ArticleRheumatology international2013
Proton pump inhibitors are not the key for therapying non-steroidal anti-inflammatory drugs-induced small intestinal injury.
Article in Rheumatology international, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 14 citations in OpenAlex.
- The effect of rebamipide on non-steroidal anti-inflammatory drug-induced gastro-enteropathy: a multi-center, randomized pilot study.The Korean journal of internal medicine · 2022Trial
- Muscovite is protective against non-steroidal anti-inflammatory drug-induced small bowel injury.World journal of gastroenterology · 2014Trial
- A novel drug-like water-soluble small molecule Focal Adhesion Kinase (FAK) activator promotes intestinal mucosal healing.Current research in pharmacology and drug discovery · 2023Article
- Uncovering the uncertainty: Risk factors and clinical relevance of P1 lesions on small bowel capsule endoscopy of anemic patients.World journal of gastroenterology · 2016Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ability of non-steroidal anti-inflammatory drugs (NSAIDs) to injure the small intestine has been well established in humans and animals. Proton pump inhibitors (PPIs) are frequently prescribed to reduce gastric and duodenal injury caused in high-risk patients taking NSAIDs. However, scarce information is available concerning the effects of PPIs on intestinal damage induced by NSAIDs, and the suppression of gastric acid secretion by PPIs is hard to provide any protection against the damage caused by NSAIDs in the small intestine. The present study was designed to examine the effects of intragastric treatment of two PPIs widely used in clinical practice, namely omeprazole and pantoprazole, on the intestinal damage induced by administration of diclofenac in rat. Male SD rats were treated with omeprazole or pantoprazole for 9 days, with concomitant treatment with anti-inflammatory doses of diclofenac on the final 5 days. The anatomical lesion, villous height, the thickness, and the section area of small intestine were quantitatively analyzed. The change of ultrastructural organization was observed. Endotoxin level in blood was measured by photometry. Epidermal growth factor was observed by immunohistochemistry. Omeprazole and pantoprazole didn't decrease the macroscopic and histologic damage induced by diclofenac in the rat's small intestine. In the two PPI groups, villous height was (89.6 ± 11.8 and 92.6 ± 19.3 μm) lower than which of the control group (P < 0.05). The thickness became thinning, and the section area became small. LPS levels in the portal blood of omeprazole and pantoprazole were (4.36 ± 1.26 and 4.25 ± 1.17 EU/ml), significantly higher than in controls (P < 0.05). The EFG of PPI group descended significantly compared with the control group (P < 0.05). Omeprazole and pantoprazole cannot protect the small intestine from the damage induced by diclofenac in the conscious rat. PPIs cannot repair NSAID-induced intestinal damage at least in part because of significant lesion in mechanical barrier function and reduction in epidermal growth factor.
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