University of Kentucky Researchers Identify COVID-19 Blood Clotting Cause
By Elizabeth Chapin
September 17, 2020 -- A new
University of Kentucky College of Medicine study may provide answers for why so
many COVID-19 patients experience thrombosis, or the formation of blood clots
that obstruct blood flow through the circulatory system.
The research led by Jeremy Wood, Zach
Porterfield and Jamie Sturgill in the Department of Internal Medicine; Beth
Garvy in Microbiology, Immunology & Molecular Genetics; and Wally
Whiteheart in Molecular & Cellular Biochemistry, suggests that localized
inflammation in the lungs caused by COVID-19 may be responsible for the
increased presence of blood clots in patients. The study also provides evidence
suggesting the risk of thrombosis could persist after the infection
clears.
The study examined the blood of 30
COVID-19 patients including 15 who were inpatients in the intensive care unit,
and 15 who received care as outpatients at UK’s Infectious Diseases Clinic,
along with eight disease-free volunteers who acted as a control group.
Compared to baseline, the COVID-19
patients had elevated levels of tissue factor, a protein found in blood that
initiates the clotting process. Patients also had reduced levels of protein S,
an anticoagulant that helps prevent blood clotting.
The researchers concluded that lung
inflammation caused by COVID-19 is what leads to a decrease in protein S.
This inflammation also causes immune and possible endothelial cell
activation, which leads to increased tissue factor protein.
“What we’ve learned is that the clotting
is not caused by anything systemic. Localized inflammation in the lungs is
what’s driving this whole process,” Wood said. “With an increase in tissue
factor and a deficiency in protein S, COVID-19 patients get more blood clotting
without the ability to shut it down or control it.”
The study additionally showed that
protein S levels remained low in some patients even after they tested negative
for COVID-19, which suggests that blood clotting issues may persist after
infection and long-term monitoring of thrombotic risk may be necessary.
Wood says this preliminary data could be
a cause for concern. Certain viruses like HIV are linked to a long-term
deficiency in protein S, which causes an ongoing risk of thrombosis in
patients. It is not yet known if COVID-19 could cause a similar persisting
protein S deficiency.
“Tissue factor and protein S are good
markers to monitor for long-term thrombosis risk and the data suggest that we
need to be monitoring these patients because we’re not seeing these parameters
corrected immediately,” Wood said.
The research team recently received a
grant from UK’s Center for Clinical and Translational Science (CCTS) to
begin a longitudinal study to look at these levels in patients over the next
year.
“This will help answer the question:
will this risk remain like it is in the HIV patients or will it go away?”
The study was funded in part by an Alliance
Grant through the College of Medicine as well as UK’s COVID-19
Unified Research Experts (CURE) Alliance through the Vice President
for Research and the College of Medicine and the CCTS. It was a product of
collaboration between a number of different groups at UK that have been
studying COVID-19.
Additional collaborators
include Martha Sim, Meenakshi Banerjee and Hammodah Alfar in the
Department of Molecular and Cellular Biochemistry; Melissa Hollifield and Jerry
Woodward with Microbiology, Immunology and Molecular Genetics; Xian Li with the
Saha Cardiovascular Research Center; Alice Thornton with the Division of
Infectious Disease; and Gail Sievert, Marietta Barton-Baxter and Kenneth
Campbell with CCTS.
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