Patients with severe COVID-19 disease caused by the SARS-CoV-2 virus can develop blood clots in medical lines (intravenous lines, catheters, etc), and in arteries, lungs, and extremities, including the toes.
Yet the mechanisms underlying coagulation disorders in patients with COVID-19 are still unknown.
In a recent study at Massachusetts General Hospital (MGH), researchers found patients with severe COVID-19 infections who have high levels of the blood-clotting protein factor V are at a higher risk for serious injury from blood clots such as deep vein thrombosis or pulmonary embolism.
On the other hand, critically ill patients with COVID-19 and low levels of factor V appear to be at increased risk for death from a coagulopathy that resembles disseminated intravascular coagulation (DIC).
DIC is a devastating, often fatal abnormality in which blood clots form in small vessels throughout the body, leading to exhaustion of clotting factors and proteins that control coagulation.
These findings, based on studies of patients with COVID-19 in MGH intensive care units (ICUs), point to disturbances in factor V activity as a potential cause of blood clotting disorders with COVID-19.
One author of the study is Elizabeth M. Van Cott, MD from the department of pathology at MGH and colleagues.
The study is published in the American Journal of Hematology.
In March 2020, in the early days of the COVID-19 pandemic in Massachusetts, the team found that a blood sample from a patient with severe COVID-19 on a ventilator contained factor V levels high above the normal reference range.
Four days later, this patient developed a saddle pulmonary embolism, a potentially fatal blood clot occurring at the junction of the left and right pulmonary arteries.
This pointed the team to the activity of factor V as well as factor VIII and factor X, two other major clotting factors.
They studied the levels of these clotting factors and other parameters in a group of 102 consecutive patients with COVID-19, and compared the results with those of current critically ill patients without COVID-19, and with historical controls.
They found that factor V levels were significantly elevated among patients with COVID-19 compared with controls and that the association between high factor V activity and COVID-19 was the strongest among all clinical parameters studied.
In all, 33% of patients with factor V activity well above the reference range had either deep vein thrombosis or a pulmonary embolism, compared with only 13% of patients with lower levels.
Death rates were much higher for patients with lower levels of factor V (30% vs. 12%), with evidence that this was due to a clinical decline toward a DIC-like state.
Importantly, the researchers note that factor V elevation in COVID-19 could cause misdiagnosis of some patients because under normal circumstances factor V levels are low in the presence of liver dysfunction or DIC.
Physicians might therefore mistakenly assume that patients instead have a deficiency in vitamin K.
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