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Coagulation in gout: is there a link with disease activity?
Daisy Vedder1,2, Martijn Gerritsen3, Joost C M Meijers4,5
1Amsterdam Rheumatology & Immunology Center, Reade, Amsterdam, Netherlands. d.vedder@reade.nl.
Insights
Patients with active gout show higher thrombin generation markers, suggesting a link between gout disease activity and coagulation. However, changes in disease activity over one year did not significantly alter coagulation markers, possibly due to persistent inflammation.
Area of Science:
- Rheumatology
- Hematology
- Cardiovascular Medicine
Background:
- Gout is a chronic inflammatory condition associated with an increased risk of cardiovascular events.
- The relationship between gout disease activity and the coagulation system requires further elucidation.
Purpose of the Study:
- To investigate coagulation markers in gout patients.
- To explore associations between gout disease activity and coagulation marker levels.
Main Methods:
- A prospective cohort study involving 30 Dutch gout patients.
- Analysis of coagulation markers (APTT, PT, D-dimer, prothrombin F1+2, vWF, thrombin generation) at baseline and 1-year follow-up.
- Correlation of coagulation markers with gout disease activity using the Gout Activity Score (GAS).
Main Results:
- Higher Gout Activity Score (GAS) correlated with increased thrombin generation parameters (ETP, peak thrombin, velocity index).
- Tophaceous gout and elevated serum uric acid (SUA) levels were linked to thrombin generation.
- Despite a moderate decrease in disease activity over one year, thrombin generation parameters showed a slight procoagulant trend.
Conclusions:
- Active gout is associated with elevated thrombin generation markers, indicating a connection between disease activity and coagulation.
- Changes in gout disease activity over one year did not lead to significant alterations in coagulation markers, potentially due to ongoing low-grade inflammation.
- Further research is recommended to compare coagulation marker levels in gout patients with the general population and to assess the impact of effective gout treatment.
Objective:
To investigate the coagulation system in gout patients and associations between disease activity and levels of coagulation markers.
Methods:
A prospective cohort study was performed with data from 30 Dutch gout patients. Levels of coagulation markers including APTT, PT, D-dimer, prothrombin F1 + 2, von Willebrand factor, and thrombin generation parameters were analyzed at baseline and 1-year visit. These markers were related to clinical markers of gout disease activity including the Gout Activity Score (GAS). Our hypothesis was that patients with gout and active disease have increased levels of coagulation markers and that a decrease in disease activity would lead to normalization of coagulation activity.
Results:
A higher GAS was associated with increased levels of thrombin generation parameters including ETP (ß = 0.48, p = 0.01), peak thrombin (ß = 0.60, p = 0.001), and velocity index (ß = 0.57, p = 0.002). Tophaceous gout and higher SUA levels were associated with thrombin generation parameters. After 1 year, thrombin generation parameters showed a small procoagulant trend despite a moderate decrease in disease activity. Prospectively measured changes in disease activity according to the GAS were not associated with any of the coagulation markers.
Conclusion:
Patients with active gout have higher levels of thrombin generation markers, indicating a link between disease activity and coagulation. A change in disease activity after 1 year was not associated with significant changes in coagulation markers, probably due to prolonged low-grade inflammation. Future studies should focus on levels of coagulation markers in comparison with the general population and the effect of adequate gout treatment. Key Points • Patients with gout have an increased risk of cardiovascular events. • High disease activity was associated with higher levels of thrombin generation markers. • Over time, small decreases in inflammation were associated with a decrease in D-dimer and thrombin generation.
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