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Inflammatory Bowel Disease and Stroke: Exploring Hidden Vascular Risks
Abdallah Khan1, Maysoon A Azzam1
1Internal Medicine, RAK Medical and Health Sciences University, Ras Al Khaimah, ARE.
Insights
Inflammatory bowel disease (IBD) increases stroke risk due to chronic inflammation and prothrombotic states. Management requires a multidisciplinary approach addressing vascular mechanisms and risk factors.
Area of Science:
- Gastroenterology and Neurology
- Vascular Medicine
- Systemic Inflammation Research
Background:
- Inflammatory bowel disease (IBD), including Crohn's disease and ulcerative colitis, is linked to gastrointestinal issues.
- Emerging evidence suggests IBD may increase stroke risk via chronic inflammation, endothelial dysfunction, and prothrombotic states.
- The precise mechanisms and extent of the IBD-stroke association require further elucidation.
Purpose of the Study:
- To systematically review the association between IBD and stroke.
- To explore underlying vascular mechanisms and risk factors for cerebrovascular events in IBD patients.
- To identify knowledge gaps in understanding this relationship.
Main Methods:
- A systematic literature search was performed using PRISMA guidelines.
- Databases searched included PubMed, Scopus, and Google Scholar.
- Six studies were included after screening 150 articles based on specific criteria.
Main Results:
- Chronic inflammation in IBD contributes to stroke risk through endothelial dysfunction and a prothrombotic state.
- Active IBD flares, particularly with atrial fibrillation, further elevate cerebrovascular event risk.
- The efficacy of biologic therapies, like TNF-alpha inhibitors, in reducing stroke risk is inconclusive.
Conclusions:
- IBD may be an independent risk factor for stroke, necessitating a multidisciplinary management approach.
- Addressing modifiable risks with biologics, statins, antiplatelet agents, and lifestyle changes may reduce cerebrovascular complications.
- Further research is essential for personalized strategies and preventive guidelines for IBD patients at risk of stroke.
Abstract:
Inflammatory bowel disease (IBD), encompassing Crohn's disease and ulcerative colitis, is primarily known for its gastrointestinal manifestations. However, emerging evidence suggests a potential link between IBD and an increased risk of stroke, likely mediated by chronic systemic inflammation, endothelial dysfunction, and a prothrombotic state. Despite this growing recognition, the exact mechanisms and extent of this association remain unclear, highlighting a critical knowledge gap. This review aims to systematically analyze the association between IBD and stroke, exploring the underlying vascular mechanisms and identifying potential risk factors contributing to cerebrovascular events in IBD patients. A comprehensive literature search was conducted following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines across PubMed, Scopus, and Google Scholar using keywords such as "IBD," "Stroke," "Chronic inflammation," "Cerebrovascular risk," and "Gut-brain axis." After screening 150 studies and applying inclusion and exclusion criteria, six studies were included in the final synthesis. The findings suggest that chronic inflammation in IBD plays a key role in increasing stroke risk through endothelial dysfunction and a heightened prothrombotic state, with additional risk factors such as atrial fibrillation during active IBD flares further contributing to cerebrovascular events. While biologic therapies, including tumor necrosis factor (TNF)-alpha inhibitors, are effective in reducing systemic inflammation, their impact on mitigating stroke risk remains inconclusive. Given the potential role of IBD as an independent risk factor for stroke, a multidisciplinary approach to management is crucial. Addressing modifiable risk factors through pharmacologic interventions such as biologics, statins, and antiplatelet agents, alongside lifestyle modifications, could help reduce cerebrovascular complications in IBD patients. Further research is needed to explore personalized therapeutic strategies and establish clearer preventive guidelines for this at-risk population.
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