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NSAID enteropathy and bacteria: a complicated relationship
Stephanie D Syer1, Rory W Blackler, Rebeca Martin
1Department of Medicine, McMaster University, Hamilton, Canada.
Abstract:
The clinical significance of small intestinal damage caused by nonsteroidal anti-inflammatory drugs (NSAIDs) remains under-appreciated. It occurs with greater frequency than the damage caused by these drugs in the upper gastrointestinal tract, but is much more difficult to diagnose and treat. Although the pathogenesis of NSAID enteropathy remains incompletely understood, it is clear that bacteria, bile, and the enterohepatic circulation of NSAIDs are all important factors. However, they are also interrelated with one another. Bacterial enzymes can affect the cytotoxicity of bile and are essential for enterohepatic circulation of NSAIDs. Gram-negative bacteria appear to be particularly important in the pathogenesis of NSAID enteropathy, possibly through release of endotoxin. Inhibitors of gastric acid secretion significantly aggravate NSAID enteropathy, and this effect is due to significant changes in the intestinal microbiome. Treatment with antibiotics can, in some circumstances, reduce the severity of NSAID enteropathy, but published results are inconsistent. Specific antibiotic-induced changes in the microbiota have not been causally linked to prevention of intestinal damage. Treatment with probiotics, particularly Bifidobacterium, Lactobacillus, and Faecalibacteriaum prausnitzii, has shown promising effects in animal models. Our studies suggest that these beneficial effects are due to colonization by the bacteria, rather than to products released by the bacteria.
Insights
Nonsteroidal anti-inflammatory drug (NSAID) enteropathy, or small intestinal damage, is common and hard to treat. Beneficial bacteria like Bifidobacterium may prevent NSAID-induced gut injury through colonization.
Area of Science:
- Gastroenterology
- Microbiology
- Pharmacology
Background:
- Small intestinal damage from nonsteroidal anti-inflammatory drugs (NSAIDs) is frequent but underdiagnosed.
- NSAID enteropathy pathogenesis involves bacteria, bile, and enterohepatic circulation, with Gram-negative bacteria playing a key role.
- Gastric acid secretion inhibitors worsen NSAID enteropathy by altering the intestinal microbiome.
Purpose of the Study:
- To elucidate the pathogenesis of NSAID enteropathy.
- To investigate the role of the intestinal microbiome in NSAID enteropathy.
- To evaluate the therapeutic potential of probiotics in preventing NSAID-induced intestinal damage.
Main Methods:
- Analysis of factors contributing to NSAID enteropathy, including bacterial and bile interactions.
- Investigation of the impact of gastric acid inhibitors on the intestinal microbiome.
- Assessment of antibiotic and probiotic interventions in animal models of NSAID enteropathy.
Main Results:
- NSAID enteropathy is multifactorial, with bacterial enzymes, bile, and enterohepatic circulation being crucial.
- Gram-negative bacteria and endotoxin may contribute to NSAID enteropathy pathogenesis.
- Probiotics, specifically Bifidobacterium, Lactobacillus, and Faecalibacteriaum prausnitzii, showed promise in animal models, likely via colonization.
Conclusions:
- NSAID enteropathy is a significant clinical issue requiring further understanding.
- The intestinal microbiome is a critical factor in NSAID enteropathy development and potential treatment.
- Probiotic colonization, rather than secreted products, appears to be the mechanism for therapeutic benefit in NSAID enteropathy.
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