One reason for the variable effect of Helicobacter pylori infection and its eradication on acid secretion is the dependence on the type and distribution of gastritis . Non-atrophic predominantly antral
Table 1. Odds ratio for prevalence of Helicobacter pylori in patients with esophagitis , 
_ Goldblum et al(1998)
Varanasi etal (1998) . Vicari etal (1998)
_ Schubert etal (1989)
Fal lone etal (2000) Far East
Shirota et al (1999) Wu etal (1999) Mihari etal (1996) Harumaetal (2000) Koike etal (2001)
gastritis results in hypergastrinaemia and acid hypersecretion. Corpus predominant or atrophic pangastritis lead to decreased acid production and therefor can play a somehow protective role for oesophageal acid exposure (—, Figs. 2 and 3).
If Helicobacter pylori is eradicated, gastritis with low acid output is healed leading to higher acid exposure of the esophagus and possibly resulting in GORD  if gastro-oesophageal reflux barrier is impaired . As many Helicobacter pylori infected patients without disease have a mixed pattern of gastritis, the elevated gastrin resulting from antral inflammation fails to cause gastric acid secretion because of corpus inflammation.
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