title: [Prevalence of intestinal metaplasia of the gastric cardia and its relation with Helicobacter pylori strains cagA and vacA].
abstract: BACKGROUND
  Esophageal metaplasia progression is a consequence of chronic gastroesophageal reflux (CGR). Patients with this condition are frequently infected by Helicobacter pylori and show several symptoms including gastritis as well as ulcer formation. In addition, they present an increased risk for the development of gastric adenocarcinoma. Several pathogenic markers for Helicobacter pylori such as ureC, vacA and cagA genes have been described. Evidence indicates that direct injury to the epithelial mucosa is caused by cytotoxins and enzymes codified by these genes. We undertook this study to establish a relationship between the presence of pathogenic Helicobacter pylori strains and the presence of metaplasia progression in patients with CGR.
  
  
  METHODS
  We detected the presence of Helicobacter pylori cagA and vacA positive strains in patients with CGR. Using polymerase chain reaction, we analyzed 120 samples obtained from 60 patients with CGR and 60 control group patients, including samples from both anatomic areas: cardia and gastric antrum.
  
  
  RESULTS
  We detected 56% of Helicobacter pylori positive patients; 57.5% of these patients were positive for either cagA(+) and/or vacA(+) Helicobacter pylori strains. Cardiac intestinal metaplasia was observed in 35% of the patients. A marked tendency was observed to develop cardiac intestinal metaplasia in those patients diagnosed with high-pathogenicity strains infected in both anatomic areas.
  
  
  CONCLUSIONS
  These results suggest that infection with Helicobacter pylori can be considered a risk factor for developing gastric cardiac intestinal metaplasia.
authors.affiliation: Dirección General Adjunta Médica, Hospital General de México OD, Secretaría de Salud, México, D. F., Mexico. drjuanmiguelabdo@yahoo.com.mx
authors.forename: Juan Miguel
authors.initials: JM
authors.lastname: Abdo-Francis
authors.forename: Sergio
authors.initials: S
authors.lastname: Sobrino-Cossío
authors.forename: Fernando
authors.initials: F
authors.lastname: Bernal-Sahagún
authors.forename: Angélica
authors.initials: A
authors.lastname: Hernández-Guerrero
mesh_terms: D000328:Adult; D000368:Aged; D000942:Antigens, Bacterial / Q000235:genetics*; D001426:Bacterial Proteins / Q000235:genetics*; D001471:Barrett Esophagus / Q000453:epidemiology* / Q000209:etiology / Q000382:microbiology / Q000473:pathology; D001706:Biopsy; D002299:Cardia / Q000473:pathology*; D003430:Cross-Sectional Studies; D005260:Female; D005757:Gastritis, Atrophic / Q000150:complications / Q000382:microbiology / Q000473:pathology*; D005764:Gastroesophageal Reflux / Q000150:complications; D005773:Gastroscopy; D016481:Helicobacter Infections / Q000150:complications / Q000382:microbiology / Q000473:pathology*; D016480:Helicobacter pylori / Q000235:genetics / Q000302:isolation & purification / Q000472:pathogenicity*; D006801:Humans; D008297:Male; D008679:Metaplasia / Q000453:epidemiology / Q000209:etiology; D008875:Middle Aged; D009504:Neutrophils / Q000473:pathology; D011230:Precancerous Conditions / Q000453:epidemiology / Q000209:etiology / Q000382:microbiology / Q000473:pathology; D011446:Prospective Studies; D013045:Species Specificity; D014774:Virulence; D055815:Young Adult
chemical_list: D000942:Antigens, Bacterial; D001426:Bacterial Proteins; C074689:VacA protein, Helicobacter pylori; C080866:cagA protein, Helicobacter pylori