title: Gastric acidity in patients with follicular gastritis is significantly reduced, but can be normalized after eradication for Helicobacter pylori.
abstract: BACKGROUND
  Follicular gastritis is thought to be caused by Helicobacter pylori infection. However, the pathophysiology of it remains unclear.
  
  
  METHODS
  We assessed gastric acidity in 15 patients with follicular gastritis, aged 20-37 years, using a 24-hour intragastric pH-metry, as well as by histologic and serologic evaluations; and compared it with that in other age-matched groups: 18 cases of H. pylori-positive antrum-predominant gastritis, 12 of pangastritis, and 24 H. pylori-negative normals. In eight cases with follicular gastritis, it was re-assessed 6 months after the eradication therapy for H. pylori.
  
  
  RESULTS
  During nighttime, the percentage of time with intragastric pH above 3.0 in follicular gastritis was significantly higher than that in normals (p<.0001), and in antrum-predominant gastritis (p<.001), but was comparable with that in pangastritis. In the daytime period, this parameter in follicular gastritis was significantly higher than that in normal (p<.001), in antrum-predominant gastritis (p<.001), and in pangastritis (p<.05). Marked mononuclear cell and neutrophil infiltration but no apparent glandular atrophy were observed in both the antrum and corpus. Serum pepsinogen I/II ratio was significantly lower in follicular gastritis than that in normals (p<.0001) and in antrum-predominant gastritis (p<.001), whereas serum gastrin was significantly higher than that in normals (p<.0001), in antrum-predominant gastritis (p<.01) and in pangastritis (p<.05). After eradication for H. pylori, all of the parameters in follicular gastritis were altered to the same ranges as those in normals.
  
  
  CONCLUSIONS
  In follicular gastritis, gastric acidity is significantly reduced, but can be normalized by eradication of H. pylori. It can thus be speculated that inflammatory cytokines or H. pylori-infection-induced prostaglandins might strongly inhibit gastric acid secretion in follicular gastritis.
authors.affiliation: Department of General Medicine, Hiroshima University Hospital, Hiroshima, Japan. tshima@hiroshima-u.ac.jp
authors.forename: Tomohiko
authors.initials: T
authors.lastname: Shimatani
authors.forename: Masaki
authors.initials: M
authors.lastname: Inoue
authors.forename: Keiko
authors.initials: K
authors.lastname: Iwamoto
authors.forename: Hideyuki
authors.initials: H
authors.lastname: Hyogo
authors.forename: Michiya
authors.initials: M
authors.lastname: Yokozaki
authors.forename: Toshinari
authors.initials: T
authors.lastname: Saeki
authors.forename: Susumu
authors.initials: S
authors.lastname: Tazuma
authors.forename: Yoko
authors.initials: Y
authors.lastname: Horikawa
authors.forename: Nobue
authors.initials: N
authors.lastname: Harada
mesh_terms: D000328:Adult; D005260:Female; D005744:Gastric Acid / Q000378:metabolism; D005755:Gastrins / Q000097:blood; D005756:Gastritis; D016481:Helicobacter Infections / Q000188:drug therapy* / Q000382:microbiology; D016480:Helicobacter pylori / Q000187:drug effects*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D008297:Male; D010435:Pepsinogens / Q000097:blood; D011706:Pyloric Antrum / Q000382:microbiology / Q000473:pathology* / Q000502:physiology*
chemical_list: D005755:Gastrins; D010435:Pepsinogens