A new study shows that the novel coronavirus can trigger the production of clot-causing autoantibodies. This finding may explain the high rate of blood clots among COVID-19 patients.
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Alongside the respiratory features of COVID-19, many people with the illness have experienced thromboses, better known as blood clots.
Some estimates suggest that the novel coronavirus causes blood clots in 30% of critically ill patients, which can lead to serious complications, including strokes.
These findings have motivated researchers to test whether existing blood-thinning drugs typically used to prevent blood clots after a heart attack, for example, could improve outcomes for people with COVID-19. However, precisely what causes the blood clots to form in people with the illness remains unclear.
New research led by a team from the University of Michigan suggests that a type of autoantibody usually seen in people with the autoimmune disease antiphospholipid syndrome could be behind blood clots in people with COVID-19.
The researchers found the clot-causing antibodies in more than half of the COVID-19 patients in their analysis, and these antibodies were also associated with impaired renal function.
The study could lead to new treatment options and is available in the journal
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Scientists have proposed various explanations for the presence of blood clots in people with COVID-19, including the “cytokine storm” generated by an excessive immune response, blockages to blood vessels caused by very low oxygen levels, and direct damage to blood vessels caused by SARS-CoV-2, the virus responsible for COVID-19.
The present study, however, investigated a new mechanism that involves a type of antibody called an autoantibody, which attacks lipids in the body.
These antibodies, known as antiphospholipid (aPL) autoantibodies, are a feature of the autoimmune disease antiphospholipid syndrome, which is associated with blood clots in veins and arteries.
aPL antibodies activate various factors in the blood, including platelets, to trigger the blood clotting process.
However, data on aPL antibodies and their ability to trigger blood clots in people with COVID-19 are still limited. To add to the evidence, this study tested for aPL antibodies in 172 people receiving inpatient treatment COVID-19.
The scientists found that more than half of the samples from the patients contained aPL autoantibodies, using the threshold recommended by the test’s manufacturer. They also found evidence to support the theory that the antibodies could cause blood clots in COVID-19 patients.
Higher levels of the antibodies were associated with having more platelets and the release of neutrophil extracellular traps (NETs). Platelets trigger the blood clotting process, and NETs are sticky webs that help trap viruses — but also promote the formation of blood clots.
The team also found that antibodies taken from COVID-19 patients caused the release of NETs in blood samples from healthy people and, when injected into mice, caused the formation of blood clots in two mouse models.
“Antibodies from patients with active COVID-19 infection created a striking amount of clotting in animals — some of the worst clotting we’ve ever seen,” says co-author Dr. Yogendra Kanthi, a cardiologist and specialist in vascular medicine at the University of Michigan.
The researchers say that they’ve found a new mechanism by which COVID-19 patients may develop blood clots.
The aPL antibodies were also associated with impaired kidney function, and some, but not all, aPL antibodies were associated with worse respiratory function. This suggests that blocking these antibodies might improve outcomes for patients.
“People with the highest levels of autoantibodies did worse, in terms of respiratory function, and the antibodies caused inflammation even in healthy cells,” explains first author Dr. Yu Zuo, a rheumatologist and assistant professor of internal medicine at the university.
The researchers are now investigating what might trigger the body to produce the antibodies in the first place, in the hope of finding a treatment.
They observe that the patients may benefit from plasmapheresis, which involves filtering the blood to remove the clot-causing antibodies and replacing it with plasma that does not contain the antibodies. However, this very aggressive treatment is usually reserved for people with severe autoimmune diseases.
The team is also trialing an existing blood thinner called dipyridamole (Persantine), which stops blood clots from forming.
“Dipyridamole is an old drug that is safe, inexpensive, and scalable,” explains Dr. Kanthi. “The [Food and Drug Administration] approved it 20 years ago to prevent clotting, but we only recently discovered its potential to block this specific type of inflammation that occurs in [people with COVID-19].”
The researchers have already begun a clinical trial to test the use of dipyridamole in people with this illness, and they expect to publish the results early next year.
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