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NSAID-induced small intestinal damage--roles of various pathogenic factors
1Department of Pharmacology and Experimental Therapeutics, Division of Pathological Sciences, Kyoto Pharmaceutical University, Misasagi, Yamashina, Japan.
Background/Aims:
NSAID-induced enteropathy has been the focus of recent basic and clinical research subsequent to the development of the capsule endoscope and double-balloon endoscope. We review the possible pathogenic mechanisms underlying NSAID-induced enteropathy and discuss the role of the inhibition of COX-1/COX-2 and the influences of food as well as various prophylactic treatments on these lesions.
Methods:
Studies were performed in experimental animals.
Results:
Multiple factors, such as intestinal hypermotility, decreased mucus secretion, enterobacteria, and upregulation of iNOS/NO expression, are involved in the pathogenesis of NSAID-induced enteropathy, in addition to the decreased production of PGs due to the inhibition of COX. Enterobacterial invasion is the most important pathogenic event, and intestinal hypermotility, which was associated with this event, is essential for the development of these lesions. NSAIDs also upregulate the expression of COX-2, and the inhibition of both COX-1 and COX-2 is required for the intestinal ulcerogenic properties of NSAIDs to manifest. NSAID-induced enteropathy is prevented by PGE2, atropine, ampicillin, and aminoguanidine as well as soluble dietary fiber, and exacerbated by antisecretory drugs such as proton pump inhibitors.
Conclusion:
These findings on the pathogenesis of NSAID-induced enteropathy will be useful for the future development of intestinal-sparing alternatives to standard NSAIDs.
Insights
Non-steroidal anti-inflammatory drug (NSAID)-induced enteropathy involves intestinal hypermotility and enterobacteria, with cyclooxygenase (COX) inhibition playing a key role. Prophylactic treatments like PGE2 and soluble fiber show promise in preventing these NSAID-induced intestinal lesions.
Area of Science:
- Gastroenterology
- Pharmacology
- Pathogenesis Research
Background:
- NSAID-induced enteropathy is a growing concern, with advancements in endoscopic technology enabling better detection.
- Understanding the underlying mechanisms is crucial for developing effective treatments.
Purpose of the Study:
- To review the pathogenic mechanisms of NSAID-induced enteropathy.
- To discuss the role of COX inhibition, food, and prophylactic treatments.
Main Methods:
- Experimental animal studies were conducted to investigate NSAID-induced enteropathy.
Main Results:
- Pathogenesis involves intestinal hypermotility, decreased mucus, enterobacteria, and iNOS/NO upregulation, alongside COX inhibition.
- Enterobacterial invasion and associated intestinal hypermotility are critical pathogenic events.
- Inhibition of both COX-1 and COX-2 is necessary for NSAID ulcerogenicity; PGE2, atropine, ampicillin, aminoguanidine, and soluble fiber prevent lesions, while PPIs exacerbate them.
Conclusions:
- Findings elucidate NSAID-induced enteropathy pathogenesis.
- This knowledge will aid in developing intestinal-sparing NSAID alternatives.
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