title: Effect of eradication of Helicobacter pylori on the histology and cellular phenotype of gastric intestinal metaplasia.
abstract: OBJECTIVE
  Eradication of Helicobacter pylori appears to reduce gastric cancer incidence. We examined the effect of successful H pylori therapy on histology, phenotype of gastric intestinal metaplasia (GIM) (complete vs incomplete), and expression of several biomarkers related to carcinogenesis.
  
  
  METHODS
  Ninety-six H pylori-positive patients from Japan were treated successfully and followed up prospectively over 4 years with yearly endoscopy and were classified into 3 groups: group CG, chronic gastritis without GIM (n = 36); group IM, chronic gastritis with GIM (n = 33); group DYS, and GIM with dysplasia/cancer in a different location of the stomach (n = 27). A total of 288 endoscopic procedures were performed. Histology, mucin-histochemistry, and immunoperoxidase assays using monoclonal antibodies (mAbs) for cell phenotype (monoclonal antibody Das-1/colonic) and for neoplasia (TC22 and p53) were performed.
  
  
  RESULTS
  The GIM histologic score was higher in group DYS than in group IM (P < .05) and group CG (P < .0001). The GIM scores did not change in groups IM and DYS over 4 years. mAb Das-1 reactivity was higher in group DYS (63%) than in group IM (39%) and group GC (0%). After eradication of H pylori, mAb Das-1 reactivity disappeared in 40% of patients (P < .0001) despite the unchanged GIM scores, and regression of TC22-4 was noted in the same patients.
  
  
  CONCLUSIONS
  H pylori eradication does not reduce the histologic GIM score, but changes the cellular phenotype of GIM. This change of phenotype may be an important factor in the reduction of cancer incidence after eradication of H pylori.
authors.affiliation: Division of Gastroenterology and Hematology/Oncology, Department of Medicine, Asahikawa Medical College, Asahikawa, Japan.
authors.forename: Jiro
authors.initials: J
authors.lastname: Watari
authors.forename: Koushik K
authors.initials: KK
authors.lastname: Das
authors.forename: Peter S
authors.initials: PS
authors.lastname: Amenta
authors.forename: Hiroki
authors.initials: H
authors.lastname: Tanabe
authors.forename: Atsumi
authors.initials: A
authors.lastname: Tanaka
authors.forename: Xin
authors.initials: X
authors.lastname: Geng
authors.forename: Jim J-C
authors.initials: JJ
authors.lastname: Lin
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Kohgo
authors.forename: Kiron M
authors.initials: KM
authors.lastname: Das
mesh_terms: D053799:2-Pyridinylmethylsulfinylbenzimidazoles / Q000627:therapeutic use; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000658:Amoxicillin / Q000627:therapeutic use; D000890:Anti-Infective Agents / Q000627:therapeutic use; D000906:Antibodies / Q000276:immunology; D001706:Biopsy; D002908:Chronic Disease; D017291:Clarithromycin / Q000627:therapeutic use; D004359:Drug Therapy, Combination; D005260:Female; D005500:Follow-Up Studies; D005756:Gastritis / Q000150:complications / Q000473:pathology; D005773:Gastroscopy; D016481:Helicobacter Infections / Q000188:drug therapy*; D016480:Helicobacter pylori; D006801:Humans; D064747:Lansoprazole; D008297:Male; D008679:Metaplasia / Q000276:immunology / Q000473:pathology; D008875:Middle Aged; D010641:Phenotype; D011446:Prospective Studies; D013270:Stomach / Q000382:microbiology / Q000473:pathology*; D013274:Stomach Neoplasms / Q000150:complications / Q000473:pathology; D014335:Tropomyosin / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
chemical_list: D053799:2-Pyridinylmethylsulfinylbenzimidazoles; D000890:Anti-Infective Agents; D000906:Antibodies; C467479:DAS-1 protein, human; D014335:Tropomyosin; D016159:Tumor Suppressor Protein p53; D064747:Lansoprazole; D000658:Amoxicillin; D017291:Clarithromycin