Intragastric pH during Treatment with Omeprazole: Role ofHelicobacter pyloriandH. pylori-Associated Gastritis

Verdú, Elena F.; Armstrong, David; Idström, JP; Labenz, Joachim; Stolte, Manfred; Börsch, G; Blum, A. L.

doi:10.3109/00365529609036903

Cited by 63 publications

(41 citation statements)

References 10 publications

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“…pylori eradication therapy also has the potential to impact significantly on reflux disease, through the effects of H. pylori eradication on acid secretory capacity and the pH of the gastric content [36,37]. When H. pylori infection is cured, a significant component of non-atrophic gastritis resolves, and acid secretory capacity can recover substantially [37].…”

Section: H Pylori Infection and Reflux Diseasementioning

confidence: 99%

Gastro-Oesophageal Reflux Disease

Dent¹

1998

Digestion

107

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New approaches to the grading of reflux oesophagitis and the definition of reflux disease have been proposed which should improve the precision of descriptions of this common problem. Endoscopy and 24-hour pH monitoring studies, though of great value, have significant limitations for assessment of reflux disease. Only about one third of reflux disease patients have oesophageal mucosal erosion or ulceration. Analysis of symptoms is probably the most useful method for diagnosis. Further research is needed into the best strategies for maximising the potential of symptom analysis. In the pathogenesis of reflux disease, Helicobacter pylori infection is not a major factor but the interaction of H. pylori gastritis and eradication therapy are important areas of great current interest. Troublesome reflux disease arises primarily from abnormally frequent gastro-oesophageal reflux, though heightened oesophageal mucosal sensitivity and defective oesophageal clearance play a role in some patients. Transient lower oesophageal sphincter relaxation appears to be the most important mechanism of reflux. This distinctive, swallow-independent type of lower oesophageal sphincter relaxation has a complex triggering system, apparently located in the brain stem. Medical and surgical treatments of reflux disease are now well characterised and have improved very substantially over recent years. Drugs that inhibit the occurrence of transient lower oesophageal sphincter relaxation are an intriguing possible future therapy.

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Section: H Pylori Infection and Reflux Diseasementioning

confidence: 99%

Gastro-Oesophageal Reflux Disease

Dent¹

1998

Digestion

107

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“…It has been shown that the intragastric pH is significantly higher with the same dose of PPI before as compared to after H. pylori eradication [31,32]. …”

Section: Helicobacter Pylori Infection and Interaction With Acid-inhimentioning

confidence: 99%

The Intriguing Relationship of Helicobacter pylori Infection and Acid Secretion in Peptic Ulcer Disease and Gastric Cancer

Malfertheiner

2011

Dig Dis

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Helicobacter pylori infection induces chronic inflammation of the gastric mucosa and thus profoundly affects gastric physiology. In the acute phase of infection, gastric acid secretion is transiently impaired. The morphological damage of the gastric mucosa, changes in gastric hormone release, and disruption of neural pathways all contribute to influence gastric acid secretion in a distinct manner. Changes in gastric acid secretion, whether impaired or increased, are intimately related with the topographic phenotypes of gastritis and the presence of atrophy or absence of corpus atrophy. The interplay of gastritis phenotype and acid secretion are key determinants in disease outcomes. Corpus-predominant gastritis and corpus atrophy are accompanied by hypochlorhydria and carry the highest risk for gastric cancer, whereas antrum-predominant gastritis with little involvement of the corpus-fundic mucosa is associated with hyperchlorhydria and predisposes to duodenal ulcer disease.

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“…All of these pathophysiological factors might be indicative of an increased gastro-oesophageal reflux [6]. Two arguments that would militate against such a relationship would be the buffering effect of the ammonia produced by the bacteria, resulting in a reduction in the amount of acid in the stomach [7, 8], and elevated gastrin levels [9]leading to an increase in lower oesophageal sphincter pressure [10]. The question arises whether the Hp-induced gastritis can protect against the development of gastro-oesophageal reflux disease (GORD) [11, 12].…”

Section: Introductionmentioning

confidence: 99%

Helicobacter pylori Infection: Protection against Barrett’s Mucosa and Neoplasia?

et al. 2000

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Background: Since Helicobacter pylori (Hp) infection provokes intestinal and gastric metaplasia, the question arises whether the specialized metaplasia (Barrett’s mucosa (BM)) and dysplasia or carcinoma in Barrett’s epithelium seen in gastro-oesophageal reflux disease (GORD) might not also be correlated with Hp infection, or whether the latter offers protection against Barrett’s oesophagus and Barrett’s adenocarcinoma. Patients: Gastric and oesophageal biopsies obtained from a total of 2,201 patients were analysed retrospectively. 297 of these patients had GORD (age 53.5 ± 13.4 years; m:f ratio 2.1:1), 1,192 patients had BM (age 62.8 ± 14.6 years; m:f 2.3:1) with or without neoplasia. 1,054 of these patients were diagnosed as having BM alone, 138 patients having BM neoplasia (high-grade dysplasia or adenocarcinoma). Patients with BM and low-grade dysplasia were excluded from this study because of the uncertainty in differentiating low-grade dysplasia from regenerative epithelium. A total of 712 patients with non-ulcer dyspepsia (NUD; average age 40.0 ± 16.1 years; m:f 0.3:1) served as a control group. Results: The percentage of Hp infection did not differ between patients with GORD with (53.3%)/without BM (51.4%) and neoplasia (47.8%), but is statistically significantly lower than in patients with NUD (65.7%). Conclusion: Our analysis shows that patients with GORD and Hp infection have no increased risk for the development of BM or neoplasia in BM. Since Hp infection is significantly less frequent in GORD than in NUD patients, a protective effect of the Hp infection is a possibility worth discussing.

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Intragastric pH during Treatment with Omeprazole: Role ofHelicobacter pyloriandH. pylori-Associated Gastritis

Abstract: The increased pH produced by omeprazole during H. pylori infection is likely to be due to neutralizing substances produced by H. pylori and not to H. pylori-induced gastritis.

Cited by 63 publications

References 10 publications

Gastro-Oesophageal Reflux Disease

Gastro-Oesophageal Reflux Disease

The Intriguing Relationship of <i>Helicobacter pylori</i> Infection and Acid Secretion in Peptic Ulcer Disease and Gastric Cancer

<i>Helicobacter pylori</i> Infection: Protection against Barrett’s Mucosa and Neoplasia?

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