title: Normalization of phospholipids concentration of the gastric mucosa was observed in patients with peptic ulcer after eradication of Helicobacter pylori.
abstract: BACKGROUND
  Phospholipids concentration in the gastric mucosa decreased in patients with Helicobacter pylori infection. The aim of this study is to examine the effects of eradication of H. pylori on decreasing the phospholipids concentration in the gastric mucosa in patients with gastric or duodenal ulcer.
  
  
  METHODS
  Phospholipids (phosphatidylcholine, phosphatidylethanolamine, and sphingonomyeline) were measured in biopsy specimens from the antrum and corpus using thin-layer chromatography. In H. pylori positive patients with gastric ulcer (n = 26) and duodenal ulcer (n = 13), and H. pylori negative controls (n = 20), the biopsy specimens were obtained before and 3 months after eradication. Eradication was performed using lansoprazole, amoxycillin, and clarithromycin.
  
  
  RESULTS
  Compared with the H. pylori negative control group, the concentrations of phosphatidylcholine and phosphatidylethanolamine decreased significantly in the gastric ulcer group in both antrum and corpus mucosa, and in the duodenal ulcer group in antrum mucosa. This decrease returned to the control level after eradication.
  
  
  CONCLUSIONS
  This study demonstrates that the eradication of H. pylori in patients with peptic ulcer normalized the decrease of phosphatidylcholine and phosphatidylethanolamine in the gastric mucosa.
authors.affiliation: Department of Internal Medicine, Saga Medical School, Saga, Saga 849-8501, Saga, Japan.
authors.forename: Sadatoshi
authors.initials: S
authors.lastname: Ishibashi
authors.forename: Ryuichi
authors.initials: R
authors.lastname: Iwakiri
authors.forename: Ryo
authors.initials: R
authors.lastname: Shimoda
authors.forename: Hibiki
authors.initials: H
authors.lastname: Ootani
authors.forename: Seiji
authors.initials: S
authors.lastname: Kawasaki
authors.forename: Jutarou
authors.initials: J
authors.lastname: Tadano
authors.forename: Atsushi
authors.initials: A
authors.lastname: Kikkawa
authors.forename: Akifumi
authors.initials: A
authors.lastname: Ootani
authors.forename: Kayoko
authors.initials: K
authors.lastname: Oda
authors.forename: Takehiro
authors.initials: T
authors.lastname: Fujise
authors.forename: Toshifumi
authors.initials: T
authors.lastname: Yoshida
authors.forename: Seiji
authors.initials: S
authors.lastname: Tsunada
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Sakata
authors.forename: Kazuma
authors.initials: K
authors.lastname: Fujimoto
mesh_terms: D053799:2-Pyridinylmethylsulfinylbenzimidazoles; D000328:Adult; D000368:Aged; D000658:Amoxicillin / Q000627:therapeutic use; D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D000897:Anti-Ulcer Agents / Q000627:therapeutic use; D017291:Clarithromycin / Q000627:therapeutic use; D004359:Drug Therapy, Combination; D004381:Duodenal Ulcer / Q000188:drug therapy* / Q000382:microbiology; D005260:Female; D005753:Gastric Mucosa / Q000737:chemistry*; D016481:Helicobacter Infections / Q000188:drug therapy / Q000382:microbiology; D016480:Helicobacter pylori / Q000187:drug effects*; D006801:Humans; D064747:Lansoprazole; D008297:Male; D008875:Middle Aged; D009853:Omeprazole / Q000031:analogs & derivatives* / Q000627:therapeutic use; D010743:Phospholipids / Q000032:analysis*; D013276:Stomach Ulcer / Q000188:drug therapy* / Q000382:microbiology; D016896:Treatment Outcome
chemical_list: D053799:2-Pyridinylmethylsulfinylbenzimidazoles; D000900:Anti-Bacterial Agents; D000897:Anti-Ulcer Agents; D010743:Phospholipids; D064747:Lansoprazole; D000658:Amoxicillin; D017291:Clarithromycin; D009853:Omeprazole