title: Prevalence and pattern of Helicobacter pylori gastritis in the gastric cardia.
abstract: OBJECTIVE
  Helicobacter pylori has a predilection for antral colonization. Local acid production is the major determinant of colonization. Because production is low in the antrum and cardia, H. pylori should also colonize the cardia. We therefore investigated the histologic pattern of gastritis and the prevalence of H. pylori in the cardia compared with the antrum and corpus.
  
  
  METHODS
  From 135 H. pylori-infected patients with gastritis, ulcer disease, or reflux esophagitis, biopsies were obtained from the antrum, corpus, and cardia. The prevalence, topography, and histologic parameters of gastritis were examined.
  
  
  RESULTS
  All 135 patients had active antral H. pylori gastritis: in the cardia, 132 of these patients (97.7%) showed active gastritis, and 124 patients (91.9%) had H. pylori visible on staining. Gastritis of the cardia in most patients resembled antral gastritis, but the density of bacteria and the inflammatory responses were less marked. The most striking finding in the cardia of patients with gastroesophageal reflux was a lower density of bacteria compared with antrum and corpus. Intestinal metaplasia was found in 32 patients in antral mucosa (23.7%) versus 28 patients in the cardia (20.7%), versus 11 patients in the corpus (8.1%), and was multifocal in 17 patients (12.6%).
  
  
  CONCLUSIONS
  H. pylori gastritis commonly involves the cardia. The histologic density of the bacteria and inflammatory responses are lower than in the antrum. Intestinal metaplasia in the cardia is a common finding in H. pylori gastritis. The cause of the lower bacterial density in the cardia of patients with reflux esophagitis needs further investigation.
authors.affiliation: Department of Gastroenterology, Otto-von-Guericke-University of Magdeburg, Germany.
authors.forename: A
authors.initials: A
authors.lastname: Hackelsberger
authors.forename: T
authors.initials: T
authors.lastname: Günther
authors.forename: V
authors.initials: V
authors.lastname: Schultze
authors.forename: J
authors.initials: J
authors.lastname: Labenz
authors.forename: A
authors.initials: A
authors.lastname: Roessner
authors.forename: P
authors.initials: P
authors.lastname: Malfertheiner
mesh_terms: D001284:Atrophy; D001706:Biopsy; D002299:Cardia / Q000382:microbiology* / Q000473:pathology; D015169:Colony Count, Microbial; D004396:Coloring Agents; D004381:Duodenal Ulcer / Q000382:microbiology / Q000473:pathology; D004942:Esophagitis, Peptic / Q000382:microbiology / Q000473:pathology; D005260:Female; D005744:Gastric Acid / Q000378:metabolism; D005753:Gastric Mucosa / Q000473:pathology; D005756:Gastritis / Q000382:microbiology* / Q000473:pathology; D016481:Helicobacter Infections / Q000473:pathology; D016480:Helicobacter pylori / Q000302:isolation & purification*; D006801:Humans; D007413:Intestinal Mucosa / Q000473:pathology; D008297:Male; D008679:Metaplasia; D008875:Middle Aged; D015995:Prevalence; D011706:Pyloric Antrum / Q000382:microbiology / Q000473:pathology; D013270:Stomach / Q000382:microbiology / Q000473:pathology; D013276:Stomach Ulcer / Q000382:microbiology / Q000473:pathology
chemical_list: D004396:Coloring Agents