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From Inflammation to Thrombosis: The Prothrombotic State and Cardiovascular Risk in Inflammatory Bowel Disease
Vlad Dumitru Brata1, Dana Alina Crisan2,3, Angela Cozma4
1Department of Gastroenterology, Regional Institute of Gastroenterology and Hepatology "Prof. Dr. Octavian Fodor", 400394 Cluj-Napoca, Romania.
Inflammatory bowel disease (IBD) increases the risk of blood clots. Managing IBD effectively and preventing cardiovascular events are key to reducing these risks.
Area of Science:
- Cardiovascular Medicine
- Gastroenterology
- Immunology
Background:
- Inflammatory bowel disease (IBD) is linked to higher risks of venous thromboembolic events (VTEs) and arterial cardiovascular events.
- A thromboinflammatory state, driven by gut inflammation, impacts vascular homeostasis via immune activation and coagulation pathways.
Purpose of the Study:
- To review the association between IBD and cardiovascular events.
- To discuss the pathophysiological mechanisms linking gut inflammation to thrombosis.
- To outline clinical strategies for prevention and management.
Main Methods:
- Review of pathophysiological data and clinical evidence.
- Analysis of the interplay between intestinal inflammation, immune response, and vascular events.
- Synthesis of current guidelines for VTE prophylaxis and cardiovascular prevention in IBD patients.
Main Results:
- IBD patients face increased VTE and moderate arterial cardiovascular event risks, influenced by disease activity and acute care.
- The thromboinflammatory phenotype involves innate immunity, coagulation-platelet interactions, endothelial dysfunction, and impaired fibrinolysis.
- Recurrence of VTE depends on anticoagulation and minimizing inflammatory/treatment exposures.
Conclusions:
- Integrated care focusing on sustained, steroid-sparing IBD control and guideline-based thromboprophylaxis is crucial.
- Cardiovascular risk assessment and optimization of modifiable factors are recommended before escalating IBD therapy.
- Future strategies may involve personalized risk assessment and targeted therapies for the gut-vascular interface and immunothrombosis.
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