Digestive Diseases and Sciences

, Volume 40, Supplement 2, pp 50S–62S

Effects of hypochlorhydria and hypergastrinemia on structure and function of gastrointestinal cells

A review and analysis
  • James W. Freston
  • Kurt Borch
  • Stephen J. Brand
  • Enar Carlsson
  • W. Creutzfeldt
  • Rolf Håkanson
  • Lars Olbe
  • Enrico Solcia
  • John H. Walsh
  • M. Michael Wolfe
Article

DOI: 10.1007/BF02214871

Cite this article as:
Freston, J.W., Borch, K., Brand, S.J. et al. Digest Dis Sci (1995) 40(Suppl 2): 50S. doi:10.1007/BF02214871

Abstract

Since hypochlorhydria can induce hypergastrinemia, and gastrin has a trophic effect on some gastrointestinal cells, states that cause elevated plasma gastrin levels are of interest in terms of effects on cell growth and function. This article reviews the relationship between gastric mucosal cells during periods of acid stimulation and inhibition and analyses the effects of hypochlorhydria and hypergastrinemia on gastric and colonic cells and tumors. Hypochlorhydria releases the inhibitory effect of antral gastrin cells, inducing them to release gastrin in the presence of peptides or amino acids in the gastric lumen or in response to antral distension. Gastrin stimulates the oxyntic mucosa, which may lead to hyperplasia of enterochromaffin-like cells, resulting in enterochromaffin-like carcinoid tumors in aged rats and, rarely, in patients with chronic atrophic gastritis or gastrinomas. In addition to hypergastrinemia, other factors appear to be required for the progression of enterochromaffin-like hyperplasia to carcinoids; genetic factors may be involved. Gastrin elevations due to antisecretory drug therapy are indirectly proportional to the degree of acid inhibition and are reversible upon cessation of therapy. The gastrin levels during omeprazole therapy are similar to those caused by gastric vagotomy. Available evidence does not support a relationship between hypergastrinemia and the occurrence or growth of gastric carcinoma or colonic tumors.

Key Words

omeprazole hypochlorhydria hypergastrinemia enterochromaffin-like cell carcinoids peptic ulcer 

Copyright information

© Plenum Publishing Corporation 1995

Authors and Affiliations

  • James W. Freston
    • 1
    • 2
    • 3
    • 4
    • 5
    • 6
    • 7
    • 8
    • 9
    • 10
  • Kurt Borch
    • 1
    • 2
    • 3
    • 4
    • 5
    • 6
    • 7
    • 8
    • 9
    • 10
  • Stephen J. Brand
    • 1
    • 2
    • 3
    • 4
    • 5
    • 6
    • 7
    • 8
    • 9
    • 10
  • Enar Carlsson
    • 1
    • 2
    • 3
    • 4
    • 5
    • 6
    • 7
    • 8
    • 9
    • 10
  • W. Creutzfeldt
    • 1
    • 2
    • 3
    • 4
    • 5
    • 6
    • 7
    • 8
    • 9
    • 10
  • Rolf Håkanson
    • 1
    • 2
    • 3
    • 4
    • 5
    • 6
    • 7
    • 8
    • 9
    • 10
  • Lars Olbe
    • 1
    • 2
    • 3
    • 4
    • 5
    • 6
    • 7
    • 8
    • 9
    • 10
  • Enrico Solcia
    • 1
    • 2
    • 3
    • 4
    • 5
    • 6
    • 7
    • 8
    • 9
    • 10
  • John H. Walsh
    • 1
    • 2
    • 3
    • 4
    • 5
    • 6
    • 7
    • 8
    • 9
    • 10
  • M. Michael Wolfe
    • 1
    • 2
    • 3
    • 4
    • 5
    • 6
    • 7
    • 8
    • 9
    • 10
  1. 1.Department of MedicineUniversity of Connecticut Health CenterFarmingtonUSA
  2. 2.Department of SurgeryUniversity Hospital of LinköpingLinköpingSweden
  3. 3.Gastrointestinal UnitMassachusetts General HospitalBostonUSA
  4. 4.Astra Hässle ABMölndalSweden
  5. 5.Division of Gastroenterology and EndocrinologyUniversity of GöttingenGöttingenGermany
  6. 6.Department of PharmacologyUniversity of LundLundSweden
  7. 7.Department of Surgery IISahlgrenska HospitalGöteborgSweden
  8. 8.Department of Human PathologyUniversity of PaviaPaviaItaly
  9. 9.UCLA Medical SchoolVA WadsworthLos AngelesUSA
  10. 10.Gastroenterology DivisionBrigham and Women's Hospital, Harvard Medical SchoolBostonUSA

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