title: Helicobacter pylori CagA status, mucosal oxidative damage and gastritis phenotype: a potential pathway to cancer?
abstract: BACKGROUND
  Oxidative DNA damage is associated with Helicobacter pylori infection, atrophy and intestinal metaplasia. H. pylori-cagA-positive strains are associated with the highest risk of gastric cancer.
  
  
  OBJECTIVE
  To ascertain whether cagA-positive H. pylori infection correlates with higher concentrations of 8OHdG and the presence of precancerous changes.
  
  
  METHODS
  118 patients were studied (65M/53F, age 61 +/- 14 years). Twelve were H. pylori-negative. Among the H. pylori-positive patients, 34 were cagA-positive and 40 were cagA negative. In 32 patients H. pylori had been eradicated at least 6 months before endoscopic sampling. The phenotype of the gastritis (atrophic compared with nonatrophic, with and without intestinal metaplasia) was scored in biopsy samples obtained from the antrum, corpus, and angularis incisura. In antral biopsy samples, 8-hydroxydeoxyguanosine was assessed by HPLC (electrochemical detector). CagA status was determined by PCR.
  
  
  RESULTS
  The highest scores for both mononuclear inflammation and activity of gastritis were significantly associated with cagA status (p = 0.036 antrum and p = 0.02 corpus). cagA-positive infection significantly correlated with a higher prevalence of atrophic-metaplastic lesions (p = 0.04). cagA-positive patients had higher 8-hydroxydeoxyguanosine levels than both cagA-negative and H. pylori-negative cases (p = 0.01). The 8-hydroxydeoxyguanosine levels were significantly higher in multifocal atrophic gastritis (p = 0.04). The odds ratio for cagA-positive patients having 8OHdG levels above a cut-off calculated on the basis of the ROC curves were 7.12, overall, reaching 11.25 when only patients younger than 50 were considered.
  
  
  CONCLUSIONS
  cagA-positive patients were characterized: first, for higher scores for gastritis, activity and atrophic and metaplastic lesions; and second for greater oxidative DNA damage overall, at younger age and in the presence of multifocal atrophy. This setting may represent a cancer-prone biological context.
authors.affiliation: Dipartimento di Scienze Chirurgiche e Gastroenterologiche - Sezione di Gastroenterologia, Università degli Studi di Padova, Italy.
authors.forename: Fabio
authors.initials: F
authors.lastname: Farinati
authors.forename: Romilda
authors.initials: R
authors.lastname: Cardin
authors.forename: Valentina M
authors.initials: VM
authors.lastname: Russo
authors.forename: Graziella
authors.initials: G
authors.lastname: Busatto
authors.forename: Monica
authors.initials: M
authors.lastname: Franco
authors.forename: Massimo
authors.initials: M
authors.lastname: Rugge
mesh_terms: D000080242:8-Hydroxy-2'-Deoxyguanosine; D000368:Aged; D000942:Antigens, Bacterial / Q000235:genetics*; D001426:Bacterial Proteins / Q000235:genetics*; D018736:DNA Adducts / Q000378:metabolism; D004249:DNA Damage; D003849:Deoxyguanosine / Q000031:analogs & derivatives* / Q000378:metabolism; D005260:Female; D005753:Gastric Mucosa / Q000378:metabolism* / Q000382:microbiology; D005756:Gastritis / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D016481:Helicobacter Infections / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D016480:Helicobacter pylori / Q000235:genetics*; D006801:Humans; D007422:Intestines / Q000473:pathology; D008297:Male; D008679:Metaplasia; D008875:Middle Aged; D018384:Oxidative Stress; D010641:Phenotype; D012044:Regression Analysis; D013274:Stomach Neoplasms / Q000378:metabolism / Q000382:microbiology*
chemical_list: D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D018736:DNA Adducts; C080866:cagA protein, Helicobacter pylori; D000080242:8-Hydroxy-2'-Deoxyguanosine; D003849:Deoxyguanosine