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Diagnosis of Helicobacter pylori infections

Pictogramme horloge Véronique Jacomo Pictogramme horloge April 2014

Helicobacter pylori is a Gram negative, highly mobile, helical bacteria that was characterised by Warren and Marshall in 1983, whose work in the role of this bacteria in the etiopathogenesis of gastroduodenal ulcers won them the Nobel prize in medicine in 2005. H. pylori infection is the most widely-spread bacterial infection in the world, afflicting 50% of the world’s population with vast geographic disparity.

Helicobacter pylori infection manifestations include acute gastritis that extends into chronic gastritis and may lead to a gastroduodenal ulcer.

In children, an ulcer is rare and less specific symptoms can be observed: abdominal pain, iron deficiency anaemia and thrombocytopenic purpura. In terms of epidemiology, the stomach of humans and primates is the reservoir for this bacteria and human-to-human contamination occurs in a faecal-oral and oral-oral manner.

Once the bacteria enters into the body, it provokes an inflammatory reaction of the gastric mucosa with both a tissue and humoral immune response. Amongst those suffering from such an infection, only 1-2% develop symptoms. The gastritis can remain stable or develop further to become an ulcer or evoke mucosal atrophy and a adenocarcinoma. It has been noted that over 90% of those with a gastroduodenal ulcer are infected with H. pylori.

The indications for the screening of Helicobacter pylori are listed in the Maastricht IV consensus report (2010) and are as follows:

  • Active or former gastroduodenal ulcer
  • Non-ulcer dyspepsia
  • Long-term low-dose aspirin treatment or NSAIDs treatment
  • Patients with a high risk of cancer (those suffering from pre-neoplastic lesions or with a family history of gastric cancer)
  • Extra digestive diseases: Idiopathic thrombocytopenic purpura, iron deficiency anaemia of unknown cause and vitamin B12 deficiency

The screening and biological diagnosis relies on both invasive and non-invasive methods.

Among the non-invasive methods, the breath test relies on the urease activity of this bacteria and measures this activity in the patient’s expired breath via mass spectrometry analysis of the different proportions of C13/C12 before and after ingestion of labelled urea. To perform this test, the patient must stop all antibiotic treatments one month prior to examination and stop proton pump inhibitors (PPI) 15 days prior to examination.

  • The detection of antigens in stool samples is reserved for the monitoring of patient progress following treatment in order to verify the eradication of Helicobacter pylori (except in children, where this test can be used as a screening technique).
  • Serology testing does not distinguish between a recent past infection because it does not detect IgM (too transient). It detects IgG antibodies which are associated with the infection but appear relatively late in the infection (3 weeks after initial infection) and remain raised throughout the duration of the infection. They return to a normal level after approximately 1 year. Furthermore, asymptomatic Helicobacter pylori carrier patients have a positive serology result and represent 50% of the adult population. Its positivity several months following eradication means it cannot be used as a tool for post-treatment verifications. Its indications are therefore limited to digestive bleeding, gastric atrophy, MALT lymphomas and gastric carcinoma as the bacterial inoculum is weak in this clinical setting, thus compromising the use of other laboratory tests.

The invasive methods are performed on biopsy fragments collected from the gastric antrum and gastric fundus during a gastroduodenal fibroscopy. At the same time, the biopsies are crushed and cultured under microaerophilic conditions for 12 days. This micro-organism of often fastidious growth can also be screened for using PCR analysis on biopsy samples, which allows for simultaneous screening of clarithromycin and fluoroquinolone resistance genes. The therapeutic approach must differ according to whether the patient lives in a zone with a high incidence or low incidence of cancer. In high incidence zones, systematic eradication of this bacteria is clinically justified. In low incidence zones, such as France, it seems reasonable, in asymptomatic cases, to reserve the screening of Helicobacter pylori infection and pre-neoplastic lesions for patients with a high-risk of developing cancer.


  • Malfertheiner P, Megraud F, O’Morain C, Bazzoli F, El-Omar E, Graham D, et al.
    Current concepts in the management of Helicobacter pylori infection – The Maastricht III Consensus Report.
    Gut 2007.
  • Cambau E, Allerheiligen V, Coulon C, Corbel C, Lascols C, Deforges L, et al.
    Evaluation of a new test, genotype HelicoDR, for molecular detection of antibiotic resistance in Helicobacter pylori.
    J Clin Microbiol 2009;47(11):3600-7.
  • Graham DY, Fischbach
    L. Helicobacter pylori treatment in the era of increasing antibiotic resistance.
    Gut 2010;59(8):1143-53.


Table 1 : performance of non-invasive methods
 Performances Serology Breath Test
Ag screening in stools
Pre-therapeutic DiagnosisExcellent for certain ELISA kits Poor for all rapid testsExcellent

Excellent specificity

Sensitivity: depending on the condition and experience

Verify eradicationNot adaptedExcellentGood
CharacteristicsRecommended for initial diagnosis
when other tests prove to be defective
(haemorrhagic ulcer, MALT, antibiotic treatment,
proton pump inhibitors)
Not influenced by bacterial density
Stop antibiotic treatment
4 weeks prior and PPIs
2 weeks prior to testing
Recommended as a
confirmation test for
eradication when breath
tests are not possible
Table 2 : performance of invasive methods
 Urease Test
 Histology Culture Gene Amplification
Pre-therapeutic DiagnosisGoodExcellent (5 biopsies)Excellent specificity
Sensitivity: depending on the
condition and experience
Verify eradicationInsufficient sensitivityGoodGoodInsufficient data
Cannot be used to verify eradication
Depends on the bacterial density
Mucosal lesions detected
Reference method
Antibiotic resistance
whenever possible
(therapeutic failure)
Detection of fluoroquinone and
clarithromicin resistance genes


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