Skip to main content
The BMJ logoLink to The BMJ
. 2002 May 25;324(7348):1263. doi: 10.1136/bmj.324.7348.1263

Helicobacter pylori breath tests

Abi Berger 1
PMCID: PMC1123218  PMID: 12028983

H pylori diagnostic breath tests rely on a simple chemical reaction which is based on the natural behaviour of the bacteria. Naturally occuring gastric urea is made up of 99% carbon isotope 12C and 1% carbon isotope 13C. The breath test uses urea enriched with 13C (that is, 99%).

Patients first drink a sachet of orange juice or citric acid. This rapidly closes the duodenal sphincter to contain the stomach contents. They are then asked to blow through a straw into a glass tube with a screw cap lid. This provides the baseline sample.

Next, they consume a drink containing 13C enriched urea (about 100 ml) and after 30 minutes repeat the blowing exercise into a second tube. This provides the post-dose sample. Both samples are sent away for carbon dioxide isotope analysis by mass spectrometry (laboratories usually return the results within a few days).

The level of 13C in the baseline sample will be normal. If levels rise in the post-dose sample, this suggests the presence of H pylori. The enriched urea provided by the testing kit must have been broken down to produce high levels of 13C in the breath and this implies the presence of urease excreting H pylori in the stomach.

If the post-dose 13C concentration is 3.5 parts per 1000 more than the baseline sample, the test is considered positive for H pylori. The higher the level of 13C, the greater the extent of the infection. Levels of 30-40 parts per 1000 over the baseline result are typical of H pylori infections.

Two back-up tubes are generally also taken at baseline and post-dose stages.

The sensitivity of such diagnostic kits is 96% and the specificity is 100%. graphic file with name hpbt.f5.jpg

Figure.

Figure

1 Virtually all duodenal ulcers and 80% of gastric ulcers are associated with Helicobacter pylori infections1

Figure.

Figure

2 H pylori survives in gastric acid by excreting large amounts of urease. This enzyme breaks down any urea in the stomach to ammonia and carbon dioxide

Figure.

Figure

3 The ammonia neutralises any acid found directly in the vicinity of the bacteria, allowing the bacteria to survive

Figure.

Figure

4 The carbon dioxide is absorbed into the blood stream and then released from the lungs

References

  1. Graham DY. Helicobacter pylori infection in the pathogenesis of duodenal ulcer and gastric cancer: a model. Gastroenterology. 1997;113(6):1983–1991. doi: 10.1016/s0016-5085(97)70019-2. [DOI] [PubMed] [Google Scholar]

Articles from BMJ : British Medical Journal are provided here courtesy of BMJ Publishing Group

RESOURCES