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cagA positive and negative Helicobacter pyloristrains are simultaneously present in the stomach of most patients with non-ulcer dyspepsia: relevance to histological damage
  1. N Figuraa,
  2. C Vindignib,
  3. A Covaccic,
  4. L Presentib,
  5. D Burronic,
  6. R Vernillod,
  7. T Banduccid,
  8. F Roviellod,
  9. D Marrellid,
  10. M Biscontria,
  11. S Kristodhullua,
  12. C Gennaria,
  13. D Vairae
  1. aInstitute of Internal Medicine, University of Siena, Siena, Italy, bInstitute of Pathology, University of Siena, cIRIS, Siena, dInstitute of Surgical Clinics, University of Siena, eInstitute of Internal Medicine, University of Bologna, Bologna, Italy
  1. Dr N Figura, Institute of Internal Medicine, University of Siena, Policlinico Le Scotte, viale Bracci, I-53100 Siena, Italy.


Background/Aims—Infection with Helicobacter pylori strains harbouring the cagA gene (cagA+) is associated with an increased risk of developing peptic ulcer and gastric cancer. The aim of this study was to assess whether H pylori isolates with different cagA status were present in patients with non-ulcer dyspepsia, and whether a variable cagA status is relevant to histological gastric mucosal damage and glandular cell proliferation.

Methods—Well separated H pyloricolonies (between 2 and 25) from primary plates, per gastric area, for each of 19 patients with non-ulcer dyspepsia were examined forcagA by hybridisation. Western blotting was used to examine both representative colonies for CagA expression and the patients’ sera for antibody response to CagA. Glandular gastric cell proliferation was assessed immunohistochemically.

Results—Of the 747 colonies examined, 45.3% werecagA+. All colonies from four patients werecagA+, and all colonies from two patients werecagA−. In 13 patients (68%) both cagA+ andcagA− colonies were found. CagA expression of isolates corresponded to their cagA status. H pyloristrains with different CagA molecular masses were present in three patients. Results based on all 19 patients studied showed that the prevalence of cagA+ colonies in areas with mucosal atrophy associated or not with intestinal metaplasia (67.9%) was significantly higher than in normal mucosa (44.7%) and mucosa from patients with chronic gastritis (44.0%) (p< 0.001). High levels of cell proliferation were associated with histological atrophy with or without intestinal metaplasia, but not with the possession of cagA by organisms colonising the same mucosal sites.

Conclusions—Most patients with non-ulcer dyspepsia are infected by both cagA+ and cagA−H pylori colonies. The cagA status of infecting organisms may play a role in the development of atrophy and intestinal metaplasia.

  • gastritis; Helicobacter pyloriinfection
  • cagA
  • mucosal atrophy
  • cell proliferation

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