title: The use of clinical, histologic, and serologic parameters to predict the intragastric extent of intestinal metaplasia: a recommendation for routine practice.
abstract: BACKGROUND
  Surveillance of intestinal metaplasia (IM) of the gastric mucosa should be limited to patients at high risk of gastric cancer. Patients with extensive IM are at increased cancer risk; however, the intragastric extent of IM is usually unknown at the time of the initial diagnosis.
  
  
  OBJECTIVE
  To assess the predictive value of clinical, histologic, and serologic parameters for the intragastric extent of IM.
  
  
  METHODS
  Prospective, multicenter study.
  
  
  METHODS
  Eighty-eight patients with a previous diagnosis of IM of the gastric mucosa.
  
  
  METHODS
  Surveillance gastroscopy with extensive random biopsy sampling.
  
  
  METHODS
  Biopsy specimens were evaluated according to the Sydney classification system. In addition, serologic testing of Helicobacter pylori and cagA status, pepsinogens I and II, gastrin, and intrinsic factor antibodies was performed. The association between the available parameters and extensive IM was evaluated with logistic regression analysis.
  
  
  RESULTS
  In 51 patients (58%), IM was present in the biopsy specimens from at least 2 intragastric locations. The most important predictors of extensive IM were a family history of gastric cancer, alcohol use > or = 1 unit/d (1 glass, approximately 10 mL or 8 g ethanol), moderate or marked IM of the index biopsy specimen, and a pepsinogen I to II ratio < 3.0. A simple risk score based on these factors could identify extensive IM in 24 of 25 patients (sensitivity 96%).
  
  
  CONCLUSIONS
  A prospective cohort study should confirm the proposed risk stratification.
  
  
  CONCLUSIONS
  A risk score of clinical, histologic, and serologic parameters can predict extensive intragastric IM and may serve as a practical tool to select patients for surveillance endoscopy in routine clinical practice.
authors.affiliation: Department of Gastroenterology and Hepatology, Erasmus MC University Medical Center, Rotterdam, The Netherlands. a.c.devries@erasmusmc.nl
authors.forename: Annemarie C
authors.initials: AC
authors.lastname: de Vries
authors.forename: Jelle
authors.initials: J
authors.lastname: Haringsma
authors.forename: Richard A
authors.initials: RA
authors.lastname: de Vries
authors.forename: Frank
authors.initials: F
authors.lastname: ter Borg
authors.forename: Nicole M
authors.initials: NM
authors.lastname: Nagtzaam
authors.forename: Ewout W
authors.initials: EW
authors.lastname: Steyerberg
authors.forename: Herman
authors.initials: H
authors.lastname: van Dekken
authors.forename: Ernst J
authors.initials: EJ
authors.lastname: Kuipers
mesh_terms: D000328:Adult; D000368:Aged; D000907:Antibodies, Bacterial / Q000276:immunology*; D000942:Antigens, Bacterial / Q000097:blood / Q000276:immunology*; D001426:Bacterial Proteins / Q000097:blood / Q000276:immunology*; D001706:Biopsy; D016099:Endoscopy, Gastrointestinal; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005500:Follow-Up Studies; D005753:Gastric Mucosa / Q000276:immunology / Q000382:microbiology / Q000473:pathology*; D005755:Gastrins / Q000276:immunology; D016480:Helicobacter pylori / Q000276:immunology*; D006801:Humans; D007437:Intrinsic Factor / Q000276:immunology*; D008297:Male; D008679:Metaplasia / Q000150:complications / Q000276:immunology / Q000473:pathology; D008875:Middle Aged; D020116:Pepsinogen A / Q000276:immunology; D020115:Pepsinogen C / Q000276:immunology; D011230:Precancerous Conditions; D011379:Prognosis; D011446:Prospective Studies; D012307:Risk Factors; D013274:Stomach Neoplasms / Q000209:etiology / Q000276:immunology / Q000473:pathology*; D011795:Surveys and Questionnaires; D013997:Time Factors; D055815:Young Adult
chemical_list: D000907:Antibodies, Bacterial; D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D005755:Gastrins; C080866:cagA protein, Helicobacter pylori; D020115:Pepsinogen C; D020116:Pepsinogen A; D007437:Intrinsic Factor