Prevention of acute NSAID-related gastroduodenal damage: A meta-analysis of controlled clinical trials

Leandro, Gioacchino; Bertin, T.; Franceschi, Marilisa; Valerio, Giuseppe

doi:10.1016/s0016-5085(98)80801-9

Cited by 13 publications

(15 citation statements)

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“…A more recent international study showed similar benefit over 6 months with esomeprazole 20 mg daily in chronic NSAID users taking a variety of NSAIDs including COX 2 inhibitors [9]. Of note, a recent meta-analysis suggested that overall PPIs provide a two-fold reduction in serious NSAID-related complications and that interestingly GPA prophylaxis was more effective in healthy subjects, such as those in the current study, than in patients with arthritis [42].…”

Section: Discussionsupporting

confidence: 59%

Primary Prevention of Adverse Gastroduodenal Effects from Short-Term Use of Non-Steroidal Anti-Inflammatory Drugs by Omeprazole 20 mg in Healthy Subjects: A Randomized, Double-Blind, Placebo-Controlled Study

et al. 2008

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The effectiveness of low-dose omeprazole as primary prevention of gastrointestinal adverse events due to episodic use of non-selective NSAIDs was evaluated. Healthy adults aged 50-75 who did not take chronic NSAIDs were randomized to a 6.5-day treatment of naproxen 500 mg twice daily plus omeprazole 20 mg daily or naproxen 500 mg twice daily plus placebo. Seventy subjects were enrolled (mean age 58.6 years, proportion >60 = 41.4%). Subjects receiving naproxen plus omeprazole developed fewer gastroduodenal ulcers compared to subjects receiving naproxen plus placebo (11.8% vs. 46.9%, P = 0.002). Likewise, naproxen plus omeprazole was associated with a decreased risk of ulceration and/or >5 erosions (38.2% vs. 81.3%, P < or = 0.001), and a smaller change in dyspepsia score. Considering their relatively low cost, ready availability, and favorable safety profile, low-dose PPI co-prescription in healthy adults requiring short-term therapy with non-selective NSAIDs may be reasonable.

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Section: Discussionsupporting

confidence: 59%

Primary Prevention of Adverse Gastroduodenal Effects from Short-Term Use of Non-Steroidal Anti-Inflammatory Drugs by Omeprazole 20 mg in Healthy Subjects: A Randomized, Double-Blind, Placebo-Controlled Study

et al. 2008

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“…Antisecretory drugs such as proton pump inhibitors (PPIs) and histamine H 2 -receptor antagonists (H 2 -RAs) are commonly used for the treatment of upper gastrointestinal (GI) mucosal lesions induced by NSAIDs (Leandro et al, 2001;Peura, 2004;Yeomans et al, 2006;Scarpignato and Hunt, 2010;Sugano et al, 2011). These drugs have been thought to be ineffective in treating NSAID-induced small intestinal lesions because acid does not seem to be involved in the formation of intestinal lesions.…”

Section: Introductionmentioning

confidence: 99%

Mucosal Protective Agents Prevent Exacerbation of NSAID-Induced Small Intestinal Lesions Caused by Antisecretory Drugs in Rats

Satoh

Amagase

Takeuchi

2013

J Pharmacol Exp Ther

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Antisecretory drugs such as histamine H 2 -receptor antagonists and proton pump inhibitors are commonly used for the treatment of upper gastrointestinal mucosal lesions induced by nonsteroidal anti-inflammatory drugs (NSAIDs). However, it has recently been reported that these drugs exacerbate NSAID-induced small intestinal lesions in rats. Unfortunately, there are few effective agents for the treatment of this complication. We examined the effects of mucosal protective agents (MPAs) (misoprostol, irsogladine, and rebamipide) and mucin of porcine stomach on diclofenac-induced intestinal lesions and the exacerbation of the lesions by ranitidine or omeprazole. The effects of the drugs on intestinal motility and mucus distribution/content were also examined. Male Wistar rats (180-220 g) were used. Each drug was administered orally under fed conditions. Diclofenac (1-10 mg/kg) produced multiple lesions in the small intestine dosedependently. Both ranitidine (30 mg/kg) and omeprazole (100 mg/kg) significantly increased the intestinal lesions induced by low doses (3 and 6 mg/kg) of diclofenac. Misoprostol (0.03-0.3 mg/kg), irsogladine (3-30 mg/kg), and rebamipide (30-300 mg/kg), as well as mucin (30-300 mg/kg) inhibited the formation of intestinal lesions caused by a high dose (10 mg/kg) of diclofenac alone and prevented the exacerbation of diclofenac-induced lesions by antisecretory drugs. Diclofenac (10 mg/kg) markedly increased the intestinal motility and decreased the mucosal mucus, and the decrease of mucus was significantly inhibited by the MPAs. These results indicate the usefulness of the MPAs for the treatment of intestinal lesions induced by NSAIDs alone or by coadministration with antisecretory drugs, and suggest that mucus plays an important role in the protection of intestinal mucosa by the MPAs.

