Reduction of Aspirin-Induced Gastroduodenal Mucosal Damage with Ranitidine

Jm, Berkowitz; Sn, Adler; Jt, Sharp; Cw, Warner

doi:10.1097/00004836-198606002-00009

Cited by 41 publications

(8 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Several studies, however, have implicated the duodenum as an alternative or additional site. '10' 31 We noted a higher incidence of duodenal ulceration (mostly in patients receiving piroxicam) than of gastric ulceration. Piroxicam was associated with a higher incidence of peptic ulceration than was naproxen (16% and 9% respectively), and treatment with piroxicam was associated with eight of the 12 duodenal ulcers that developed during the study.…”

Section: Discussionmentioning

confidence: 89%

“…In a study on bleeding induced by aspirin, inhibition of acid secretion represented the best strategy to reduce gastric mucosal bleeding.28 In other studies ranitidine and cimetidine protected against damage induced by aspirin in volunteers. [29][30][31][32] We evaluated the protection given by ranitidine 150 mg twice daily in a large population of patients requiring non-steroidal anti-inflammatory drugs. In addition, we studied risk factors to target treatment to specific subgroups of patients.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

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

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.

show abstract

Section: Discussionmentioning

confidence: 89%

Section: Introductionmentioning

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

show abstract

“…Ranitidine has been demonstrated to pro tect gastric mucosa against aspirin-induced damage in vivo, in rats [3, 4] and in humans [1,2]. However, ranitidine does not protect rat gastric mucosa against ethanol-induced damage in in vivo studies (5, 17, 18], As aspirin-induced damage to gastric mucosa is dependent on the pH of gastric content [19], whereas ethanol-induced damage is not [20,21 ], the question arises as to whether ranitid ine-induced protection is limited to those agents whose damaging effect is acid depen dent.…”

Section: Discussionmentioning

confidence: 99%

“…The histamine H2 receptor antagonist, ranitidine, has been demonstrated to protect gastric mucosa against aspirin-induced dam age in vivo, in man [1,2] and rats [3,4], Tamawski et al [5] reported that ranitidine and cimetidine did not protect rat gastric mucosa in vivo against ethanol-induced 1 Dr. Romano is a visiting scientist from the Insti tute of General Medicine and Clinical Methodology, 1st Faculty of Medicine, University of Naples, Italy. damage (which is acid-independent unlike aspirin) so questioning the ability of H2 blockers to protect gastric mucosa indepen dent of acid inhibition.…”

mentioning

confidence: 99%

Effect of Ranitidine on Taurocholate-, Ethanol-, and Indomethacin-Induced Damage to Gastric Epithelial Cells in vitro

Romano

Razandi²,

Ivey³

1989

Digestion

View full text Add to dashboard Cite

We evaluated whether ranitidine protects gastric epithelial cells against damage induced by sodium taurocholate, ethanol or indomethacin, under conditions independent of its acid inhibitory effect as well as of systemic factors. We also studied the role of prostaglandins and sulfhydryls in any such protection. Ranitidine significantly reduced the amount of damage induced by taurocholate, but did not afford protection against ethanol- and indo-methacin-induced damage. Incubation with ranitidine did not increase PGE₂ production by cultured cells nor did it affect the cellular content of sulfhydryls. The protective effect of ranitidine against taurocholate was not prevented by indomethacin or by the sulfhydryl blocker, N-ethylmaleimide. In conclusion, this in vitro study confirms that H₂ blockers such as ranitidine have a limited cytoprotective ability independent of acid secretion, which is not as extensive as agents such as prostaglandins and sulfhydryls. This may be because prostaglandins and sulfhydryls play no role in the protective effect of ranitidine.

show abstract

“…The results of a recent study of 110 patients taking NSAIDs confirmed the predominance of gastric damage and found no difference between placebo and ranitidine in the prevention of either gastric or duodenal injury (33). Ranitidine has only been shown to prevent gastric damage in two studies (106,107). T h e results of all 11 published controlled trials of H, blockers in the healing of NSAID-induced lesions or ulcers while NSAID use was continued are shown in Table 5.…”

Section: Prevention and Healing Of Nsaid-induced Damage By Other Thermentioning

confidence: 99%

Misoprostol—a Logical Therapeutic Approach to Gastroduodenal Mucosal Injury Induced by Non-Steroidal Anti-Inflammatory Drugs?

Fenn¹,

Robinson²

1991

J Clin Pharm Ther

View full text Add to dashboard Cite

SUMMARYMisoprostol is a synthetic analogue of naturally occurring prostaglandin El.T h e basis of the damaging actions of non-steroidal anti-inflammatory drugs (NSAIDs) on the gastrointestinal (GI) tract is believed to be a consequence of two events: a direct damaging action on mucosal integrity and depletion of endogenous mucosal prostaglandins (PGs). Due to the latter effect, and because current evidence indicates that PGs play an important role in maintaining the integrity of the G I tract, misoprostol has been developed as a logical therapy to prevent and heal gastric and duodenal damage caused b y NSAIDs. T h e purpose of this review is to consider the need for such a therapy, to describe its pharmaceutical development, to review its pharmacology and to review its efficacy compared with other available agents.

show abstract

Reduction of Aspirin-Induced Gastroduodenal Mucosal Damage with Ranitidine

Cited by 41 publications

References 0 publications

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

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

Effect of Ranitidine on Taurocholate-, Ethanol-, and Indomethacin-Induced Damage to Gastric Epithelial Cells in vitro

Misoprostol—a Logical Therapeutic Approach to Gastroduodenal Mucosal Injury Induced by Non-Steroidal Anti-Inflammatory Drugs?

Contact Info

Product

Resources

About