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Ischemic Stroke May Increase the Risk of Crohn's Disease and Ulcerative Colitis: Evidence from a Bidirectional
Xin Luo1, Liping Yao1, Yinchao Chen1
1The Third Hospital of Changsha (Changsha Hospital Affiliated to Hunan University), Changsha City, Hunan Province, People's Republic of China.
Insights
Ischemic stroke (IS) increases the risk of Crohn's disease (CD) and ulcerative colitis (UC). However, inflammatory bowel disease (IBD) does not appear to cause IS. Monitor IBD risks in IS patients.
Area of Science:
- Genetics
- Epidemiology
- Internal Medicine
Background:
- The causal link between ischemic stroke (IS) and inflammatory bowel disease (IBD) is not well understood.
- A bidirectional Mendelian randomization (MR) study was proposed to investigate this relationship.
Purpose of the Study:
- To determine if IS causes IBD or if IBD causes IS.
- To explore the bidirectional causal relationship between IS and IBD, including its subtypes Crohn's disease (CD) and ulcerative colitis (UC).
Main Methods:
- Utilized large-scale genetic data from the MEGASTROKE consortium and the International Inflammatory Bowel Disease Genetics Consortium.
- Employed inverse variance weighting (IVW) as the primary analysis, with MR-Egger regression, weighted median, MR-PRESSO, and MR-Robust adjusted profile score for sensitivity analyses.
- Conducted a meta-analysis combining data from the International Inflammatory Bowel Disease Genetics Consortium and the FinnGen database for robust causal association assessment.
Main Results:
- Ischemic stroke (IS) was found to be causally associated with an increased risk of Crohn's disease (CD) (OR IVW = 1.38) and ulcerative colitis (UC) (OR IVW = 1.27).
- No significant causal relationship was observed between IBD (as a whole or its subtypes) and the risk of IS.
- Replication phase using FinnGen data did not reveal significant correlations, but combined meta-analysis supported IS as a risk factor for CD and UC.
Conclusions:
- Ischemic stroke (IS) is causally linked to an increased risk of developing Crohn's disease (CD) and ulcerative colitis (UC).
- Inflammatory bowel disease (IBD) and its subtypes were not found to be causally associated with the risk of IS.
- Close monitoring for CD and UC is recommended for patients with a history of IS.
Background:
The bidirectional causal relationship between ischemic stroke (IS) and inflammatory bowel disease (IBD) remains unclear, prompting us to propose a bidirectional Mendelian randomization (MR) study to investigate this relationship further.
Methods:
We obtained IS data from the MEGASTROKE consortium and IBD data, including its subtypes ulcerative colitis (UC) and Crohn's disease (CD), from the International Inflammatory Bowel Disease Genetics Consortium. In this study, we utilized IBD and its subtypes as exposure variables and IS as the outcome variable, and vice versa, to explore the bidirectional relationship between them. We used the IBD genetic data from the FinnGen database as replication data to further explore the causality. In this study, we employed the inverse variance weighting method as our primary approach. For sensitivity analyses, we utilized additional methods including MR-Egger regression, weighted median estimation, MR pleiotropy residual sum and outlier (MR-PRESSO), and MR-Robust adjusted profile score. Furthermore, we conducted a random effects meta-analysis to combine the causal relationships derived from both the International Inflammatory Bowel Disease Genetics Consortium and FinnGen datasets, aiming to ascertain more robust causal associations.
Results:
The initial phase of the bidirectional MR study revealed a causal relationship between IS and the risk of CD (odds ratio [OR] = 1.56, 95% confidence interval [CI]: 1.20-2.02, P = 0.0008) and UC (OR = 1.33, 95% CI: 1.05-1.69, P = 0.0179), but did not find a causal relationship between IBD as a whole and the risk of IS, nor between IBD subtypes and the risk of IS. During the replication phase, the FinnGen database did not reveal any significant correlation between IS and the risk of IBD, including its subtypes CD and UC. However, additional meta-analysis of the combined data from both databases indicated that IS is significantly associated with an increased risk of CD (OR inverse-variance weighted (IVW) = 1.38, 95% CI: 1.07-1.69, P < 0.05) and UC (ORIVW = 1.27, 95% CI: 1.04-1.50, P < 0.05), but not with the overall risk of IBD (ORIVW = 1.05, 95% CI: 0.87-1.16, P > 0.05). No significant effects were observed between IBD and IS risk, nor were there significant effects between IS and the risks of IBD, CD, or UC. To ensure the robustness of these findings, heterogeneity and pleiotropy tests were conducted.
Conclusions:
IBD and its subtypes were not found to be causally associated with the risk of IS, whereas IS was found to be causally associated with the risk of CD and UC. This suggests that the risks of CD and UC should be closely monitored in patients with IS.
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