title: Gastric epithelial dysplasia. How clinicopathologic background relates to management.
abstract: BACKGROUND
  Gastric epithelial dysplasia (GED) in metaplastic mucosa is considered the most advanced preinvasive lesion in the multistep morphogenesis of intestinal-type gastric cancer (GC). The rate of GED's evolution into GC is still under debate and probably is related to pathologic and clinical parameters other than the dysplasia itself. The aim of this study was to evaluate whether clinical aspects (sex and age) and/or morphologic variables (GED grade, coexisting atrophic gastritis) are relevant to the outcome of dysplasia, with a view toward initiating the establishment of a rational follow-up protocol for practical GED management.
  
  
  METHODS
  Ninety-three patients harboring GED (G1: 56, G2:34, G3:18) were followed for more than 12 months according to a previously-agreed protocol. Regression, progression, or evolution into GC were detected for each grade of GED. Multivariate analysis was used to check the independence of clinical and pathologic variables in the progression of GED into more severe dysplastic lesions and/or as risk factors for evolution into GC.
  
  
  RESULTS
  Age, male sex, GED grade and grade of coexisting atrophic gastritis proved independent risk factors for GED progression, with no significant interactions. Only GED grade (G2 and G3) was significantly associated with carcinomatous evolution. In G1-GED, age and the grade of coexisting atrophy proved to be independent risk factors for carcinomatous evolution.
  
  
  CONCLUSIONS
  In G1-GED, more stringent follow-up should be recommended for older patients with coexisting high grade atrophic gastritis; stringent follow-up is always mandatory for G2-GED; and a surgical approach is justified in G3-GED.
authors.affiliation: Department of Pathology, University of Padova-ULSS, Italy.
authors.forename: M
authors.initials: M
authors.lastname: Rugge
authors.forename: G
authors.initials: G
authors.lastname: Leandro
authors.forename: F
authors.initials: F
authors.lastname: Farinati
authors.forename: F
authors.initials: F
authors.lastname: Di Mario
authors.forename: F
authors.initials: F
authors.lastname: Sonego
authors.forename: M
authors.initials: M
authors.lastname: Cassaro
authors.forename: M
authors.initials: M
authors.lastname: Guido
authors.forename: V
authors.initials: V
authors.lastname: Ninfo
mesh_terms: D000230:Adenocarcinoma / Q000473:pathology* / Q000628:therapy; D005260:Female; D005753:Gastric Mucosa / Q000473:pathology*; D005757:Gastritis, Atrophic / Q000150:complications / Q000473:pathology; D016481:Helicobacter Infections / Q000150:complications / Q000473:pathology; D016480:Helicobacter pylori; D006801:Humans; D008297:Male; D008875:Middle Aged; D011230:Precancerous Conditions / Q000473:pathology* / Q000628:therapy; D012044:Regression Analysis; D012307:Risk Factors; D013272:Stomach Diseases / Q000473:pathology; D013274:Stomach Neoplasms / Q000473:pathology* / Q000628:therapy