title: Cell proliferation in type C gastritis affecting the intact stomach.
abstract: OBJECTIVE
  Type C gastritis caused by bile reflux has a characteristic appearance, similar to that seen in other forms of chemical gastritis, such as those associated with NSAIDs or alcohol. An increase in mucosal cell proliferation increases the likelihood of a neoplastic clone of epithelial cells emerging, particularly where there is chronic epithelial injury associated with bile reflux. It has been shown previously that type C gastritis is associated with increased cell proliferation in the postsurgical stomach. The aim of this study was to determine cell proliferation in type C gastritis caused by bile reflux affecting the intact stomach.
  
  
  METHODS
  Specimens from 15 patients with a histological diagnosis of type C gastritis on antral biopsy were obtained from the pathology archives between 1994 and 1997. A control group of nine normal antral biopsies was also selected and all underwent MIB-1 immunostaining. The gastric glands were divided into three zones (zone 1, gastric pit; zone 2, isthmus; and zone 3, gland base) and the numbers of positively staining nuclei for 500 epithelial cell nuclei were counted in each zone to determine the percentage labelling index (LI%).
  
  
  RESULTS
  Cell proliferation was significantly higher in all three zones of the gastric glands with type C gastritis compared with controls as follows: zone 1, median LI% in type C gastritis 64.7 (range, 7.8-99.2), controls 4.7 (range, 2.0-11.3); zone 2, median LI% in type C gastritis 94.7 (range, 28.8-98.7), controls 40.2 (range, 23.1-70.3); and zone 3, median LI% in type C gastritis 20.0 (range, 1.3-96.0), controls 2.6 (range, 0.9-8.7).
  
  
  CONCLUSIONS
  Bile reflux is thought to act as a promoter of gastric carcinogenesis in the postsurgical stomach. The same may be true in the intact stomach.
authors.affiliation: Department of Gastroenterology, Blackburn Royal Infirmary, UK.
authors.forename: J E
authors.initials: JE
authors.lastname: Dowall
authors.forename: P
authors.initials: P
authors.lastname: Willis
authors.forename: R
authors.initials: R
authors.lastname: Prescott
authors.forename: S
authors.initials: S
authors.lastname: Lamonby
authors.forename: D A
authors.initials: DA
authors.lastname: Lynch
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D034961:Antigens, Nuclear; D001655:Bile Reflux / Q000150:complications; D015415:Biomarkers; D002455:Cell Division; D005260:Female; D005756:Gastritis / Q000209:etiology / Q000473:pathology*; D006801:Humans; D007124:Immunoenzyme Techniques; D019394:Ki-67 Antigen; D008297:Male; D008875:Middle Aged; D009687:Nuclear Proteins / Q000378:metabolism; D011230:Precancerous Conditions / Q000473:pathology*; D011706:Pyloric Antrum / Q000473:pathology; D012189:Retrospective Studies; D013274:Stomach Neoplasms / Q000473:pathology*
chemical_list: D034961:Antigens, Nuclear; D015415:Biomarkers; D019394:Ki-67 Antigen; D009687:Nuclear Proteins