title: Helicobacter pylori, ethnicity, and the gastroesophageal reflux disease spectrum: a study from the East.
abstract: BACKGROUND
  Ethnic differences in gastroesophageal reflux disease (GERD) and its complications as well as racial variations in the prevalence of Helicobacter pylori infection are well documented. Nevertheless, the association between reflux disease, H. pylori, and race has not been adequately explored.
  
  
  OBJECTIVE
  We estimated the strength of the association between H. pylori, ethnicity, and the gastroesophageal reflux disease (GERD) spectrum, including Barrett's esophagus, in Asian patients presenting for endoscopy in a tertiary referral center.
  
  
  METHODS
  Prospectively, we studied 188 consecutive patients with GERD, short- and long-segment Barrett's esophagus, and controls. All patients underwent gastroscopy with gastric biopsies to assess H. pylori, gastritis, and atrophy. CagA status and H. pylori infection were determined by immunoblot assay.
  
  
  RESULTS
  The overall prevalence of H. pylori infection was 52.1% (of which 77.6% were cagA(+)) and was lowest in the long-segment Barrett's esophagus group (36.7%) (p = .048). When Barrett's esophagus was present, the length of abnormality was 44.8% shorter in the presence of H. pylori (p = .015). Indians had the highest prevalence of H. pylori (75%) and Malays the lowest (19.6%) (p < .001). In Indians, increased prevalence of H. pylori and cagA-positive strains was associated with reduced severity of GERD (p < .004 and p < .001, respectively), a trend not apparent in the other races. Corpus atrophy, which was almost exclusively associated with H. pylori, was highest in Indians as compared to the other races (p = .013).
  
  
  CONCLUSIONS
  Presence of H. pylori was associated with a reduced severity of GERD spectrum disease in Asians, especially Indians. H. pylori infection may protect against complicated reflux disease via induction of corpus atrophy.
authors.affiliation: Division of Gastroenterology, Department of Medicine, Royal College of Medicine, Perak, Malaysia. shanraj@dhhs.tas.gov.au
authors.forename: Shanmugarajah
authors.initials: S
authors.lastname: Rajendra
authors.forename: Roger
authors.initials: R
authors.lastname: Ackroyd
authors.forename: Iain K
authors.initials: IK
authors.lastname: Robertson
authors.forename: Jacqueline J
authors.initials: JJ
authors.lastname: Ho
authors.forename: Norain
authors.initials: N
authors.lastname: Karim
authors.forename: Kannan M
authors.initials: KM
authors.lastname: Kutty
mesh_terms: D000328:Adult; D000942:Antigens, Bacterial / Q000235:genetics; D001426:Bacterial Proteins / Q000235:genetics; D001471:Barrett Esophagus / Q000453:epidemiology / Q000382:microbiology; D016022:Case-Control Studies; D005260:Female; D005764:Gastroesophageal Reflux / Q000453:epidemiology / Q000208:ethnology* / Q000473:pathology; D016481:Helicobacter Infections / Q000453:epidemiology / Q000208:ethnology*; D016480:Helicobacter pylori / Q000235:genetics / Q000472:pathogenicity; D006801:Humans; D008296:Malaysia / Q000453:epidemiology / Q000208:ethnology; D008297:Male; D008875:Middle Aged; D015995:Prevalence; D011446:Prospective Studies
chemical_list: D000942:Antigens, Bacterial; D001426:Bacterial Proteins; C080866:cagA protein, Helicobacter pylori