Scientists from Michigan Medicine found that “rogue” antibodies found circulating in the blood of COVID-19 patients have the potential to cause cells to lose their resistance to clotting.
The research is published in Arthritis & Rheumatology and was conducted by Hui Shi et al.
In the study, the team examined the blood samples of nearly 250 patients hospitalized for COVID-19.
They found higher-than-expected levels of antiphospholipid autoantibodies, which can trigger blood clots in the arteries and veins of patients with autoimmune disorders, including lupus and antiphospholipid syndrome.
Antibodies typically help the body neutralize infections.
Autoantibodies are antibodies produced by the immune system that mistakenly target and sometimes damage the body’s own systems and organs.
In a previous study, the researchers found that autoantibodies from patients with active COVID-19 infections caused “a striking amount of clotting” in mice.
In this study, they uncover the possible reason: the autoantibodies appear to stress the endothelial cells that make up the inner lining of blood vessels and, in doing so, cause the cells to lose their ability to prevent blood clots from forming.
The finding provides an even stronger connection between autoantibody formation and clotting in COVID-19.
The team says when endothelial cells are activated, they cause healthy blood vessels to become ‘sticky,’ attracting other cells to the vessel walls and becoming more prone to thrombosis.
This can affect many of the body’s essential organs.
They found that when they removed the antiphospholipid autoantibodies from COVID-19 blood samples, the endothelial cell activation that promotes clotting was lost.
Future studies need to decide if it is beneficial to screen patients with severe COVID-19 for these autoantibodies to evaluate their risk of clotting and progressive respiratory failure.
Eventually, doctors may be able to repurpose treatments used in traditional cases of antiphospholipid syndrome for COVID-19.
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