Digestive Diseases and Sciences

, Volume 47, Issue 1, pp 162–169

Atrophic Corpus Gastritis and Helicobacter pylori Infection in Primary Biliary Cirrhosis

Authors

  • Kazufumi Dohmen
    • Department of Internal MedicineSaga Prefectural Hospital Koseikan
    • Department of Internal MedicineOkabe Hospital
  • Hirohisa Shigematsu
    • Department of Internal MedicineSaga Prefectural Hospital Koseikan
  • Yuichi Miyamoto
    • Department of Internal MedicineSaga Prefectural Hospital Koseikan
  • Fumio Yamasaki
    • Department of PathologySaga Prefectural Hospital Koseikan
  • Koji Irie
    • Department of PathologySaga Prefectural Hospital Koseikan
  • Hiromi Ishibashi
    • Department of Internal Medicine, Faculty of MedicineKyushu University
Article

DOI: 10.1023/A:1013292210036

Cite this article as:
Dohmen, K., Shigematsu, H., Miyamoto, Y. et al. Dig Dis Sci (2002) 47: 162. doi:10.1023/A:1013292210036

Abstract

Chronic atrophic corpus gastritis, termed as autoimmune corpus gastritis or type A gastritis, and primary biliary cirrhosis (PBC) are characterized by a common immunological process against the exocrine glandular structures of both the stomach and bile duct. However, there has been controversy over whether atrophic corpus gastritis is associated with PBC. Recently, it has been suggested that Helicobacter pylori plays an important role in the early stage of atrophic corpus gastritis due to the induction of autoantibodies that are reactive with a protein in the gastric parietal cells. One hypothesis is that molecular mimicry, possibly resulting from H. pylori infection, might be responsible for initiating an autoimmune response in a predisposed host due to cross-reactivity among gastric mucosal, bile ductular, and bacterial antigens. The aim of this study is to assess whether atrophic changes of the gastric corpus could affect patients with PBC, and to determine the correlation with H. pylori infection. Sixteen patients with PBC were enrolled in this study. All patients were examined by serological studies of anti-pyruvate dehydrogenase (PDH) antibody, anti-H. pylori antibody, gastrin and vitamin B12. Gastroscopy was performed on all patients in order to verify the histological findings and to microscopically identify H. pylori. Atrophic corpus gastritis was found in 2 of 16 patients with PBC (12.5%), one of whom was confirmed to have pernicious anemia, a developed stage of atrophic corpus gastritis. H. pylori infection in the gastric corpus and the anti-H. pylori antibody were found in 7 (43.8%) and 11 (68.8%) of 16 patients, respectively. Anti-H. pylori antibody was confirmed to be positive in both of the patients with atrophic corpus gastritis, although H. pylori was absent in the gastric biopsy specimen. There was a positive correlation between anti-PDH antibodies and anti-H. pylori antibodies in sera from patients with PBC. Atrophic corpus gastritis is not frequently involved in PBC. However, H. pylori is a possible pathogenic factor in atrophic corpus gastritis in PBC patients because of the presence of anti-H. pylori antibody. A positive correlation between the titer of anti-PDH antibodies and the titer of anti-H. pylori antibodies was confirmed. Consequently, H. pylori infection could induce autoimmune responses in the development of both PBC and atrophic corpus gastritis. H. pylori infection associated with PBC requires further study.

primary biliary cirrhosis type A gastritis atrophic gastritis autoimmune gastritis Helicobacter pylori molecular mimicry

Copyright information

© Plenum Publishing Corporation 2002