title: Autoimmune gastritis: histology phenotype and OLGA staging.
abstract: BACKGROUND
  Among Western populations, the declining incidence of Helicobacter pylori infection coincides with a growing clinical impact of autoimmune gastritis.
  
  
  OBJECTIVE
  To describe the histological phenotype of autoimmune gastritis, also to test the prognostic impact of OLGA staging in the autoimmune setting.
  
  
  METHODS
  A single-institutional series (spanning the years 2003-2011) of 562 consecutive patients (M:F ratio: 1:3.7; mean age = 57.6 ± 14.4 years) with serologically confirmed autoimmune gastritis underwent histology review and OLGA staging.
  
  
  RESULTS
  Helicobacter pylori infection was ascertained histologically in 44/562 cases (7.8%). Forty six biopsy sets (8.2%) featured OLGA stages III-IV; they included all four cases of incidental epithelial neoplasia (three intraepithelial and one invasive; three of these four cases had concomitant H. pylori infection). There were 230 (40.9%) and 139 (24.7%) cases, respectively, of linear and micro-nodular enterochromaffin-like cell hyperplasia; 19 (3.4%) type I carcinoids were detected. The series included 116 patients who underwent repeated endoscopy/biopsy sampling (mean time elapsing between the two procedures = 54 months; range 24-108). Paired histology showed a significant (P = 0.009) trend towards a stage progression [the stage increased in 25/116 cases (22%); it remained unchanged in 87/116 cases (75%)].
  
  
  CONCLUSIONS
  In autoimmune gastritis, the cancer risk is restricted to high-risk gastritis stages (III-IV), and is associated mainly with concomitant H. pylori infection. OLGA staging consistently depicts the time-dependent organic progression of the autoimmune disease and provides key information for secondary gastric cancer prevention strategies.
authors.affiliation: Department of Medicine, University of Padua, PD, Italy. massimo.rugge@unipd.it
authors.forename: M
authors.initials: M
authors.lastname: Rugge
authors.forename: M
authors.initials: M
authors.lastname: Fassan
authors.forename: M
authors.initials: M
authors.lastname: Pizzi
authors.forename: V
authors.initials: V
authors.lastname: Zorzetto
authors.forename: G
authors.initials: G
authors.lastname: Maddalo
authors.forename: S
authors.initials: S
authors.lastname: Realdon
authors.forename: M
authors.initials: M
authors.lastname: De Bernard
authors.forename: C
authors.initials: C
authors.lastname: Betterle
authors.forename: R
authors.initials: R
authors.lastname: Cappellesso
authors.forename: G
authors.initials: G
authors.lastname: Pennelli
authors.forename: M
authors.initials: M
authors.lastname: de Boni
authors.forename: F
authors.initials: F
authors.lastname: Farinati
mesh_terms: D000328:Adult; D000368:Aged; D001327:Autoimmune Diseases / Q000382:microbiology / Q000473:pathology*; D001706:Biopsy; D002276:Carcinoid Tumor / Q000473:pathology; D018450:Disease Progression; D016099:Endoscopy, Gastrointestinal / Q000379:methods; D005260:Female; D005756:Gastritis / Q000382:microbiology / Q000473:pathology*; D016481:Helicobacter Infections / Q000473:pathology; D016480:Helicobacter pylori / Q000302:isolation & purification*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D011230:Precancerous Conditions / Q000473:pathology; D012307:Risk Factors; D012720:Severity of Illness Index; D013274:Stomach Neoplasms / Q000276:immunology / Q000473:pathology