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Published on: September 22, 2019
Causal associations between inflammatory bowel disease and sepsis: a two-sample Mendelian randomization study
Renyang Tong1, Ziting Liang1, Chengui Zhuo2
1Department of Respiratory and Critical Care Medicine, Beijing Institute of Respiratory Medicine and Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China.
Genetic liability to Crohn's disease (CD) causally increases the risk of sepsis-related death in critical care. This study used Mendelian randomization to explore the link between inflammatory bowel disease (IBD) and sepsis outcomes.
Area of Science:
- Genetics
- Gastroenterology
- Critical Care Medicine
Background:
- Observational studies show an unclear link between inflammatory bowel disease (IBD) and sepsis.
- The causal relationship between IBD and sepsis remains poorly understood.
- A Mendelian randomization (MR) approach was used to investigate causality.
Purpose of the Study:
- To determine the causal effect of IBD on sepsis using genetic data.
- To differentiate the impact of Crohn's disease (CD) and ulcerative colitis (UC) on sepsis risk.
- To identify potential genetic targets for therapeutic development.
Main Methods:
- Two-sample Mendelian randomization (MR) was employed.
- Genome-wide significant single nucleotide polymorphisms (SNPs) were used as instrumental variables for CD and UC.
- SNPs were analyzed for association with sepsis, critical care sepsis, and 28-day sepsis mortality.
Main Results:
- A significant causal association was found between genetic liability to CD and sepsis with 28-day death in critical care (OR, 1.246; P=0.0012).
- No significant causal association was observed between CD and overall sepsis or critical care sepsis.
- Ulcerative colitis (UC) showed a non-significant trend towards increased risk for sepsis (OR, 1.031; P=0.064).
Conclusions:
- Genetic evidence supports a causal link between Crohn's disease and sepsis-related mortality.
- Future research should specify IBD subtypes and sepsis severity for clarity.
- Identified genetic risk loci may serve as targets for novel drug development.
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