Mechanism of acid hypersecretion post curative gastrinoma resection

Jeremiah V. Ojeaburu, Tetsuhide Ito, Pellegrino Crafa, Cesare Bordi, Robert T. Jensen

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Background: Some patients with Zollinger-Ellison syndrome post curative gastrinoma resection continue to show gastric acid hypersecretion; however, the mechanism is unknown. Aim: 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.

Original languageEnglish
Pages (from-to)139-154
Number of pages16
JournalDigestive Diseases and Sciences
Volume56
Issue number1
DOIs
Publication statusPublished - Jan 1 2011

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Gastrinoma
Enterochromaffin-like Cells
Acids
Zollinger-Ellison Syndrome
Gastric Acid
Monoamine Oxidase
Gastroesophageal Reflux
Statistical Factor Analysis
Fasting
Stomach
Biopsy
Serum
Pharmaceutical Preparations

All Science Journal Classification (ASJC) codes

  • Physiology
  • Gastroenterology

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Mechanism of acid hypersecretion post curative gastrinoma resection. / Ojeaburu, Jeremiah V.; Ito, Tetsuhide; Crafa, Pellegrino; Bordi, Cesare; Jensen, Robert T.

In: Digestive Diseases and Sciences, Vol. 56, No. 1, 01.01.2011, p. 139-154.

Research output: Contribution to journalArticle

Ojeaburu, JV, Ito, T, Crafa, P, Bordi, C & Jensen, RT 2011, 'Mechanism of acid hypersecretion post curative gastrinoma resection', Digestive Diseases and Sciences, vol. 56, no. 1, pp. 139-154. https://doi.org/10.1007/s10620-010-1234-1
Ojeaburu, Jeremiah V. ; Ito, Tetsuhide ; Crafa, Pellegrino ; Bordi, Cesare ; Jensen, Robert T. / Mechanism of acid hypersecretion post curative gastrinoma resection. In: Digestive Diseases and Sciences. 2011 ; Vol. 56, No. 1. pp. 139-154.
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AU - Jensen, Robert T.

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N2 - Background: Some patients with Zollinger-Ellison syndrome post curative gastrinoma resection continue to show gastric acid hypersecretion; however, the mechanism is unknown. Aim: 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.

AB - Background: Some patients with Zollinger-Ellison syndrome post curative gastrinoma resection continue to show gastric acid hypersecretion; however, the mechanism is unknown. Aim: 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.

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