation that makes people who were already struggling even sicker.”

The next step for the researchers is to figure out whether severely ill patients will get better if these autoantibodies are blocked, which could require an aggressive treatment such plasmapheresis, according to coauthor Dr. Yu (Ray) Zuo, an assistant professor at Michigan Medicine. For plasmapheresis, the blood is drained through an IV, filtered and replaced with plasma that lacks the “bad” antibodies. Dr Zuo notes that study patients who had the most autoantibodies also had the worst respiratory function. The offending antibodies were also associated with inflammation in healthy cells.

Dr. Knight adds that the scientists still don’t know what makes the body create autoantibodies in COVID-19 infections. They are looking into how long the antibodies last in the body after an COVID-19 infection ends.

The team is participating in a trial to see whether the anticlotting agent dipyridamole can help reduce dangerous blood clotting in COVID-19 patients. The drug has been approved by the U.S. Food and Drug Administration for 20 years to prevent clotting but recently was found to have anti-inflammatory properties. According to Dr. Kanthi, repurposing it for use in COVID-19 should be easier than finding a new drug.

Disclaimer: This article does not provide medical advice. Do not take action based solely on this article and always consult with an appropriate healthcare professional. This article is purely for informational purposes.

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