title: Circadian gastric acidity in Helicobacter pylori positive ulcer patients with and without gastric metaplasia in the duodenum.
abstract: BACKGROUND
  The presence of gastric metaplasia allows helicobacter pylori to colonise the duodenum and this condition is thought to be acquired as a response to acid hypersecretion. This functional disorder, however, is present only in a subgroup of duodenal ulcer patients and, in addition, surface gastric metaplasia has been frequently found in the proximal duodenum of normal subjects and patients with non-ulcer dyspepsia, who cannot be certainly considered as acid hypersecretors.
  
  
  OBJECTIVE
  To clarify the role of acid in inducing gastric type epithelium in the duodenum. This study aimed at assessing whether the pattern of circadian gastric acidity differs between H pylori positive duodenal ulcer patients with and without duodenal gastric metaplasia.
  
  
  METHODS
  Seventy one patients with duodenal ulcer confirmed by endoscopy and who were found to be positive for H pylori infection by histology on antrum biopsy specimens were enrolled into this study.
  
  
  METHODS
  Gastric type epithelium in the duodenum was found in 49 of 71 ulcer patients (69%). Continuous 24 hour gastric pH metry was performed in 50 healthy subjects and in the two subgroups of duodenal ulcer patients with and without gastric metaplasia in the duodenum. Gastric acidity was calculated for 24 hours (1700-1659), night (2000-0759) and day-time (0800-1959).
  
  
  RESULTS
  Ulcer patients without gastric metaplasia showed a significantly higher gastric acidity (p < 0.001) than controls for every time interval considered, while the ulcer subgroup with gastric metaplasia was more acid than healthy subjects (p < 0.001) during the whole 24 hour period and the daytime. There was no difference between the two subgroups of duodenal ulcer patients with and without gastric metaplasia during the various time segments analysed.
  
  
  CONCLUSIONS
  The findings confirm that the circadian gastric acidity of duodenal ulcer patients is higher than that of controls. As there is no difference in gastric pH between duodenal ulcer patients with and without gastric metaplasia, gastric hyperacidity is not specific to patients with duodenal gastric metaplasia. It is probable that this histological change is a non-specific response to mucosal injury resulting from various factors and not exclusively to acid.
authors.affiliation: Dipartimento di Medicina Interna, Università di Genova, Italy.
authors.forename: V
authors.initials: V
authors.lastname: Savarino
authors.forename: G S
authors.initials: GS
authors.lastname: Mela
authors.forename: P
authors.initials: P
authors.lastname: Zentilin
authors.forename: M R
authors.initials: MR
authors.lastname: Mele
authors.forename: L
authors.initials: L
authors.lastname: Lapertosa
authors.forename: R
authors.initials: R
authors.lastname: Patetta
authors.forename: E
authors.initials: E
authors.lastname: Dallorto
authors.forename: A
authors.initials: A
authors.lastname: Vassallo
authors.forename: C
authors.initials: C
authors.lastname: Mansi
authors.forename: S
authors.initials: S
authors.lastname: Vigneri
authors.forename: G
authors.initials: G
authors.lastname: Celle
mesh_terms: D000328:Adult; D000704:Analysis of Variance; D002940:Circadian Rhythm; D004381:Duodenal Ulcer / Q000382:microbiology / Q000473:pathology* / Q000503:physiopathology; D004386:Duodenum / Q000473:pathology*; D004848:Epithelium / Q000473:pathology; D005260:Female; D005744:Gastric Acid / Q000378:metabolism*; D005753:Gastric Mucosa / Q000378:metabolism; D016481:Helicobacter Infections / Q000473:pathology* / Q000503:physiopathology; D016480:Helicobacter pylori; D006801:Humans; D006863:Hydrogen-Ion Concentration; D008297:Male; D008679:Metaplasia; D008875:Middle Aged; D008991:Monitoring, Physiologic; D013270:Stomach / Q000473:pathology