Effect of naproxen on gastric acid secretion and gastric pH

Rodriguez–Stanley, Sheila; Redinger, Nancy; Miner, Philip B.

doi:10.1111/j.1365-2036.2006.02897.x

Cited by 11 publications

(10 citation statements)

References 22 publications

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“…Different studies showed a direct relation between acid and GI injuries induced by NSAIDs, in fact the main prescribed drugs to prevent such injuries are the proton-pump inhibitors (PPI) [36,37], Fornai suggests that beneficial effects of PPIs on mucosal injury are likely to be independent from the COX-2/PGE 2 /VEGF pathway [38] so considering all the involved cellular pathways it can be deduced that the intact mucus layer protects epithelium from the action of acid pepsin, protons, [H+] and, in addition, when the barrier is damaged, acid aggravates gastric injuries. There are also evidences of an increased basal gastric acid concentration mediated by NSAIDs due to the basal gastric fluid volume reduction [39].…”

Section: Figurementioning

confidence: 99%

Study of Melatonin as Preventive Agent of Gastrointestinal Damage Induced by Sodium Diclofenac

Rivero-Sánchez

Clares

Rodríguez-Lagunas

et al. 2020

Cells

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Safety profile of nonsteroidal anti-inflammatory drugs (NSAIDs) has been widely studied and both therapeutic and side effects at the gastric and cardiovascular level have been generally associated with the inhibitory effect of isoform 1 (COX-1) and 2 (COX-2) cyclooxygenase enzymes. Now there are evidences of the involvement of multiple cellular pathways in the NSAIDs-mediated-gastrointestinal (GI) damage related to enterocyte redox state. In a previous review we summarized the key role of melatonin (MLT), as an antioxidant, in the inhibition of inflammation pathways mediated by oxidative stress in several diseases, which makes us wonder if MLT could minimize GI NSAIDs side effects. So, the aim of this work is to study the effect of MLT as preventive agent of GI injury caused by NSAIDs. With this objective sodium diclofenac (SD) was administered alone and together with MLT in two experimental models, ex vivo studies in pig intestine, using Franz cells, and in vivo studies in mice where stomach and intestine were studied. The histological evaluation of pig intestine samples showed that SD induced the villi alteration, which was prevented by MLT. In vivo experiments showed that SD altered the mice stomach mucosa and induced tissue damage that was prevented by MLT. The evaluation by quantitative reverse transcription PCR (RT-qPCR) of two biochemical markers, COX-2 and iNOS, showed an increase of both molecules in less injured tissues, suggesting that MLT promotes tissue healing by improving redox state and by increasing iNOS/NO that under non-oxidative condition is responsible for the maintenance of GI-epithelium integrity, increasing blood flow and promoting angiogenesis and that in presence of MLT, COX-2 may be responsible for wound healing in enterocyte. Therefore, we found that MLT may be a preventive agent of GI damages induced by NSAIDs.

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Section: Figurementioning

confidence: 99%

Study of Melatonin as Preventive Agent of Gastrointestinal Damage Induced by Sodium Diclofenac

Rivero-Sánchez

Clares

Rodríguez-Lagunas

et al. 2020

Cells

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“…In humans, NSAID‐induced acute gastric injury has been shown to be greater in volunteers who had the lowest fasting pH following naproxen administration 24 . Naproxen has been demonstrated to reduce total gastric acid volume with concomitant increase in gastric acid concentration in humans 25 . Funatsu et al.…”

Section: Systemic Effectsmentioning

confidence: 99%

Review article: cellular and molecular mechanisms of NSAID‐induced peptic ulcers

Musumba

Pritchard

Pirmohamed

2009

Aliment Pharmacol Ther

212

139

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“…This review concluded that most studies showed that indomethacin does not affect basal acid secretion, but some showed that it increased histamine‐stimulated secretion [28] . Subsequent studies seem to support these conclusions [29,30] . Thus, it might appear that NSAIDs have some, albeit relatively minor, effects on gastric acidity in humans.…”

Section: Resultsmentioning

confidence: 99%

NSAIDs: take with food or after fasting?

Rainsford

Bjarnason

2012

Journal of Pharmacy and Pharmacology

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Objective Published and regulatory advice is to take NSAIDs with fluids and/or food irrespective whether NSAIDs are taken over the counter or long-term. The basis for this recommendation is not clear and we sought to establish the reasons for it through a search of published literature and personal files. Results Results from experimental animals show that fasting increases the gastric side effects of NSAIDs while food increases small bowel damage, but this has not been tested in humans. The possible effects of food in modifying the gastric damage caused by NSAIDs are complex, as food quantity and composition modify the responses substantially. Food usually delays peak levels of NSAIDs (and hence onset of action) without affecting total bioavailability. This may not be important when a steady state is achieved, but rapid onset of action is highly relevant for over-thecounter use of NSAIDs. The safety of over-the-counter use of ibuprofen and naproxen appears to be excellent and comparable with paracetamol. Conclusion The rapid onset of action of NSAIDs is most important during overthe-counter use, in which case it may be more appropriate to take the drugs on a fasting stomach.

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Effect of naproxen on gastric acid secretion and gastric pH

Abstract: SUMMARY BackgroundThe mechanisms for the non-steroidal anti-inflammatory drug-induced inflammation in the stomach are unclear.

Cited by 11 publications

References 22 publications

Study of Melatonin as Preventive Agent of Gastrointestinal Damage Induced by Sodium Diclofenac

Study of Melatonin as Preventive Agent of Gastrointestinal Damage Induced by Sodium Diclofenac

Review article: cellular and molecular mechanisms of NSAID‐induced peptic ulcers

NSAIDs: take with food or after fasting?

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