Abstract

The role of Helicobacter pylori in non-ulcer dyspepsia continues to be controversial. While there is general agreement that incident infection with H. pylori can induce self-limited symptoms, the evidence linking the infection to chronic upper abdominal pain or discomfort in the absence of peptic ulceration is equivocal. The prevalence of H. pylori is at most only slightly increased in non-ulcer dyspepsia over the background population taking into account age, socioeconomic status and past ulcer history. However, it is yet to be convincingly shown that H. pylori precedes the onset of non-ulcer dyspepsia. It is now accepted that H. pylori is not associated with a specific symptom profile. Recent evidence suggests that a subgroup with H. pylori and non-ulcer dyspepsia have increased acid secretion in response to gastrin-releasing peptide, but gastric motor and sensory function appears not to be affected by the infection. The most persuasive evidence for a causal relationship between the infection and non-ulcer dyspepsia will come from ongoing large multicentre randomized placebo controlled trials, as the relatively small therapeutic trials to date have been unconvincing.

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