title: Serological assessment of gastric mucosal atrophy in gastric cancer.
abstract: BACKGROUND
  Non-invasive tools for gastric cancer screening and diagnosis are lacking. Serological testing with the detection of pepsinogen 1 (PG1), pepsinogen 2 (PG2) and gastrin 17 (G17) offers the possibility to detect preneoplastic gastric mucosal conditions. Aim of this study was to assess the performance of these serological tests in the presence of gastric neoplasia.
  
  
  METHODS
  Histological and serological samples of 118 patients with gastric cancer have been assessed for tumor specific characteristics (Laurén type, localisation), degree of mucosal abnormalities (intestinal metaplasia, atrophy) and serological parameters (PG1, PG2, PG1/2-ratio, G17, H. pylori IgG, CagA status). Association of the general factors to the different serological values have been statistically analyzed.
  
  
  RESULTS
  Patients with intestinal type gastric cancer had lower PG1 levels and a lower PG1/2-ratio compared to those with diffuse type cancer (p = 0.003). The serum levels of PG2 itself and G17 were not significantly altered. H. pylori infection in general had no influence on the levels of PG1, PG2 and G17 in the serum of gastric cancer patients. There was a trend towards lower PG1 levels in case of positive CagA-status (p = 0.058). The degree of both intestinal metaplasia and atrophy correlated inversely with serum levels for PG1 and the PG1/2-ratio (p < 0.01). Laurén-specific analysis revealed that this is only true for intestinal type tumors. Univariate ANOVA revealed atrophy and CagA-status as the only independent factors for low PG1 and a low PG1/2-ratio.
  
  
  CONCLUSIONS
  Glandular atrophy and a positive CagA status are determinant factors for decreased pepsinogen 1 levels in the serum of patients with gastric cancer. The serological assessment of gastric atrophy by analysis of serum pepsinogen is only adequate for patients with intestinal type cancer.
authors.affiliation: Department of Gastroenterology, Hepatology and Infectious Diseases, Otto-von-Guericke-University of Magdeburg, Magdeburg, Germany.
authors.forename: Jan
authors.initials: J
authors.lastname: Bornschein
authors.forename: Michael
authors.initials: M
authors.lastname: Selgrad
authors.forename: Thomas
authors.initials: T
authors.lastname: Wex
authors.forename: Doerthe
authors.initials: D
authors.lastname: Kuester
authors.forename: Peter
authors.initials: P
authors.lastname: Malfertheiner
mesh_terms: D000230:Adenocarcinoma / Q000097:blood* / Q000473:pathology*; D000368:Aged; D000907:Antibodies, Bacterial / Q000097:blood; D000942:Antigens, Bacterial / Q000097:blood; D001284:Atrophy; D001426:Bacterial Proteins / Q000097:blood; D014408:Biomarkers, Tumor / Q000097:blood*; D005260:Female; D005753:Gastric Mucosa / Q000473:pathology*; D005755:Gastrins / Q000097:blood; D016481:Helicobacter Infections / Q000097:blood; D016480:Helicobacter pylori / Q000276:immunology; D006801:Humans; D008297:Male; D008875:Middle Aged; D020116:Pepsinogen A / Q000097:blood; D011230:Precancerous Conditions / Q000097:blood; D012189:Retrospective Studies; D013274:Stomach Neoplasms / Q000097:blood* / Q000473:pathology*
chemical_list: D000907:Antibodies, Bacterial; D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D014408:Biomarkers, Tumor; D005755:Gastrins; C080866:cagA protein, Helicobacter pylori; C013550:gastrin 17; D020116:Pepsinogen A