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Helicobacter pylori infection prevents erosive reflux oesophagitis by decreasing gastric acid secretion

BACKGROUND Helicobacter pylori infection is less prevalent and atrophic gastritis is less extensive in patients with reflux oesophagitis than those without it, but few studies have examined this relationship directly. AIMS We investigated the relationship between H pylori infection, acid secretion,...

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Bibliographic Details
Published in:Gut 2001-09, Vol.49 (3), p.330-334
Main Authors: Koike, T, Ohara, S, Sekine, H, Iijima, K, Abe, Y, Kato, K, Toyota, T, Shimosegawa, T
Format: Article
Language:English
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Summary:BACKGROUND Helicobacter pylori infection is less prevalent and atrophic gastritis is less extensive in patients with reflux oesophagitis than those without it, but few studies have examined this relationship directly. AIMS We investigated the relationship between H pylori infection, acid secretion, and reflux oesophagitis in Japanese subjects. SUBJECTS A total of 105 patients with erosive reflux oesophagitis were compared with 105 sex and age matched patients without reflux oesophagitis. METHODS The diagnosis of H pylori infection was made by histological examination of gastric mucosal biopsy specimens, rapid urease test, and detection of serum IgG antibodies. Acid secretion was assessed by the endoscopic gastrin test. RESULTS H pylori infection was present in 36 patients with erosive reflux oesophagitis (34.3%) and in 80 control subjects (76.2%) (odds ratio 0.163, 95% confidence interval 0.09–0.29). Overall acid secretion was significantly greater in patients with reflux oesophagitis. AmongH pylori positive patients, acid secretion was greater in patients with reflux oesophagitis than those without oesophagitis. CONCLUSION In Japan, erosive reflux oesophagitis occurs most often in the absence ofH pylori infection and gastric hyposecretion. Even in the presence of H pylori infection, reflux oesophagitis is more likely to develop in patients without gastric hyposecretion. H pylori infection may inhibit reflux oesophagitis by inducing hypoacidity.
ISSN:0017-5749
1468-3288
1458-3288
DOI:10.1136/gut.49.3.330