Curing Helicobacter pylori infection in patients with duodenal ulcer may provoke reflux esophagitis

Labenz, Joachim; Al, Blum; Bayerdörffer, Ekkehard; Meining, Alexander; Stolte, Manfred; Börsch, G

doi:10.1016/s0016-5085(97)70024-6

Cited by 629 publications

(510 citation statements)

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“…KUPCINSKAS et al (16) also followed patients with duodenal ulcer for 1 year after H. pylori eradication and have not observed any increase in reflux esophagitis incidence, either. Other studies, obtained similar data in patients with gastric ulcers (12) .…”

Section: Discussionmentioning

confidence: 99%

Neither genotype nor the gastric colonization site of Helicobacter pylori are predictive factors for the development of erosive esophagitis in patients with peptic ulcer disease, 1 year after eradication

Batista

Silva

Eisig

et al. 2009

Arq. Gastroenterol.

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-Context -WhetherHelicobacter pylori infection is a protective or predisposing factor for the development of gastroesophageal reflux disease remains controversial. The most virulent strains, such as those expressing the cytotoxin-associated gene A (CagA), and the site of gastric colonization have been correlated with the prevention or development of esophagitis. Aim -To determine the incidence of erosive esophagitis following eradication of H. pylori in patients with peptic ulcer disease and to evaluate the association of erosive esophagitis with virulent strains of H. pylori and the site of gastric colonization. Methods -Triple therapy with lansoprazole, amoxicillin and clarithromycin was administered to 159 patients with peptic ulcer disease. Endoscopy, histopathology, urease and carbon-14 urea breath tests were performed prior to treatment, at 3 months and 1 year following treatment. Genotyping of H. pylori strains using polymerase chain reaction was performed separately on samples from the corpus and antrum. Results -One year after treatment, 148 successfully treated patients were reevaluated. Twenty-eight patients (19%) had erosive esophagitis, classified as Los Angeles grade A in 24 and B in 4. The samples taken from the corpus were CagA-positive in 18 patients (64%), while the samples taken from the antrum were CagA-positive in 21 patients (75%). Conclusions -The incidence of erosive esophagitis in peptic ulcer patients who had their H. pylori eradicated was 19%. No correlation was found between the gastric site colonized by H. pylori or strains expressing CagA and the prevention or development of erosive esophagitis in patients with peptic ulcer disease, 1 year after infection eradication. HEADINGS -Helicobacter pylori. Peptic ulcer. Esophagitis.

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Section: Discussionmentioning

confidence: 99%

Neither genotype nor the gastric colonization site of Helicobacter pylori are predictive factors for the development of erosive esophagitis in patients with peptic ulcer disease, 1 year after eradication

Batista

Silva

Eisig

et al. 2009

Arq. Gastroenterol.

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“…Antibiotic therapy 2 and 6 months after infection resulted in reversal of atrophy and restoration of normal gastric architecture, whereas bacterial eradication 1 year after infection resulted in some restoration of parietal cell mass and prevention of further progression of dysplasia in most animals (94). Although some questions have been raised regarding the worsening of gastroesophageal reflux after H. pylori eradication (115), most studies have not confirmed an increase in gastroesophageal reflux in patients whose H. pylori infection has been eradicated (116)(117)(118)(119). Further studies are clearly needed to determine whether eliminating both Helicobacter and non-Helicobacter spp.…”

Section: Strategies For Treating H Pylori Infection In At-risk Populmentioning

confidence: 99%

Inflammation, atrophy, and gastric cancer

Fox

Wang²

2007

J. Clin. Invest.

694

626

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The association between chronic inflammation and cancer is now well established. This association has recently received renewed interest with the recognition that microbial pathogens can be responsible for the chronic inflammation observed in many cancers, particularly those originating in the gastrointestinal system. A prime example is Helicobacter pylori, which infects 50% of the world's population and is now known to be responsible for inducing chronic gastric inflammation that progresses to atrophy, metaplasia, dysplasia, and gastric cancer. This Review provides an overview of recent progress in elucidating the bacterial properties responsible for colonization of the stomach, persistence in the stomach, and triggering of inflammation, as well as the host factors that have a role in determining whether gastritis progresses to gastric cancer. We also discuss how the increased understanding of the relationship between inflammation and gastric cancer still leaves many questions unanswered regarding recommendations for prevention and treatment.

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“…16 Eradication of H. pylori to cure peptic ulcer disease can result in new onset of gastro-oesophageal reflux disease. 17,18 It is conceivable that eradication of H. pylori to reduce the medical and economic load of gastric cancer or peptic ulcer would lead to a surge of gastro-oesophageal reflux disease and costs associated with its management.…”

Section: Discussionmentioning

confidence: 99%

Medical decision models of Helicobacter pylori therapy to prevent gastric cancer

Sonnenberg

Inadomi

1998

Aliment Pharmacol Ther

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tration on its essential features. A model would defy its very purpose if it tried to be overly detailed and simulate the medical phenomenon by considering all influences that occur in the real world. A good model should be simple and easily appreciated. Classic examples of elegant and conceptually simple mathematical models are, for instance, the differential equations that were developed by mathematicians to describe the complex and seemingly bewildering phenomena of physics. The majority of problems encountered in medicine, unfortunately, involve too many interrelated variables to be summarized in such a fashion. In essence, linear and logistic regression analyses represent two types of mathematic tools to model the influence of multiple variables on one medical outcome of interest. Compartment models and path

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Curing Helicobacter pylori infection in patients with duodenal ulcer may provoke reflux esophagitis

Cited by 629 publications

References 1 publication

Neither genotype nor the gastric colonization site of Helicobacter pylori are predictive factors for the development of erosive esophagitis in patients with peptic ulcer disease, 1 year after eradication

Neither genotype nor the gastric colonization site of Helicobacter pylori are predictive factors for the development of erosive esophagitis in patients with peptic ulcer disease, 1 year after eradication

Inflammation, atrophy, and gastric cancer

Medical decision models of Helicobacter pylori therapy to prevent gastric cancer

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