Long Covid Syndrome Is Likely To Be Caused By Blood Clotting

Recent research indicates that the linking factor between COVID-19 infection, severe acute COVID-19 infection and progression to Long COVID syndrome may be persistent endotheliopathy, inducing symptoms such as breathlessness, fatigue and decreased exercise tolerance.

Long COVID syndrome is experienced by individuals who have contracted COVID-19 and continue to exhibit a wide-range of fluctuating symptoms including, but not limited to, breathlessness, chronic fatigue, anxiety, stress and decreased exercise tolerance. Such symptoms may develop during initial COVID-19 infection or following the infection period. Often the condition changes over time and may affect multiple systems in the body leading to generalised pain, persistent high temperature and even psychiatric problems. These symptoms are attributed to Long COVID syndrome when they cannot be attributed to an alternative diagnosis.

The present study was conducted by researchers from &RCSI University of Medicine and Health Sciences &(Dublin, Ireland) and has been accepted for publication in the &Journal of Thrombosis and Haemostasis. This research proceeds earlier findings establishing that &patients admitted to hospital with severe acute COVID-19 infection experienced abnormal blood clotting &which in some cases contributed to death. Furthermore, the groups previous study investigated why this blood clotting takes place and identified a &severe imbalance between von Willebrand Factor (VWF& a molecule that causes clotting) and ADAMTS13 &(VWF regulating molecule) in patients with severe COVID-19 infections.

Researchers studied clotting markers in 50 individuals with symptoms of Long COVID syndrome and observed a significant elevation of these markers in the test group in comparison to healthy controls. Interestingly, levels of clotting markers were persistently high in individuals who managed their initial COVID-19 infection at home as well as those who required hospitalization.

Increased clotting was found to be one of the only physiological effects persisting in convalescent COVID-19 patients despite acute phase markers such as CRP, neutrophil and white blood cell counts normalizing in most patients. This demonstrated that the sustained endothelial cell activation and ongoing endotheliopathy in Long COVID syndrome occurs independently of the acute phase response and can remain persistently elevated despite apparent resolution of acute COVID-19. Additionally, these elevated clotting markers were correlated with reduced physical fitness and fatigue, common Long COVID syndrome symptoms. Sustained endotheliopathy was more frequent in older, comorbid patients and those requiring hospitalization.

The study’s lead author, Helen Fogarty, explained “Because clotting markers were elevated while inflammation markers had returned to normal, our results suggest that the clotting system may be involved in the root cause of Long COVID syndrome.”

“Understanding the root cause of a disease is the first step toward developing effective treatments,” commented corresponding author, James O’Donnell.

The group hypothesize that shedding of the endothelial cell surface receptor thrombomodulin may play a role in modulating the loss of normal endothelial cell quiescence, which in turn could influence VWF expression in Long COVID syndrome. A potential avenue of future research into how sustained endothiopathy may contribute to Long COVID pathogenesis.

Sources: lt;/strong>Fogarty H, Townsend L, Morrin H &et al. Persistent Endotheliopathy in the Pathogenesis of Long COVID Syndrome. &J. Thromb. &doi:10.1111/jth.15490 (2021) [Epub ahead of print].

Ward S, Fogarty H, Karampini E &et al. ADAMTS13 regulation of VWF multimer distribution in severe COVID-19. &J. Thromb. 19(8), 1914-1921 doi:10.1111/jth.15409 (2021).

Fogarty h, Townsend L, Cheallaigh CN &et al. &COVID-19 coagulopathy in Caucasian patients. &J. Haem. &189(6), 1044-1049 doi:10.1111/bjh.16749 (2020).