Exploring Hypercoagulability in Post-COVID Syndrome PCS: An Attempt at Unraveling the Endothelial Dysfunction, 2025, Muys et al.

[SNT Gatchaman]

Exploring Hypercoagulability in Post-COVID Syndrome PCS: An Attempt at Unraveling the Endothelial Dysfunction
Muys, Maxim; Demulder, Anne; Besse-Hammer, Tatiana; Ghorra, Nathalie; Rozen, Laurence

BACKGROUND
The lingering effects of SARS-CoV-2 infection, collectively known as post-COVID syndrome (PCS), affect a significant proportion of recovered patients, manifesting as persistent symptoms like fatigue, cognitive dysfunction, and exercise intolerance. Increasing evidence suggests that endothelial dysfunction and coagulation abnormalities play a central role in PCS pathophysiology. This study investigates hypercoagulability and endothelial dysfunction in PCS through thrombin generation and the von Willebrand factor (VWF)/ADAMTS13 axis.

METHODS
Plasma samples from 97 PCS patients recruited since October 2020 by the clinical research unit of the Brugmann University Hospital were analyzed. A thrombin generation test was performed on a St-Genesia® analyzer (Stago) using the Thromboscreen kit; VWF antigen was determined on a CS-2500 analyzer (Siemens); and ADAMTS-13 activity was determined using an ELISA kit (Technozym®) on an ElX808 plate reader.

RESULTS
Thrombin generation testing revealed elevated thrombin production in PCS patients, particularly when thrombomodulin was included. Although most PCS patients showed normalized VWF/ADAMTS13 ratios, 11.3% exhibited elevated ratios (≥1.5), associated with advanced age.

CONCLUSIONS
Patients with PCS show a consistent pattern of prolonged thrombo-inflammatory dysregulation, highlighted by elevated in vitro thrombin generation and the persistence of abnormal VWF/ADAMTS-13 ratios in a subset of patients.

Link | PDF (Journal of Clinical Medicine) [Open Access]

 

[Utsikt]

Increasing evidence suggests that endothelial dysfunction and coagulation abnormalities play a central role in PCS pathophysiology.

Why does everyone have to include lies like this? I get that they want to highlight the relevance of their work, but you can do that on the basis of the burden of PCS, you don’t have to go beyond the evidence..

 

[forestglip]

From introduction:

Of particular interest is the role of thrombomodulin (TM), a membrane-bound protein expressed on endothelial cells that is essential for the proper functioning of the protein C anticoagulant pathway. TM binds to thrombin, converting it from a procoagulant enzyme into an activator of protein C. This activation of protein C subsequently suppresses clotting by inactivating factor Va and factor VIIIa, thereby limiting further thrombin generation and promoting fibrinolysis. Impaired TM function, as suggested by the reduced inhibition of thrombin generation, may contribute to the hypercoagulable state observed in PCS patients [10].

This looks like the main finding:

Differences among healthy subjects, severe and non-severe acute COVID-19 patients were already described in our previous work [4]. This study focuses on assessing coagulation abnormalities in patients diagnosed with PCS (Table 2). Thrombin generation tests without TM did not reveal any statistically significant differences between the PCS cohort and the other cohorts (acute COVID and healthy subjects). Abnormalities became evident through TGT analysis in the presence of TM. When TM was included, the ETP inhibition was lower in patients with PCS compared to healthy controls, meaning the thrombin generation was notably higher in those patients, albeit to a lesser extent when compared to those with severe acute COVID-19 (Figure 2).

Figure 2. Comparisons among healthy subjects (n = 81), PCS patients (n = 97), acute COVID severe cases (n = 8), and acute COVID non-severe cases (n = 15) including the following: (A) endogenous thrombin potential with TM (ETP TM+); (B) endogenous thrombin potential inhibition. Data are presented as the median and the interquartile range. Comparisons between groups were assessed using Dunn’s post hoc test following a Kruskal–Wallis test (* p < 0.1, ** p < 0.01).