title: Long-term acid suppression by omeprazole in gastro-oesophageal reflux disease patients does not lead to anti-gastric autoantibody production.
abstract: BACKGROUND
  Helicobacter pylori-associated atrophy of the gastric corpus is associated with the presence of anti-canalicular autoantibodies. Also, long-term profound acid suppression in H. pylori-infected subjects may cause atrophic corpus gastritis.
  
  
  OBJECTIVE
  To investigate whether long-term acid suppression by omeprazole leads to antigastric autoantibodies.
  
  
  METHODS
  Fifty patients, of which 34 H. pylori-positive on entry of the study, were treated with omeprazole (20-40 mg once daily) for reflux oesophagitis, and were evaluated for anti-gastric autoantibody responses by immunohistochemistry before and after treatment. H. pylori was not eradicated and patients were followed for an average of 6.6 years (range 3-14.1 years). In addition to immunohistochemistry, anti-H(+), K(+)-ATPase reactivity was assessed by Western blot in paired sera of 41 patients (26 H. pylori-positive and 15 uninfected) and results are critically evaluated.
  
  
  RESULTS
  In immunohistochemistry, all patients were negative for anti-canalicular autoantibodies when omeprazole therapy started, except for two patients with corpus-predominant gastritis in the presence of H. pylori. One patient, who was H. pylori-negative, newly developed an anti-canalicular antibody response during therapy.
  
  
  CONCLUSIONS
  Our results indicate that, as compared with non-infected patients, long-term profound acid suppression therapy in H. pylori-infected gastro-oesophageal reflux disease patients does not increase or accelerate gastric autoimmunity.
authors.affiliation: Departments of Medical Microbiology and Infection Control, Vrije Universiteit Medical Center, Amsterdam, The Netherlands. m.bergman@erasmusmc.nl
authors.forename: M P
authors.initials: MP
authors.lastname: Bergman
authors.forename: E C
authors.initials: EC
authors.lastname: Klinkenberg-Knol
authors.forename: G
authors.initials: G
authors.lastname: Faller
authors.forename: A
authors.initials: A
authors.lastname: Aar
authors.forename: W
authors.initials: W
authors.lastname: Lakhai
authors.forename: C M J E
authors.initials: CM
authors.lastname: Vandenbroucke-Grauls
authors.forename: E J
authors.initials: EJ
authors.lastname: Kuipers
authors.forename: B J
authors.initials: BJ
authors.lastname: Appelmelk
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000897:Anti-Ulcer Agents / Q000627:therapeutic use*; D000917:Antibody Formation; D001323:Autoantibodies / Q000276:immunology*; D015153:Blotting, Western; D015331:Cohort Studies; D005260:Female; D005744:Gastric Acid / Q000502:physiology*; D005764:Gastroesophageal Reflux / Q000188:drug therapy* / Q000276:immunology*; D016481:Helicobacter Infections; D016480:Helicobacter pylori; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009853:Omeprazole / Q000627:therapeutic use*
chemical_list: D000897:Anti-Ulcer Agents; D001323:Autoantibodies; D009853:Omeprazole