title: Role of anti-parietal cell antibody in Helicobacter pylori-associated atrophic gastritis: evaluation in a country of high prevalence of atrophic gastritis.
abstract: BACKGROUND
  Helicobacter pylori plays an important part in the progression of atrophic gastritis; however, markers for predicting the progression of atrophic gastritis remain unidentified. We investigated the relation between the degree of atrophic gastritis and the amount of anti-parietal cell antibodies (APCAs) present.
  
  
  METHODS
  In 219 Japanese patients, APCA was investigated by enzyme-linked immunosorbent assay (ELISA) and by Western blotting. The grade of corpus atrophy was estimated by histology and serum pepsinogen levels. Serum levels of pepsinogen were evaluated by radioimmunoassay.
  
  
  RESULTS
  Helicobacter pylori infection did not affect the APCA levels determined by ELISA. Long-term administration of proton-pump inhibitors and H. pylori eradication did not influence the levels of APCAs. However, in H. pylori-positive patients, the levels of APCA determined by ELISA were statistically higher in patients with severe atrophy than in those with mild atrophy as determined histologically (0.67+/-0.48 versus 0.45+/-0.40; A492, mean+/-s, P=0.01) and serologically by pepsinogen levels (0.66+/-0.51 versus 0.44+/-0.40. P=0.002). The levels of pepsinogen I/II ratio were correlated with APCA levels only in the H. pylori-positive group. Western blotting showed that major antigen was identical with the beta-subunit of H+,K+-ATPase.
  
  
  CONCLUSIONS
  APCA plays an important part in the progression of corpus atrophy after H. pylori infection.
authors.affiliation: First Dept. of Internal Medicine, Hiroshima University School of Medicine, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Ito
authors.forename: K
authors.initials: K
authors.lastname: Haruma
authors.forename: S
authors.initials: S
authors.lastname: Kaya
authors.forename: T
authors.initials: T
authors.lastname: Kamada
authors.forename: S
authors.initials: S
authors.lastname: Kim
authors.forename: A
authors.initials: A
authors.lastname: Sasaki
authors.forename: M
authors.initials: M
authors.lastname: Sumii
authors.forename: S
authors.initials: S
authors.lastname: Tanaka
authors.forename: M
authors.initials: M
authors.lastname: Yoshihara
authors.forename: K
authors.initials: K
authors.lastname: Chayama
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000888:Antibodies, Anti-Idiotypic / Q000032:analysis*; D015153:Blotting, Western; D016009:Chi-Square Distribution; D002648:Child; D015331:Cohort Studies; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005753:Gastric Mucosa / Q000276:immunology / Q000473:pathology; D005757:Gastritis, Atrophic / Q000453:epidemiology / Q000276:immunology / Q000382:microbiology*; D016481:Helicobacter Infections / Q000453:epidemiology / Q000276:immunology*; D016480:Helicobacter pylori / Q000276:immunology* / Q000302:isolation & purification; D006801:Humans; D007564:Japan / Q000453:epidemiology; D008297:Male; D008875:Middle Aged; D015995:Prevalence; D011336:Probability; D011446:Prospective Studies; D012307:Risk Factors
chemical_list: D000888:Antibodies, Anti-Idiotypic