title: [CagA status and virulence of Helicobacter pylori strains. Results of a French multicentric prospective study].
abstract: Previous experimental and epidemiological studies with few patients suggested that the presence of the cagA gene was a virulence factor for Helicobacter pylori (H. pylori).
  
  
  OBJECTIVE
  To establish in this large epidemiological cohort study the relationship between the histological virulence of H. pylori infection and the cagA status of the bacteria.
  
  
  METHODS
  This prospective cohort study (6 month follow-up) was conducted on adult patients undergoing endoscopy for upper gastrointestinal symptoms. The cagA status of H. pylori-positive patients was established using the polymerase chain reaction (PCR) method on an antral biopsy. A score of histological virulence (inflammation, activity) was recorded on the basis of the Sydney system (on antral, angular and fundic biopsies). Eradication treatment given was not imposed and a clinical follow-up was performed at 3 and 6 months. H. pylori eradication was verified by a 13C urea breath test at 3 months.
  
  
  RESULTS
  Four hundred and twenty two centers recruited 652 patients (mean age: 51 +/- 15 years, 55% female). Upper GI endoscopy was abnormal in 80% of the patients of whom 68% had a gastritis aspect; 38% were infected by H. pylori, and among them 51% were cagA-positive. The histological virulence scores associated with the cagA-positive strains were significantly higher than those associated with the cagA-negative strains, globally (P = 0.0035), in the antrum (P = 0.0063), and in the angulus (P = 0.046), but not in the fundus (P = 0.05). The cagA status was correlated neither with the symptom severity at inclusion and at 6 months (P > 0.05), nor with the H. pylori eradication rate at 3 months (75% in cagA-positive and 70% in cagA-negative strains, P = 0.52).
  
  
  CONCLUSIONS
  This study on a large cohort of patients confirms the greater histological virulence of H. pylori cagA-positive strains. However, this virulence was not associated with more severe symptoms nor with an increase in resistance to H. pylori eradication treatment.
authors.affiliation: Service d'Hépato-Gastroentérologie, Hôtel Dieu, Clermont-Ferrand.
authors.forename: G
authors.initials: G
authors.lastname: Bommelaer
authors.forename: S
authors.initials: S
authors.lastname: Bruley Des Varannes
authors.forename: J F
authors.initials: JF
authors.lastname: Fléjou
authors.forename: T
authors.initials: T
authors.lastname: Matysiak
authors.forename: T
authors.initials: T
authors.lastname: Poynard
authors.forename: A
authors.initials: A
authors.lastname: Richard
authors.forename: A
authors.initials: A
authors.lastname: Slama
authors.forename: F
authors.initials: F
authors.lastname: Mégraud
mesh_terms: D000328:Adult; D000368:Aged; D000942:Antigens, Bacterial; D001426:Bacterial Proteins / Q000276:immunology*; D001706:Biopsy; D001944:Breath Tests; D015331:Cohort Studies; D005260:Female; D005602:France; D016481:Helicobacter Infections / Q000382:microbiology* / Q000473:pathology; D016480:Helicobacter pylori / Q000472:pathogenicity*; D006801:Humans; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D011446:Prospective Studies; D014508:Urea / Q000032:analysis; D014774:Virulence / Q000235:genetics
chemical_list: D000942:Antigens, Bacterial; D001426:Bacterial Proteins; C080866:cagA protein, Helicobacter pylori; D014508:Urea