ArticleDigestive diseases and sciences2004
Gastric acid normosecretion is not essential in the pathogenesis of mild erosive gastroesophageal reflux disease in relation to Helicobacter pylori status.
Article in Digestive diseases and sciences, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.
- Risk factors and 26-years worldwide prevalence of endoscopic erosive esophagitis from 1997 to 2022: a meta-analysis.Scientific reports · 2023Pooled it
- Pathophysiology of Gastroesophageal Reflux Disease.Digestion · 2026Review
- Comparing the acid-suppressive effects of three brands of generic lansoprazole with the original: pharmacokinetic bioequivalence tests do not necessarily guarantee pharmacodynamic equivalence.Digestive diseases and sciences · 2009Article
- Prevalence of gastroesophageal reflux disease and its association with Helicobacter pylori infection in chronic renal failure patients and in renal transplant recipients.Saudi journal of gastroenterology : official journal of the Saudi Gastroenterology Association · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the pathogenesis of gastroesophageal reflux disease (GERD), gastric acid is considered to be one of the most important factors, but little is known about the degree of gastric acid secretion in GERD patients. In this study, we evaluated it in GERD patients and control subjects by 24-h intragastric pH, and serological and histological investigations, in relation to Helicobacter pylori (H. pylori) status. In H. pylori-negative GERD patients gastric acid secretion was similar to that in H. pylori-negative control subjects. In H. pylori-positive GERD patients, in particular, mild GERD patients, it decreased significantly compared to that in H. pylori-negative control subjects, but the degree of decrease was smaller than in H. pylori-positive control subjects. Results of serological and histological evaluation were supportive. In conclusion, in some GERD patients, gastric acid secretion was significantly decreased. Increased or maintained gastric acid secretion was not essential in the pathogenesis of mild GERD.
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Registered trials
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