Failure of Helicobacter pylori eradication to influence site-specific relapse in high risk NSAID users: Results of a large six month double blind randomised controlled clinical trial

Hawkey, C. J.; Tullassay, Z; Szcepanski, L; Rensburg, C. Van; Filipowicz-Sosnowska, Anna; Lanas, Ángel; Peacock, RA; Gillon, Krw

doi:10.1016/s0016-5085(98)80590-8

Cited by 4 publications

(7 citation statements)

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“…Forty‐seven studies of 1‐week triple therapy with omeprazole, clarithromycin and amoxycillin (OCA) were identified, from which the ITT eradication rate could be determined 14 , . 17 , 19 , 20 , 23 –65 It was unavailable from another 19 studies 66 –84 …”

Section: Resultsmentioning

confidence: 99%

One‐week clarithromycin triple therapy regimens for eradication of Helicobacter pylori

Pipkin

Williamson

Wood

1998

Aliment Pharmacol Ther

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Background: One‐week triple therapies have been endorsed as the treatment regimens of choice for eradication of Helicobacter pylori infection. Those that include clarithromycin appear to be the most effective. Aim: To review reports of triple therapies that include clarithromycin. Methods: Reports were identified from the literature to May 1998. The variation between study designs prevents a formal meta‐analysis. A measure of the relative efficacies of regimens has, however, been gained by comparison and by pooling of intention‐to‐treat eradication rates. Results: One hundred and ninety‐two studies were identified which included 264 treatment arms of a 1‐week triple therapy composed of clarithromycin with amoxycillin or a nitroimidazole (metronidazole or tinidazole), and either ranitidine bismuth citrate or a proton pump inhibitor (omeprazole, lansoprazole or pantoprazole). From reports of these studies, an intention‐to‐treat H. pylori eradication rate could be determined from 210 treatment arms of 151 studies. Conclusions: There is little to choose between the efficacies of 1‐week clarithromycin‐based triple therapy eradication regimens. However, those comprising clarithromycin, a nitroimidazole and either ranitidine bismuth citrate or a high dose of omeprazole are, in general, the most effective. Against antibiotic‐resistant strains of H. pylori, regimens including ranitidine bismuth citrate may be more effective than those including a proton pump inhibitor.

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Section: Resultsmentioning

confidence: 99%

One‐week clarithromycin triple therapy regimens for eradication of Helicobacter pylori

Pipkin

Williamson

Wood

1998

Aliment Pharmacol Ther

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“…21 Functional dyspepsia provides yet another example of where a better clinical effect with proton pump inhibitors is found in H pylori infected subjects. Previous examples include treatment and prevention of recurrence of reflux oesophagitis22 as well as treatment of ulcers induced by non-steroidal anti-inflammatory drugs 23…”

Section: Discussionmentioning

confidence: 99%

Short course acid suppressive treatment for patients with functional dyspepsia: results depend on Helicobacter pylori status

Blum

2000

Gut

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Background and aims-Treatment of functional dyspepsia with acid inhibitors is controversial and it is not known if the presence of Helicobacter pylori infection influences the response. Methods-After a complete diagnostic workup, 792 patients with functional dyspepsia unresponsive to one week of low dose antacid treatment were randomised to two weeks of treatment with placebo, ranitidine 150 mg, omeprazole 10 mg, or omeprazole 20 mg daily. Individual dyspeptic and other abdominal symptoms were evaluated before and after treatment according to H pylori status. Results-The proportions of patients considered to be in remission (intention to treat) at the end of treatment with placebo, ranitidine 150 mg, omeprazole 10 mg, and omeprazole 20 mg were, respectively, 42%, 50%, 48%, and 59% in the H pylori positive group and 66%, 73%, 64%, and 71% in the H pylori negative group. In H pylori positive patients, the therapeutic gain over placebo was significant for omeprazole 20 mg (17.6%, 95% confidence intervals (CI) 4.2-31.0; p<0.014 using the Bonferroni-adjusted p level of 0.017) but not for omeprazole 10 mg (6.8%, 95% CI −6.7-20.4) or ranitidine 150 mg (8.9%, 95% CI −4.2-21.9). There was no significant therapeutic gain from active treatment over placebo in H pylori negative patients. Complete disappearance of symptoms and improvement in quality of life also occurred most frequently with omeprazole 20 mg and was significant in both H pylori positive and H pylori negative groups. The six month relapse rate of symptoms requiring treatment was low (<20%) in all groups. Conclusions-Omeprazole 20 mg per day had a small but significant favourable eVect on outcome in H pylori positive patients. The diVerential response in these patients may be explained by an enhanced antisecretory response in the presence of H pylori. The eVect of weaker acid inhibition was unsatisfactory. (Gut 2000;47:473-480)

