Blood clots or thromboembolic complications in patients with COVID-19 are linked to increased levels of various proteins that cause blood to clot, compared to people with blood clots unrelated to COVID-19, according to a small study by researchers at the Yale Cancer Center . These results may provide insights into new therapeutic strategies for treating patients with COVID-19-related blood clots. The results were released today at the American Society of Hematology (ASH) 2021 annual meeting and exhibition in Atlanta, Georgia.
We expected to find differences in protein levels in patients who developed blood clots in the presence and without COVID-19. However, the lack of significant differences in protein levels in patients with COVID-19 with and without blood clots was unexpected and suggests that the overall difference in the concentration of proteins involved in the body’s ability to clot blood was related to COVID-19 -The disease itself is related. “
Daria Madeeva, MD, Study lead author, Medical Doctor, Yale New Haven Health
Blood drawn from 48 inpatients between December 2020 and February 2021. Of these, 24 patients had a confirmed diagnosis of COVID-19 infection and arterial or venous thromboembolism; 17 had COVID-19 infection without arterial thrombosis and without venous thromboembolism, while 7 was diagnosed with arterial or venous thromboembolism without COVID-19. The researchers found that levels of several proteins were higher in patients with COVID-19 who also developed blood clots. One of these proteins, tissue factor, has classically been linked to an injury to the vessel lining (endothelium), and since it was higher in the blood of patients with COVID-19, this suggests a deeper injury to the endothelium. Another protein, pentraxin-3, was also found to have higher levels in those who developed blood clots with COVID-19. This protein is produced by endothelial cells during inflammation and is therefore also a marker for endothelial injuries. The researchers also found that two additional proteins, C2 and C5a, were also higher in patients who developed blood clots from COVID-19, as well as lipocalin-2 and resistin. Previous studies have found that these proteins are markers of neutrophil activation in patients with COVID-19, and their higher levels are linked to more severe disease. In addition, the levels of the SAA and PECAM-1 proteins were also higher in patients who developed blood clots with COVID-19.
“Going forward, we are looking to evaluate far greater numbers of proteins and include more patients in our studies,” said Alexander B. Pine, MD, PhD, assistant professor of medicine (hematology) at Yale Cancer Center and lead author on the study. . “In addition, a similar proteomics approach could be used to assess mechanisms and factors that contribute to the development of thrombosis in inflammatory diseases other than COVID-19.”
Other Yale authors on the study are Kelly Borges, Marcus Shallow, Prerak Juthani, Stephen Wang, MD MPH, Akash Gupta, MD, Hyung Chun, MD, and Alfred Lee, MD, PhD.
This research was supported in part by a pilot grant from the DeLuca Center for Innovation in Hematology Research.
