Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013395 (dyspepsia)
 4,879 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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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PMID:Helicobacter pylori and non-ulcer dyspepsia. 889 31

A major role for Helicobacter pylori gastritis in nonulcer dyspepsia (NUD) is controversial. Gastroduodenal dysfunction may be associated with H. pylori infection, but there is little evidence for a causal link with dyspepsia. Population-based studies with appropriate methodology have generally failed to confirm an association between H. pylori and NUD. Furthermore, no definite association between subgroups of NUD (ulcer-like, dysmotility-like, reflux-like, and nonspecific) and H. pylori has been identified however the subgroups have been defined, and no specific symptom pattern characterizes patients with H. pylori infection. Whether H. pylori-induced alterations of gastric physiology can explain NUD remains open to debate while we await the results of more specific experiments. Although acid secretion in response to gastrin-releasing peptide may be increased in a subset of NUD patients who are infected with H. pylori, uninfected patients with NUD have not been assessed and the results require confirmation. Most studies suggest no association between H. pylori and gastroduodenal motor or sensory dysfunction in NUD. Treatment trials have been unconvincing. The trials with bismuth therapy have not been adequately blinded. Furthermore, some studies suggest that H. pylori-negative patients with NUD may respond to bismuth treatment, although the results have not been uniform. Therapies aimed at curing H. pylori infection have produced mixed results, with small positive and negative trials. The trials that have used adequate outcome measures have more often than not been negative. Based on current evidence, H. pylori is not established to be of causal importance in NUD.
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PMID:What role does Helicobacter pylori play in dyspepsia and nonulcer dyspepsia? Arguments for and against H. pylori being associated with dyspeptic symptoms. 939 64