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“…After 8 weeks, the patients on eradication therapy had impaired healing of gastric ulcers and developed new ulcers. 5 H. pylori infection was thought to protect against NSAIDs by stimulating prostaglandin synthesis in the gastric mucosa. 11 Furthermore, H. pylori eradication might increase intragastric acidity, thus reducing the ef®cacy of acid suppressive drugs.…”

Section: Discussionmentioning

confidence: 99%

“…Recent data suggested that H. pylori might actually protect against the ulcerogenic effects of NSAIDs in long‐term users 3 –5 . Two large‐scale endoscopic studies reported a higher rate of ulcer healing with fewer ulcer relapses in H. pylori positive NSAID users on long‐term omeprazole when compared to uninfected subjects 3 , .…”

Section: Discussionmentioning

confidence: 99%

“…2 However, controversies exist on the role of H. pylori in the pathogenesis of NSAID‐associated peptic ulcers. Recent studies have suggested that H. pylori expedited the healing of endoscopic lesions in chronic NSAID users who had no history of gastrointestinal complications 3 –5 . This raises a concern as to whether curing the infection may hamper the ulcer healing that is associated with NSAIDs, and whether H. pylori should be ‘saved’ rather than ‘eradicated’.…”

Section: Introductionmentioning

confidence: 99%

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Does eradication of Helicobacter pylori impair healing of nonsteroidal anti‐inflammatory drug associated bleeding peptic ulcers? A prospective randomized study

Chan

Sung

Suen

et al. 1998

Aliment Pharmacol Ther

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Background: Despite the widely accepted view that Helicobacter pylori is the most important cause of peptic ulcer disease, recent studies have suggested that the microbe protects against nonsteroidal anti‐inflammatory drug (NSAID)‐associated gastroduodenal lesions and promotes ulcer healing. We investigated the effects of H. pylori eradication on the healing of NSAID‐associated bleeding peptic ulcers. Methods: Chronic NSAID users presenting with peptic ulcer haemorrhage underwent endoscopy to secure haemostasis and to document H. pylori infection by rapid urease test and culture. They were prospectively randomized to receive either omeprazole (20 mg once daily) for 8 weeks or a 1‐week course of triple therapy (bismuth subcitrate 120 mg, tetracycline 500 mg, metronidazole 400 mg, all given four times daily) plus omeprazole (20 mg once daily) for 8 weeks. Endoscopy was repeated after 8 weeks. Final H. pylori status was determined by a 13C‐urea breath test that was performed at least 4 weeks after discontinuation of omeprazole. Results: 195 H. pylori‐infected NSAID users, complicated by bleeding ulcers, were randomized to receive omeprazole alone (102) or triple therapy plus omeprazole (93). 174 patients returned for second endoscopy at 8 weeks (91 in the omeprazole group, 83 in the triple therapy group). Urea breath test was negative in 14% in the omeprazole group vs. 92% in the triple therapy group (P < 0.001). Complete ulcer healing was achieved in 88 (97%) patients in the omeprazole group and 77 (93%) in the triple therapy group (P = 0.31). On intention‐to‐treat analysis, ulcers were healed in 86% of the omeprazole group and 83% of the triple therapy group (P = 0.50). There was no significant difference in the healing rates of gastric or duodenal ulcers between the two groups. Conclusion: Eradication of H. pylori did not impair the healing of NSAID‐associated bleeding peptic ulcers.

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Failure of Helicobacter pylori eradication to influence site-specific relapse in high risk NSAID users: Results of a large six month double blind randomised controlled clinical trial

Cited by 4 publications

References 0 publications

One‐week clarithromycin triple therapy regimens for eradication of Helicobacter pylori

One‐week clarithromycin triple therapy regimens for eradication of Helicobacter pylori

Short course acid suppressive treatment for patients with functional dyspepsia: results depend on Helicobacter pylori status

Does eradication of Helicobacter pylori impair healing of nonsteroidal anti‐inflammatory drug associated bleeding peptic ulcers? A prospective randomized study

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