Effect of Ranitidine and Amoxicillin plus Metronidazole on the Eradication of Helicobacter pylori and the Recurrence of Duodenal Ulcer

Hentschel, E; Brandstätter, G; Dragosics, B; Hirschl, Alexander M.; Nemec, H.; Schütze, K; Taufer, M.; Wurzer, H

doi:10.1056/nejm199302043280503

Cited by 663 publications

(301 citation statements)

References 17 publications

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“…4, 8±10 Hentschel et al reported that the combination of amoxycillin, metronidazole and an H 2 -receptor antagonist was effective in the treatment of H. pylori infection. 11 We showed that the substitution of clarithromycin for metronidazole (amoxycillin±clari-thromycin±H 2 -receptor antagonist therapy) was also effective and, as expected, effectiveness was not reduced by metronidazole resistance. 12 Subsequent studies showed that a proton pump inhibitor could be substituted for the H 2 -receptor antagonist with good SUMMARY Background: Effective anti-Helicobacter pylori therapies with few side-effects are needed.…”

Section: Introductionsupporting

confidence: 63%

Clarithromycin, amoxycillin and H₂‐receptor antagonist therapy for Helicobacter pylori peptic ulcer disease in Korea

Breuer

Kim

El‐Zimaity

et al. 1997

Aliment Pharmacol Ther

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Background: Effective anti‐Helicobacter pylori therapies with few side‐effects are needed. We previously showed that the regimen of amoxycillin, clarithromycin and an H2‐receptor antagonist was effective in the United States. The current study tested whether this therapy would also be successful in Korea. Methods: Patients with gastric or duodenal ulcers received amoxycillin (750 mg t.d.s.) plus clarithromycin (500 mg t.d.s.) for 2 weeks and nizatidine 300 mg at bedtime for 6 weeks. Endoscopic examinations were performed before treatment and 4 or more weeks after ending antimicrobial therapy. H. pylori status was confirmed by rapid urease testing and histological examination of gastric antrum and corpus biopsies using the Genta stain. Antibiotic resistance was tested using the E‐test method. Cure was defined as no evidence of H. pylori infection 4 or more weeks after ending therapy. Results: Seventy‐two patients (59 males and 13 females; mean age 46 years), including 35 with duodenal ulcers, 30 with gastric ulcers and seven with both, were studied. H. pylori infection was cured in 95.8% (69/72 patients; 95% CI = 88.3–99.1%). Two of the treatment failures had culture data and one had pre‐treatment resistance to clarithromycin. Smoking did not have an adverse effect on therapy. Ten patients (15%) developed side‐effects during treatment, but all were mild and did not require treatment interruption. No case of reinfection was noted during follow‐up. Conclusion: The combination of amoxycillin, clarithromycin and an H2‐receptor antagonist is effective in Korean patients with H. pylori infection.

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Section: Introductionsupporting

confidence: 63%

Clarithromycin, amoxycillin and H₂‐receptor antagonist therapy for Helicobacter pylori peptic ulcer disease in Korea

Breuer

Kim

El‐Zimaity

et al. 1997

Aliment Pharmacol Ther

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“…Helicobacter pylori as the cause of active chronic gastritis, this new gastric pathogen has been firmly established as the major etiological agent of peptic-ulcer disease, and it is now strongly linked to development of gastric adenocarcinoma and gastric lymphoma (9,13,18,19,24,26,37,40,42,43,52). Although gastric spiral organisms have been observed in dogs and cats for over 90 years, their presence in these species has been largely ignored and they were sometimes cited as gastric commensals (3,23,50).…”

Section: Since the Discovery In 1983 By Warren And Marshall Ofmentioning

confidence: 99%

Helicobacter pylori induced gastritis in the domestic cat

1995

Gastroenterology

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Helicobacter pylori has been cultured from the inflamed gastric mucosae of naturally infected cats; the lesions in H. pylori-infected cat stomachs mimic many of the features seen in H. pylori-infected human stomachs. To determine whether H. pylori-negative specific-pathogen-free cats with normal gastric mucosae were susceptible to colonization by this bacterium and whether gastritis developed after infections, four H. pylori-negative cats treated with cimetidine were orally dosed three times with 3 ml (1.5 ؋ 10 8 CFU/ml) of H. pylori every 4 days. All four cats became persistently colonized as determined by gastric cultures and PCRs from serial gastric biopsy samples and necropsy samples at 7 months postinfection. H. pylori was not isolated from the two control cats, nor were their gastric tissues positive by PCR; one of the two cats had a few focal lymphocytic aggregates in the body submucosa, whereas the second cat had a normal gastric mucosa. All four H. pylori-infected cats had multifocal gastritis consisting of lymphoid aggregates plus multiple large lymphoid nodules, which were most noticeable in the antral mucosa. In addition, one H. pylori-infected cat had a moderate diffuse infiltration of polymorphonuclear leukocytes in the subglandular region of the antrum. H. pylori-like organisms were focally distributed in glandular crypts of the antrum. Two of the H. pylori-infected cats had significant (eightfold) increases over baseline in levels of immunoglobulin G H. pylori serum antibody. The H. pylori isolates from the four experimentally infected cats had restriction fragment length polymorphism patterns specific for the flaA gene that were identical to those of the inoculating strain. H. pylori readily colonizes the cat stomach and produces persistent gastritis. Since the discovery in 1983 by Warren and Marshall ofHelicobacter pylori as the cause of active chronic gastritis, this new gastric pathogen has been firmly established as the major etiological agent of peptic-ulcer disease, and it is now strongly linked to development of gastric adenocarcinoma and gastric lymphoma (9,13,18,19,24,26,37,40,42,43,52). Although gastric spiral organisms have been observed in dogs and cats for over 90 years, their presence in these species has been largely ignored and they were sometimes cited as gastric commensals (3,23,50). However, because of the tremendous interest in H. pylori as a gastric pathogen, renewed interest has been focused on gastric organisms in animals, the role of these organisms in producing gastric pathology, and their potential as zoonotic gastric pathogens. Animals also have been the subjects of experiments designed to study the pathogenesis and epidemiology of H. pylori. Unfortunately, attempts to infect a variety of animal species with H. pylori were unsuccessful, with the exception of studies with gnotobiotic and (to a lesser extent) specific-pathogen-free pigs, gnotobiotic dogs, Old World macaque species, and most recently, athymic or germfree mice (2,27,28,30,44). Furthermore, early attempts t...

