title: Helicobacter pylori infection, not gastroesophageal reflux, is the major cause of inflammation and intestinal metaplasia of gastric cardiac mucosa.
abstract: OBJECTIVE
  The etiology of inflammation below the normal Z-line is an area of intense debate. Some suggest this is the earliest change of chronic gastroesophageal reflux disease (GERD), whereas others indict Helicobacter pylori (H. pylori) as the main cause. The aim of this study was to evaluate the relationship among inflammation of gastric cardiac mucosa (carditis), H. pylori infection, and intestinal metaplasia in patients with GERD and Barrett's esophagus compared with age-matched controls.
  
  
  METHODS
  Patients with GERD and Barrett's esophagus were compared with controls undergoing endoscopy for a variety of other conditions. Endoscopic biopsy specimens from the gastric cardia (obtained on retroflexed view), fundus, and antrum were evaluated for inflammation, H. pylori infection, and intestinal metaplasia.
  
  
  RESULTS
  The prevalence of H. pylori infection did not significantly differ among the study populations: controls (42%), GERD (33%), and Barrett's esophagus (27%) (p = 0.20). However, the prevalence of carditis significantly decreased from the control group (30%) to those with GERD (23%) and Barrett's esophagus (11%) (p = 0.03). Overall, 42 of 51 (82%) patients with carditis had H. pylori; all had pangastritis. The prevalence of cardia intestinal metaplasia also significantly decreased from the control group (15%) to those with GERD (4%) and Barrett's esophagus (0%) (p = 0.003). Of 13 patients with cardia intestinal metaplasia, 12 had carditis, 10 had H. pylori infection, and seven had intestinal metaplasia elsewhere in the stomach.
  
  
  CONCLUSIONS
  Inflammation of gastric cardiac mucosa decreases in prevalence from controls to patients with GERD and Barrett's esophagus and correlates strongly with H. pylori infection. Cardia intestinal metaplasia is associated with H. pylori-related cardiac inflammation and intestinal metaplasia elsewhere in the stomach.
authors.affiliation: Center for Swallowing and Esophageal Disorders and Department of Anatomic Pathology, Cleveland Clinic Foundation, Ohio 44195, USA.
authors.forename: John R
authors.initials: JR
authors.lastname: Goldblum
authors.forename: Joel E
authors.initials: JE
authors.lastname: Richter
authors.forename: Michael
authors.initials: M
authors.lastname: Vaezi
authors.forename: Gary W
authors.initials: GW
authors.lastname: Falk
authors.forename: Thomas W
authors.initials: TW
authors.lastname: Rice
authors.forename: Richard M
authors.initials: RM
authors.lastname: Peek
mesh_terms: D000328:Adult; D017677:Age Distribution; D000368:Aged; D000369:Aged, 80 and over; D000704:Analysis of Variance; D001471:Barrett Esophagus / Q000150:complications / Q000473:pathology; D001707:Biopsy, Needle; D002299:Cardia / Q000473:pathology; D016022:Case-Control Studies; D015331:Cohort Studies; D004945:Esophagoscopy / Q000379:methods; D005260:Female; D005753:Gastric Mucosa / Q000473:pathology*; D005756:Gastritis / Q000453:epidemiology* / Q000209:etiology* / Q000473:pathology; D005764:Gastroesophageal Reflux / Q000150:complications / Q000473:pathology; D005773:Gastroscopy / Q000379:methods; D016481:Helicobacter Infections / Q000150:complications* / Q000473:pathology; D016480:Helicobacter pylori / Q000302:isolation & purification*; D006801:Humans; D007413:Intestinal Mucosa / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D015995:Prevalence; D011379:Prognosis; D018570:Risk Assessment; D012307:Risk Factors; D017678:Sex Distribution