title: Helicobacter pylori genotypes can predict gastric tissue histopathology: a longitudinal study of Iranian patients.
abstract: BACKGROUND
  Several factors have been suggested to account for differences in the virulence of Helicobacter pylori infections in various populations. Evidence suggests the existence of different strains of H. pylori with different degrees of virulence. The present study aimed to investigate the gastric histopathology in Iranian patients infected with H. pylori and to investigate the relationship between the severity of gastritis and four different bacterial virulence-associated genotypes.
  
  
  METHODS
  All of the patients with positive results from a pathological examination, a rapid urease test, and PCR analysis for H. pylori infection were consecutively included into the study. The classification and grading of gastritis were performed according to the Sydney System. Esophagitis was classified endoscopically according to the Savary-Miller grading system. The primers used in this study targeted 16S rRNa (521 bp), Urease A (411 bp), Cag A (400 bp), and 26 kDa (303 bp).
  
  
  RESULTS
  Twenty-eight patients were included in the study. The presence of Cag A showed a significant relationship with higher gastritis grades (3.0±0.7 vs. 2.3±0.9, p=0.024) and higher scores for H. pylori infection (3.0±0.7 vs. 2.3±0.7, p=0.027). The patients infected with 26 kDa-positive H. pylori had significantly higher infection scores (3.5±0.6 vs. 2.5±0.6, p=0.020).
  
  
  CONCLUSIONS
  This study showed that CagA-positive H. pylori infection is associated with more severe gastritis and with increased bacterial density and inflammation in the biopsy specimens. The 303-bp positive genotype was also significantly associated with higher grades of esophagitis. Additional in-depth trials will be helpful in extending our findings.
authors.affiliation: Baqiyatallah Research Center for Gastroenterology & Liver Diseases, Tehran, Iran. Khedmat.h@gmail.com
authors.forename: Hossein
authors.initials: H
authors.lastname: Khedmat
authors.forename: Ali
authors.initials: A
authors.lastname: Karami
authors.forename: Zahra
authors.initials: Z
authors.lastname: Safiri
authors.forename: Mohsen
authors.initials: M
authors.lastname: Amini
authors.forename: Ali
authors.initials: A
authors.lastname: Bakhtiari
authors.forename: Ashraf
authors.initials: A
authors.lastname: Karbasi
authors.forename: Mojgan
authors.initials: M
authors.lastname: Jayhounian
authors.forename: Hamidreza
authors.initials: H
authors.lastname: Jalalian
authors.forename: Saeed
authors.initials: S
authors.lastname: Taheri
mesh_terms: D000328:Adult; D000368:Aged; D000942:Antigens, Bacterial / Q000235:genetics; D058491:Bacterial Load; D001426:Bacterial Proteins / Q000235:genetics; D004269:DNA, Bacterial / Q000235:genetics; D004941:Esophagitis / Q000473:pathology; D005260:Female; D005753:Gastric Mucosa / Q000473:pathology; D005756:Gastritis / Q000473:pathology; D005838:Genotype; D016481:Helicobacter Infections / Q000382:microbiology* / Q000473:pathology*; D016480:Helicobacter pylori / Q000145:classification* / Q000235:genetics / Q000302:isolation & purification / Q000472:pathogenicity*; D006651:Histocytochemistry; D006801:Humans; D007492:Iran; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D012720:Severity of Illness Index; D014510:Urease / Q000032:analysis; D014774:Virulence
chemical_list: D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D004269:DNA, Bacterial; C080866:cagA protein, Helicobacter pylori; D014510:Urease