In a groundbreaking article recently published in the journal Scientific Reports, researchers conducted an observational study in Germany to investigate the impact of ADAMTS13, a blood clotting regulator gene, on coronavirus disease 2019 (COVID-19).
ADAMTS13, also known as von Willibrand factor (VWF)-cleaving protease, plays a crucial role in preventing the formation of ultra-large VWF multimers by cleaving VWF. Deficiency in ADAMTS13 can result in a life-threatening blood disorder called thrombocytic thrombocytopenic purpura (TTP), often treated with plasmapheresis.
COVID-19 has been associated with an increased risk of autoreactivity. To understand if autoantibodies to ADAMTS13 contribute to the reduced ADAMTS13/VWF:Ag ratio observed in COVID-19, the researchers investigated this phenomenon in 156 patients from three healthcare centers in Germany, including 90 hospitalized due to COVID-19.
For the study, blood samples were collected from each participant to measure ADAMTS13 activity. The study revealed that nearly one-third of hospitalized COVID-19 patients had ADAMTS13 autoantibodies, which exhibited low activity, suggesting an inhibitory effect on the protease.
Interestingly, this phenomenon was not observed in ICU patients without a COVID-19 diagnosis. The findings suggested that measuring ADAMTS13 autoantibody levels could potentially serve as a predictor of COVID-19 severity.
It’s worth noting that none of the patients in the study developed severe thrombocytopenia, defined as a platelet count of 50,000/µl or less.
Previous studies have shown that COVID-19 patients exhibit antibody patterns resembling those seen in lupus and rheumatoid arthritis. Critically ill COVID-19 patients also display signs of B-cell activation and B-cell repertoire (BCR) observed in autoimmune conditions.
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection poses a dual risk for thrombotic microangiopathy. Excessive release of VWF leads to ADAMTS13 activity surpassing…
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