title: Marked increase in gastric acid secretory capacity after omeprazole treatment.
abstract: BACKGROUND
  In contrast with the histamine2 (H2) blockers, proton pump inhibitors have not been shown to give rebound hypersecretion of acid. Taking into consideration the hyperplasia of the enterochromaffin-like (ECL) cell provoked by hypergastrinaemia secondary to profound acid inhibition and the central role of histamine from ECL cells in the regulation of acid secretion, the lack of any rebound acid hypersecretion after treatment with proton pump inhibitors has been questioned.
  
  
  OBJECTIVE
  To reassess the effect of treatment with omeprazole on post-treatment acid secretion.
  
  
  METHODS
  Basal and pentagastrin stimulated acid secretion were determined in nine patients with reflux oesophagitis before and 14 days after termination of a 90 day treatment period with the proton pump inhibitor omeprazole (40 mg daily). Basal gastrin release were determined before and during omeprazole treatment. Furthermore, biopsy samples from the oxyntic mucosa were taken before and at the end of the treatment period for chemical (histamine and chromogranin A (CgA)) evaluation of the ECL cell mass.
  
  
  RESULTS
  A substantial increase in meal stimulated gastrin release during omeprazole treatment resulted in an increased ECL cell mass. Furthermore, CgA in serum increased during omeprazole treatment suggesting that serum CgA may be used as a test to evaluate ECL cell hyperplasia. A significant increase in basal and a marked (50%) and significant increase in pentagastrin stimulated acid secretion were found after treatment with omeprazole.
  
  
  CONCLUSIONS
  Increased acid secretion after a conventional treatment period with a proton pump inhibitor is probably due to ECL cell hyperplasia and may have negative consequences for acid related diseases.
authors.affiliation: Department of Medicine, University Hospital, Trondheim, Norway.
authors.forename: H L
authors.initials: HL
authors.lastname: Waldum
authors.forename: J S
authors.initials: JS
authors.lastname: Arnestad
authors.forename: E
authors.initials: E
authors.lastname: Brenna
authors.forename: I
authors.initials: I
authors.lastname: Eide
authors.forename: U
authors.initials: U
authors.lastname: Syversen
authors.forename: A K
authors.initials: AK
authors.lastname: Sandvik
mesh_terms: D000328:Adult; D000368:Aged; D000897:Anti-Ulcer Agents / Q000009:adverse effects / Q000627:therapeutic use*; D053379:Chromogranin A; D002864:Chromogranins / Q000032:analysis / Q000097:blood; D004759:Enterochromaffin Cells / Q000187:drug effects / Q000473:pathology; D004942:Esophagitis, Peptic / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D005744:Gastric Acid / Q000378:metabolism*; D005753:Gastric Mucosa / Q000737:chemistry / Q000187:drug effects / Q000473:pathology; D006801:Humans; D006965:Hyperplasia; D008297:Male; D008875:Middle Aged; D009853:Omeprazole / Q000009:adverse effects / Q000627:therapeutic use*; D010418:Pentagastrin; D054328:Proton Pump Inhibitors
chemical_list: D000897:Anti-Ulcer Agents; D053379:Chromogranin A; D002864:Chromogranins; D054328:Proton Pump Inhibitors; D010418:Pentagastrin; D009853:Omeprazole