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Gut 45:653-661 doi:10.1136/gut.45.5.653
  • Small intestine

Morphological and functional restoration of parietal cells inHelicobacter pylori associated enlarged fold gastritis after eradication

  1. Y Murayama,
  2. J Miyagawa,
  3. Y Shinomura,
  4. S Kanayama,
  5. Y Yasunaga,
  6. H Nishibayashi,
  7. K Yamamori,
  8. Y Higashimoto,
  9. Y Matsuzawa
  1. Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan
  1. Dr Y Murayama, Department of Internal Medicine and Molecular Science, Graduate School of Medicine, B5, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan.
  • Accepted 2 June 1999

Abstract

BACKGROUND/AIM Helicobacter pylori infections are associated with hypochlorhydria in patients with pangastritis. It has previously been shown that eradication of H pylori leads to an increase in acid secretion in H pylori associated enlarged fold gastritis, suggesting that H pylori infection affects parietal cell function in the gastric body. The aim of this study was to evaluate the effects ofH pylori infection on parietal cell morphology and function in hypochlorhydric patients.

PATIENTS/METHODS The presence of H pylori infection, mucosal length, and inflammatory infiltration were investigated in six patients with enlarged fold gastritis and 12 patients without enlarged folds. Parietal cell morphology was examined by immunohistochemistry using an antibody against the α subunit of H+,K+-ATPase and electron microscopy. In addition, gastric acid secretion and fasting serum gastrin concentration were determined before and after the eradication ofH pylori.

RESULTS In theH pylori positive patients with enlarged fold gastritis, fold width, foveolar length, and inflammatory infiltration were increased. In addition, the immunostaining pattern of H+, K+-ATPase was less uniform, and the percentage of altered parietal cells showing dilated canaliculi with vacuole-like structures and few short microvilli was greatly increased compared with that in H pylori positive patients without enlarged folds. After eradication, fold width, foveolar length, and inflammatory infiltrates decreased and nearly all parietal cells were restored to normal morphology. On the other hand, altered parietal cells were negligible in H pylori negative patients. In addition, the basal acid output and tetragastrin stimulated maximal acid output increased significantly from 0.5 (0.5) to 4.1 (1.5) mmol/h and from 2.5 (1.2) to 13.8 (0.7) mmol/h (p<0.01), and fasting serum gastrin concentrations decreased significantly from 213.5 (31.6) to 70.2 (7.5) pg/ml (p<0.01) after eradication in patients with enlarged fold gastritis.

CONCLUSION The morphological changes in parietal cells associated withH pylori infection may be functionally associated with the inhibition of acid secretion seen in patients with enlarged fold gastritis.

Footnotes

  • Abbreviations used in this paper:
    H+,K+-ATPase
    H+ and K+ stimulated adenosine triphosphatase