title: Mechanism of acid hypersecretion post curative gastrinoma resection.
abstract: BACKGROUND
  Some patients with Zollinger-Ellison syndrome post curative gastrinoma resection continue to show gastric acid hypersecretion; however, the mechanism is unknown.
  
  
  OBJECTIVE
  The aim of this study was to prospectively study acid secretion following curative gastrinoma resection and analyze factors contributing in patients with Zollinger-Ellison syndrome.
  
  
  METHODS
  Fifty patients cured post gastrinoma resection were studied with serial assessments of acid secretory status, cure status and ECL-cell status/activity (with serial biopsies, CgA, urinary N-MIAA). Correlative analysis was performed to determine predictive factors.
  
  
  RESULTS
  Hypersecretion occurred in 31 patients (62%) and 14 had extreme-hypersecretion. There was an initial decline (3-6 months) in BAO/MAO, which then remained stable for eight years. Preoperative BAO correlated with the postoperative secretion, but not other clinical, tumoral, laboratory variables, the degree of postoperative acid suppression or type of antisecretory drug needed. Hypersecretors had greater postoperative ECL changes (P=0.005), serum CGA (P=0.009) and 24-h urinary N-MIAA (P=0.0038).
  
  
  CONCLUSIONS
  Post curative resection, gastric hypersecretion persists long term (mean 8 years) in 62% of patients and in 28% it is extreme, despite normogastrinemia. No preoperative variable except BAO correlates with postresection hypersecretion. The persistent increased ECL-cell extent post curative resection suggests prolonged hypergastrinemia can lead to changes in ECL-cells that are either irreversible in humans or sustained by unknown mechanisms not involving fasting hypergastrinemia and which can result in hypersecretion, in a proportion of which it can be extreme. Whether similar findings may occur in patients with idiopathic GERD treated for prolonged periods (>10 years) with PPIs, at present, is unknown.
authors: Digestive Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bldg. 10, Rm. 9C-103, 10 CENTER DR MSC 1804, Bethesda, MD 20892-1804, USA. ojeaburu@hotmail.com
authors: Jeremiah V
authors: JV
authors: Ojeaburu
authors: Tetsuhide
authors: T
authors: Ito
authors: Pellegrino
authors: P
authors: Crafa
authors: Cesare
authors: C
authors: Bordi
authors: Robert T
authors: RT
authors: Jensen
mesh_terms: D004759:Enterochromaffin Cells / Q000473:pathology; D005260:Female; D005500:Follow-Up Studies; D005744:Gastric Acid / Q000378:metabolism*; D015408:Gastrinoma / Q000601:surgery*; D005755:Gastrins / Q000097:blood; D006801:Humans; D006965:Hyperplasia; D008297:Male; D008875:Middle Aged; D010190:Pancreatic Neoplasms / Q000601:surgery*; D010295:Parietal Cells, Gastric / Q000473:pathology; D011184:Postoperative Period; D015995:Prevalence; D011446:Prospective Studies; D015043:Zollinger-Ellison Syndrome / Q000453:epidemiology / Q000378:metabolism* / Q000503:physiopathology*
chemical_list: D005755:Gastrins