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“…Antisecretory drugs such as histamine H 2 -receptor antagonists (H 2 -RAs) and proton pump inhibitors (PPIs) are commonly used for the treatment of upper gastrointestinal mucosal lesions induced by NSAIDs (Leandro et al, 2001;Peura, 2004;Yeomans et al, 2006;Scarpignato and Hunt, 2010;Sugano et al, 2011). However, the effects of the drugs on small intestinal ulcers are not fully understood.…”

Section: Introductionmentioning

confidence: 99%

Exacerbation of Nonsteroidal Anti-Inflammatory Drug-Induced Small Intestinal Lesions by Antisecretory Drugs in Rats: The Role of Intestinal Motility

Satoh

Amagase

Takeuchi

2012

J Pharmacol Exp Ther

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Antisecretory drugs such as histamine H 2 -receptor antagonists (H 2 -RAs) and proton pump inhibitors (PPIs) are commonly used for the treatment of gastric and duodenal ulcers induced by nonsteroidal anti-inflammatory drugs (NSAIDs). However, the effects of these drugs on NSAID-induced small intestinal ulcers are not fully understood. The effects of H 2 -RAs and PPIs on NSAID-induced gastrointestinal lesions and small intestinal motility were examined in rats. Male Wistar rats (180 -220 g) were used. Indomethacin (10 mg/kg) was administered orally in fasted or fed rats, and gastrointestinal lesions were examined 24 h after indomethacin administration. Intestinal motility was measured by using a balloon method under urethane anesthesia. Indomethacin produced multiple lesions in the gastric corpus in fasted rats and in the small intestine in fed rats: 1) H 2 -RAs (cimetidine, ranitidine, and famotidine) and PPIs (omeprazole, lansoprazole, and rabeprazole) markedly inhibited the formation of gastric lesions. 2) The drugs, except for lansoprazole, increased intestinal lesions. 3) H 2 -RAs augmented the increase in intestinal motility caused by indomethacin, and the effects of H 2 -RAs on motility and intestinal lesions were markedly inhibited by atropine. 4) Lansoprazole inhibited the formation of intestinal lesions, and the effect was prevented by both pharmacological ablation of capsaicin-sensitive sensory neurons and pretreatment with N-nitro-L-arginine methyl ester, a selective inhibitor of nitric-oxide synthesis. The results suggest that: 1) inhibition of acid secretion by antisecretory drugs may exacerbate NSAID-induced intestinal lesions, 2) H 2 -RAs further aggravate lesions by increasing intestinal motility via the activation of cholinergic pathways, and 3) lansoprazole protects the intestinal mucosa against NSAID-related ulcerative stimuli.

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Prevention of acute NSAID-related gastroduodenal damage: A meta-analysis of controlled clinical trials

Cited by 13 publications

References 0 publications

Primary Prevention of Adverse Gastroduodenal Effects from Short-Term Use of Non-Steroidal Anti-Inflammatory Drugs by Omeprazole 20 mg in Healthy Subjects: A Randomized, Double-Blind, Placebo-Controlled Study

Primary Prevention of Adverse Gastroduodenal Effects from Short-Term Use of Non-Steroidal Anti-Inflammatory Drugs by Omeprazole 20 mg in Healthy Subjects: A Randomized, Double-Blind, Placebo-Controlled Study

Mucosal Protective Agents Prevent Exacerbation of NSAID-Induced Small Intestinal Lesions Caused by Antisecretory Drugs in Rats

Exacerbation of Nonsteroidal Anti-Inflammatory Drug-Induced Small Intestinal Lesions by Antisecretory Drugs in Rats: The Role of Intestinal Motility

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