title: Implications of anti-parietal cell antibodies and anti-Helicobacter pylori antibodies in histological gastritis and patient outcome.
abstract: OBJECTIVE
  To develop a serum or histological marker for early discovery of gastric atrophy or intestinal metaplasia.
  
  
  METHODS
  This study enrolled 44 patients with gastric adenocarcinoma, 52 patients with duodenal ulcer, 14 patients with gastric ulcer and 42 consecutive healthy adults as controls. Each patient received an endoscopy and five biopsy samples were obtained. The degrees of histological parameters of gastritis were categorized following the Updated Sydney System. Anti-parietal cell antibodies (APCA) and anti-Helicobacter pylori (H pylori) antibodies (AHPA) were analyzed by immunoassays. H pylori infection was diagnosed by rapid urease test and histological examination.
  
  
  RESULTS
  Patients with gastric cancer and gastric ulcer are significantly older than healthy subjects, while also displaying higher frequency of APCA than healthy controls. Patients with positive APCA showed higher scores in gastric atrophy and intestinal metaplasia of corpus than patients with negative APCA. Patients with positive AHPA had higher scores in gastric atrophy, intestinal metaplasia, and gastric inflammation of antrum than those patients with negative AHPA. Elderly patients had greater prevalence rates of APCA. Following multivariant logistic regression analysis, the only significant risk factor for antral atrophy is positive AHPA, while that for corpus atrophy is positive APCA.
  
  
  CONCLUSIONS
  The existence of positive APCA correlates with glandular atrophy in corpus and the presence of positive AHPA correlates with glandular atrophy in antrum. The existence of serum APCA and AHPA betokens glandular atrophy and requires further examination for gastric cancer.
authors.affiliation: Division of Gastroenterology, Department of Internal Medicine, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan, China.
authors.forename: Ching-Chu
authors.initials: CC
authors.lastname: Lo
authors.forename: Ping-I
authors.initials: PI
authors.lastname: Hsu
authors.forename: Gin-Ho
authors.initials: GH
authors.lastname: Lo
authors.forename: Kwok-Hung
authors.initials: KH
authors.lastname: Lai
authors.forename: Hui-Hwa
authors.initials: HH
authors.lastname: Tseng
authors.forename: Chiun-Ku
authors.initials: CK
authors.lastname: Lin
authors.forename: Hoi-Hung
authors.initials: HH
authors.lastname: Chan
authors.forename: Wei-Lun
authors.initials: WL
authors.lastname: Tsai
authors.forename: Wen-Chi
authors.initials: WC
authors.lastname: Chen
authors.forename: Nan-Jing
authors.initials: NJ
authors.lastname: Peng
mesh_terms: D000230:Adenocarcinoma / Q000276:immunology / Q000382:microbiology; D000328:Adult; D000368:Aged; D000907:Antibodies, Bacterial / Q000097:blood*; D001323:Autoantibodies / Q000097:blood*; D016022:Case-Control Studies; D004381:Duodenal Ulcer / Q000276:immunology / Q000382:microbiology; D005260:Female; D005757:Gastritis, Atrophic / Q000276:immunology* / Q000382:microbiology* / Q000473:pathology; D016481:Helicobacter Infections / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D016480:Helicobacter pylori / Q000276:immunology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010295:Parietal Cells, Gastric / Q000276:immunology; D013274:Stomach Neoplasms / Q000276:immunology / Q000382:microbiology; D013276:Stomach Ulcer / Q000276:immunology / Q000382:microbiology
chemical_list: D000907:Antibodies, Bacterial; D001323:Autoantibodies