Practice Uncertainties Page

Whom should we “test and treat” for Helicobacter pylori?

BMJ 2014; 348 doi: https://doi.org/10.1136/bmj.g3320 (Published 20 May 2014) Cite this as: BMJ 2014;348:g3320
  1. Alexander C Ford, associate professor and honorary consultant gastroenterologist12,
  2. Paul Moayyedi, director division of gastroenterology3
  1. 1Leeds Gastroenterology Institute, Leeds General Infirmary, Leeds, UK
  2. 2Leeds Institute of Biomedical and Clinical Sciences, Leeds University, Leeds, UK
  3. 3Farncombe Family Digestive Health Research Institute, McMaster University, McMaster University Medical Centre, Hamilton, Ontario, Canada
  1. Correspondence to: P Moayyedi moayyep{at}mcmaster.ca
  • Accepted 9 May 2014

The possibility that peptic ulcer and gastric cancer could be an infectious disease would have been dismissed as ridiculous 30 years ago. We now realise that Helicobacter pylori infection is the major cause of both. As H pylori infection has been implicated in various upper gastrointestinal diseases, testing for the bacterium non-invasively and treating infected individuals (“test and treat”) has become widespread. The key question is in which group of patients is this approach appropriate?

What is the evidence of the uncertainty?

We searched MEDLINE, Clinical Evidence, the Cochrane central register of controlled trials, the Cochrane library, and http://clinicaltrials.gov to identify published and ongoing randomised controlled trials and systematic reviews that have assessed the effect of “test and treat” in patients with upper gastrointestinal diseases, including peptic ulcer disease, gastro-oesophageal reflux disease, functional dyspepsia, and uninvestigated dyspepsia, as well as in people in the community.

Peptic ulcer disease

H pylori is causally implicated in the pathogenesis of pyloric ulcer disease.1 A systematic review and meta-analysis of randomised controlled trials of eradication therapy versus placebo in H pylori positive disease showed that eradication therapy was cost effective compared with long term acid suppression and led to significantly lower rates of duodenal and gastric ulcer relapse, with numbers needed to treat (NNT) to prevent one ulcer relapse of 2 and 3 respectively.2

Gastro-oesophageal reflux disease

A systematic review of observational studies showed that the prevalence of H pylori was significantly lower in people with gastro-oesphageal reflux disease than in healthy controls, suggesting that infection may be protective.3 This is biologically plausible because H pylori can induce an atrophic gastritis, which may reduce production of gastric acid. However, the association could also be the result of a confounding by socioeconomic status (reflux disease is more common in higher socioeconomic groups,4 whereas H pylori …

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