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“…It survives in the acidic environment of the gastric mucosa and causes gastritis, peptic ulcers, mucosa-associated lymphoid tissue lymphoma, and gastric cancer [2]. Therefore, the eradication of H. pylori can markedly lower gastric and duodenal ulcer recurrence and allowing the treatment of mucosa-associated lymphoid tissue lymphoma [3]. The first-line choice of treatment for H. pylori infection in the United States and Europe consists of a conventional triple therapy, in which a proton pump inhibitor (PPI), clarithromycin, and amoxicillin are administered for 7-14 days [4][5][6].…”

Section: Introductionmentioning

confidence: 99%

Comparison of three different regimens against Helicobacter pylori as a first-line treatment: A randomized clinical trial

Kefeli

Başyiğit

Yeniova

et al. 2015

Bosn J of Basic Med Sci

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Treatments with bismuth-containing quadruple therapy (QT), sequential therapy (ST), or concomitant therapy (CT) have been proposed as empirical first-line regimens for Helicobacter pylori. We compared the efficacy and tolerability of 10 days bismuth-containing quadruple QT, 10 days ST, and 10 days CT with as first-line treatments for H. pylori in a randomized crossover study. The subjects were randomly divided into three groups. The first 130 patients were treated with rabeprazole, bismuth potassium citrate, metronidazole, and tetracycline for 10 days. The second 130 patients in the sequential group were treated with rabeprazole and amoxicillin for 5 days, and then rabeprazole, clarithromycin, and metronidazole for an additional 5 days. The last 130 patients in the concomitant group were treated with rabeprazole, amoxicillin, clarithromycin, and metronidazole for 10 days. H. pylori eradication was confirmed by urea breath test at 6 weeks. The primary outcome was eradication rates of first-line treatment by intention to treat and per protocol (PP) analyzes. There was no difference between the average ages and the male/female ratio of the groups. The PP analysis was performed on 121, 119, and 118 patients in the QT, ST, and CT groups, respectively. In the PP analysis, the successful eradication 94.2% (114/121), 95.0% (113/119), and 95.8% (113/118) the QT, ST, and CT groups, respectively. There was no significant difference among the three groups (p = 0.86). 10 days QT, ST, and CT are highly effective as empirical first-line therapies for H. pylori in the region with high clarithromycin resistance.

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Effect of Ranitidine and Amoxicillin plus Metronidazole on the Eradication of Helicobacter pylori and the Recurrence of Duodenal Ulcer

Abstract: In patients with recurrent duodenal ulcer, eradication of H. pylori by a regimen that does not have any direct action on the mucosa is followed by a marked reduction in the rate of recurrence, suggesting a causal role for H. pylori in recurrent duodenal ulcer.

Cited by 663 publications

References 17 publications

Clarithromycin, amoxycillin and H₂‐receptor antagonist therapy for Helicobacter pylori peptic ulcer disease in Korea

Clarithromycin, amoxycillin and H₂‐receptor antagonist therapy for Helicobacter pylori peptic ulcer disease in Korea

Helicobacter pylori induced gastritis in the domestic cat

Comparison of three different regimens against Helicobacter pylori as a first-line treatment: A randomized clinical trial

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Effect of Ranitidine and Amoxicillin plus Metronidazole on the Eradication of Helicobacter pylori and the Recurrence of Duodenal Ulcer

Abstract: In patients with recurrent duodenal ulcer, eradication of H. pylori by a regimen that does not have any direct action on the mucosa is followed by a marked reduction in the rate of recurrence, suggesting a causal role for H. pylori in recurrent duodenal ulcer.

Cited by 663 publications

References 17 publications

Clarithromycin, amoxycillin and H2‐receptor antagonist therapy for Helicobacter pylori peptic ulcer disease in Korea

Clarithromycin, amoxycillin and H2‐receptor antagonist therapy for Helicobacter pylori peptic ulcer disease in Korea

Helicobacter pylori induced gastritis in the domestic cat

Comparison of three different regimens against Helicobacter pylori as a first-line treatment: A randomized clinical trial

Contact Info

Product

Resources

About

Clarithromycin, amoxycillin and H₂‐receptor antagonist therapy for Helicobacter pylori peptic ulcer disease in Korea

Clarithromycin, amoxycillin and H₂‐receptor antagonist therapy for Helicobacter pylori peptic ulcer disease in Korea