Peptic ulcer and non-steroidal anti-inflammatory agents.

Jm, Duggan; Dobson, Annette; Johnson, H. Daintree; Fahey, Paul

doi:10.1136/gut.27.8.929

Cited by 93 publications

(20 citation statements)

References 14 publications

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“…These drugs, however, account for 25% of all the suspected adverse drug reactions reported to the United Kingdom Committee on Safety of Medicines each year and 21% reported to the United States Food and Drug Administration. 2 The commonest and most serious of these reactions are gastrointestinal.3'5 Up to 60% of patients taking these drugs report dyspepsia,5'7 but this has not proved to be a reliable guide to the presence of gastroduodenal lesions.8 '2 Aspirin causes gastroduodenal damage in more than 80% of subjects,'3 '" varying from acute microscopic gastric changes'5 to potentially more serious chronic gastric ulceration or haemorrhage.7 [16][17][18] In a large prospective study gastric lesions were found in a third of patients taking non-steroidal anti-inflammatory drugs for a year and in half of those receiving two or more such drugs. BMJ VOLUME 297solved this problem.…”

Section: Introductionmentioning

confidence: 99%

“…Patients-297 patients with rheumatoid arthritis or osteoarthritis over the age of 18 without lesions in the stomach and duodenum at baseline endoscopy (after one week without taking non-steroidal antiinflammatory drugs). Those taking other antirheumatic agents, concomitant ulcerogenic drugs, or treatment for peptic ulcers within the previous 30 days were excluded.…”

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confidence: 99%

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Prevention of gastroduodenal damage induced by non-steroidal anti-inflammatory drugs: controlled trial of ranitidine.

Ehsanullah

Page

Tildesley

et al. 1988

BMJ

359

118

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Objective-To evaluate the prophylactic effect of ranitidine 150 mg twice daily in patients requiring one of the following non-steroidal anti-inflammatory drugs: naproxen, piroxicam, diclofenac, and indomethacin. In addition, risk factors were studied in order to help in targeting of such treatment to specific groups of patients.Design-Double blind, placebo controlled, randomised, parallel group with endoscopic assessments at 0, 4, and 8 weeks.Setting-Multicentre outpatient study at secondary referral centres in five European countries.Patients-297 patients with rheumatoid arthritis or osteoarthritis over the age of 18 without lesions in the stomach and duodenum at baseline endoscopy (after one week without taking non-steroidal antiinflammatory drugs). Those taking other antirheumatic agents, concomitant ulcerogenic drugs, or treatment for peptic ulcers within the previous 30 days were excluded. Age, sex, arthritic disease, and type of non-steroidal anti-inflammatory drug used were comparable in the two treatment groups. In all, 263 patients completed the trial.Interventions-Ranitidine 150 mg twice daily or placebo (plus the selected non-steroidal antiinflammatory drug) was prescribed within five days after the baseline endoscopy for two consecutive periods of four weeks. Paracetamol was permitted during the study, but not antacids. Patients were withdrawn if the most severe grade of damage (including ulceration) was found at the four week endoscopy or when indicated, or with lesser damage at the investigator's discretion.End point-Frequency of gastric and duodenal ulceration or lesions, or both.Measurements and main results-The cumulative incidence of peptic ulceration by eight weeks was 10-3% (27/263); 2 out of 135 (1-5%) developed duodenal ulceration in the ranitidine group, compared with 10 out of 126 (8%) taking placebo. The frequency ofgastric ulceration was the same (6%) for the two groups at eight weeks. Though significantly fewer gastric lesions developed in the ranitidine group by four weeks, this difference was not evident by eight weeks. The frequency of non-ulcerative lesions in the duodenum did not differ greatly for the two groups at either time point. Twelve out of 75 (16%) patients taking piroxicam developed peptic ulceration, of whom two thirds had duodenal ulceration. Patients with a history of peptic ulcer were particularly susceptible to recurrent ulceration, against which ranitidine offered some protection.Conclusions-Ranitidine 150 mg twice daily significantly reduced the incidence of duodenal ulceration but not gastric ulceration when prescribed concomitantly with one of four commonly used non-steroidal anti-inflammatory drugs.

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Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

Prevention of gastroduodenal damage induced by non-steroidal anti-inflammatory drugs: controlled trial of ranitidine.

Ehsanullah

Page

Tildesley

et al. 1988

BMJ

359

118

View full text Add to dashboard Cite

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“…Non-steroidal anti-inflammatory drugs (NSAIDs), such as aspirin and indomethacin, are well-known to delay the healing of peptic ulcers or to induce the re lapse of healed ulcers (24). A drug that is able to pre vent such an adverse effect will be useful for the treat ment of patients with peptic ulcers who are receiving NSAID therapy.…”

Section: Discussionmentioning

confidence: 99%

Effects of a New Histamine H2-Receptor Antagonist, Z-300, on Gastric Secretion and Gastro-Duodenal Lesions in Rats: Comparison with Roxatidine.

et al. 1992

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ABSTRACT-We examined the effects of a new compound, N-[3-[3-(piperidinomethyl)phenoxy] propyl]-2-(2-hydroxyethyl-l-thio)acetamido • 2-(4-hydroxy benzoyl)benzoate (Z-300), on the histamine H2-receptor, gastric secretion in rats and dogs, and acute gastro-duodenal lesions or chronic gastric ulcers in rats. Roxatidine acetate hydrochloride (roxatidine), a known histamine H2-receptor antagonist , was used as a reference compound. The pA2 values for Z-300 and roxatidine for the isolated guinea pig atrium were 6.8 and 7.0, respectively. These agents at < 10-5 M did not affect the contraction of guinea pig ileum in response to carbachol. Z-300, administered either orally or parenterally, significant ly inhibited the basal and histamine-stimulated gastric acid secretion in rats. Gastric acid secretion stimulated by histamine, pentagastrin or carbachol in Heidenhain pouch dogs was also significantly in hibited by the compound. The effect persisted for >7 hr in the case of histamine-stimulation. Oral Z 300 significantly protected the gastric mucosa from water-immersion stress-, indomethacin-, aspirin and HCl • ethanol-induced lesions and protected the duodenal mucosa against mepirizole and cysteamine-in duced ulcers. These effects on gastric secretion and lesion formation were, as a whole, stronger than those observed with roxatidine. Z-300, but not roxatidine, significantly accelerated the spontaneous healing of acetic acid ulcers induced in rats and prevented the delay in ulcer healing caused by in domethacin. The mechanism of action of Z-300 on acute lesions and chronic ulcers appears to be most ly related to its potent antisecretory and mucosal-protective activities.

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“…Recently, two reports from Australia have examined the relationship of aspirin, non aspirin NSAIDs and acetaminophen to gas tric ulceration [70,71 ]. Both found the use of acetaminophen on its own was not associ ated with ulceration, whereas both aspirin and non-aspirin NSAIDs were.…”

Section: Aspirin As a Cause Of Peptic Ulcermentioning

confidence: 99%

“…Since then there have been ten studies from Aus tralia and the United States all of which have shown significant associations between regu lar aspirin intake (4-15 doses weekly [65]) and chronic gastric ulcer [66][67][68][69][70][71] (table II). No association, however, has been found with chronic duodenal ulcer.…”

Section: Aspirin As a Cause Of Peptic Ulcermentioning

confidence: 99%