Curing <i>Helicobacter pylori</i> Infection in Patients with Duodenal Ulcer Does Not Provoke Gastroesophageal Reflux Disease

Befrits, Ragnar; Sjöstedt, Svante; Ödman, Bengt; Sörngård, Heléne; Lindberg, Greger

doi:10.1046/j.1523-5378.2000.00031.x

Cited by 54 publications

(64 citation statements)

References 12 publications

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“…The association between H. pylori eradication and the development of newly and recurrent GERD is still controversial although various studies have been performed [18][19][20][21][22][23][24]. Moreover, there is still no evidence whether the presence of GERD before eradication therapy could affect the H. pylori eradication success rate.…”

Section: Discussionmentioning

confidence: 99%

Helicobacter pylori Eradication Therapy Ameliorates Latent Digestive Symptoms in Chronic Atrophic Gastritis

et al. 2018

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Background/Aims: This study investigated the effect of Helicobacter pylori eradication therapy on latent digestive symptoms in chronic atrophic gastritis. Methods: We enrolled 650 health checkup patients who underwent eradication therapy for chronic gastritis and completed a self-report questionnaire before and after the treatment between January 2014 and December 2016 at the Japanese Red Cross Society Kyoto Daiichi Hospital. Results: H. pylori eradication therapy for chronic atrophic gastritis improved latent digestive symptoms, including both the acid reflux and dyspepsia components in the frequency scale for the symptoms of gastroesophageal reflux disease (FSSG) scores. The effect was sustained until 1 year after the treatment. Higher FSSG scores (≥8 points) before H. pylori eradication therapy and age <70 years were significantly associated with the improvement of digestive symptoms after H. pylori eradication therapy. Conclusion: H. pylori eradication therapy may improve patients’ quality of life through the resolution of latent abdominal symptoms.

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Section: Discussionmentioning

confidence: 99%

Helicobacter pylori Eradication Therapy Ameliorates Latent Digestive Symptoms in Chronic Atrophic Gastritis

et al. 2018

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“…The authors reported a higher rate of esophagitis in patients who had their H. pylori eradicated compared to the group in which the infection had continued. Following this first study, other trials were carried out, either confirming LABENZ' work (8,9,14) or reporting contradictory results (1,24,36,38,41,42,44) .…”

Section: Introductionmentioning

confidence: 88%

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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“…These phenomena are seen more often in non-flat scars than in flat scars defined by chromoendoscopy (7,8). Reduced prostaglandin concentration in the ulcer scar tissue and H. pylori infection (15) are the major abnormalities seen in non-flat scars (7,8).…”

Section: S6mentioning

confidence: 99%

“…Eradication therapy is successful in 80-90% (but not 100%) but has some adverse effects and is not applicable to H. pylori-negative ulcers. In addition, elimination of H. pylori may, in some patients, aggravate reflux esophagitis (14), although this issue remains controversial (15,16). Furthermore, elimination of H. pylori may increase the appetite by altering leptin (17) and result in an increase in body weight (18).…”

Section: S6mentioning

confidence: 99%

15th Anniversary of Rebamipide: Looking Ahead to the New Mechanisms and New Applications

et al. 2005

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Rebamipide, a gastro-protective drug, was developed in Japan for the treatment of peptic ulcer disease. It was proven superior to the former same category drug cetraxate in a randomized, controlled, double-blind, comparative clinical study in 1989. Rebamipide's mechanisms of actions are different from anti-secretory drugs; it accelerates and improves the quality of ulcer healing and reduces ulcer recurrence rate. Numerous studies have been conducted to explain the mechanisms responsible for these actions, 37 papers were published by 1998. Major properties of rebamipide include: stimulation of prostaglandin and mucus glycoprotein synthesis, inhibition of reactive oxygen species, inflammatory cytokines and chemokines, and inhibition of neutrophils activation. Since 1998, 107 papers were published, clarifying further effects of rebamipide on cyclooxygenase-2, prostaglandin E receptors, growth factors (i.e., HGF, EGF, and VEGF), heat-shock proteins, nitric oxide, adhesion molecules, neutrophils, and Helicobacter pylori- and NSAID-related pathology. Moreover, inhibitory action of rebamipide on gastric cancer growth has also been shown. In this issue we reviewed recent advances in understanding of rebamipide's mechanism of action and its newest clinical applications.

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Curing Helicobacter pylori Infection in Patients with Duodenal Ulcer Does Not Provoke Gastroesophageal Reflux Disease

Abstract: Our data show that successful eradication of H. pylori infection does not increase the incidence of GERD in duodenal ulcer patients.

Cited by 54 publications

References 12 publications

Helicobacter pylori Eradication Therapy Ameliorates Latent Digestive Symptoms in Chronic Atrophic Gastritis

Helicobacter pylori Eradication Therapy Ameliorates Latent Digestive Symptoms in Chronic Atrophic Gastritis

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

15th Anniversary of Rebamipide: Looking Ahead to the New Mechanisms and New Applications

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