title: Lower prevalence of Helicobacter pylori infection with vacAs1a, cagA-positive, and babA2-positive genotype in erosive reflux esophagitis disease.
abstract: BACKGROUND
  Increased prevalence of esophagitis has been recognized in the West. Helicobacter pylori infection, particularly virulent strains, is proposed as a protective factor against the development of gastroesophageal reflux disease. To evaluate the relationship of reflux esophagitis with virulent H. pylori infection, we studied the prevalence of reflux esophagitis among H. pylori-infected and -uninfected patients and the genotype of isolates in Taiwan.
  
  
  METHODS
  Patients who had routine physical examination were investigated. The severity of esophagitis was evaluated using the Los Angeles grading system. H. pylori status was assessed by histology, rapid urease test, and bacterial culture. Genotyping of vacA, cagA, and babA2 was determined by polymerase chain reaction (PCR). Risk factors for severe esophagitis were evaluated.
  
  
  RESULTS
  Reflux esophagitis was found in 21.2% of 1622 patients. The prevalence of H. pylori infection was found in 33.0% of 276 patients with reflux esophagitis compared with 67.5% of 378 patients with normal esophagus (p < .001). Esophagitis occurred in a significantly lower rate among H. pylori-positive patients with peptic ulcer than those without peptic ulcer. cagA, babA2, and vacAs1a were detected in 100% of 143 isolates. Factors that predicted severe esophagitis included age, gender, and hiatus hernia but not H. pylori infection.
  
  
  CONCLUSIONS
  Our study suggests significantly lower incidence of H. pylori infection with the triple-positive virulent genotype in patients with reflux esophagitis in Taiwan.
authors.affiliation: Institute of Molecular and Cellular Biology and Department of Life Sciences, National Tsing Hua University, Hsinchu, Taiwan.
authors.forename: Chih-Ho
authors.initials: CH
authors.lastname: Lai
authors.forename: Sek-Kwong
authors.initials: SK
authors.lastname: Poon
authors.forename: Yun-Chu
authors.initials: YC
authors.lastname: Chen
authors.forename: Chi-Sen
authors.initials: CS
authors.lastname: Chang
authors.forename: Wen-Ching
authors.initials: WC
authors.lastname: Wang
mesh_terms: D018829:Adhesins, Bacterial / Q000235:genetics / Q000378:metabolism; D000328:Adult; D000368:Aged; D000942:Antigens, Bacterial / Q000235:genetics / Q000378:metabolism; D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism; D004942:Esophagitis, Peptic / Q000150:complications* / Q000453:epidemiology* / Q000382:microbiology; D005260:Female; D005838:Genotype; D016481:Helicobacter Infections / Q000150:complications* / Q000453:epidemiology* / Q000382:microbiology; D016480:Helicobacter pylori / Q000145:classification / Q000235:genetics / Q000378:metabolism / Q000472:pathogenicity*; D006801:Humans; D015994:Incidence; D008297:Male; D008875:Middle Aged; D015995:Prevalence; D013624:Taiwan / Q000453:epidemiology; D014774:Virulence
chemical_list: D018829:Adhesins, Bacterial; D000942:Antigens, Bacterial; C400429:BabA protein, Helicobacter pylori; D001426:Bacterial Proteins; C074689:VacA protein, Helicobacter pylori; C080866:cagA protein, Helicobacter pylori