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. 1999 Nov;45(5):653–661. doi: 10.1136/gut.45.5.653

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

Y Murayama 1, J Miyagawa 1, Y Shinomura 1, S Kanayama 1, Y Yasunaga 1, H Nishibayashi 1, K Yamamori 1, Y Higashimoto 1, Y Matsuzawa 1
PMCID: PMC1727706  PMID: 10517899

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 of H 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 of H pylori.
RESULTS—In the H 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 with H pylori infection may be functionally associated with the inhibition of acid secretion seen in patients with enlarged fold gastritis.


Keywords: Helicobacter pylori; enlarged fold gastritis; parietal cell morphology; acid secretion; gastrin

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Figure 1  .

Figure 1  

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Immunohistochemical detection of H+,K+-ATPase in human gastric mucosa. (A) Gastric mucosal tissue of an H pylori negative patient without enlarged folds. Parietal cell cytoplasm is specifically and uniformly stained (arrow). Original magnification × 210. (B) Gastric mucosal tissue of an H pylori positive patient with enlarged fold gastritis. Some parietal cells are uniformly stained as above. In other parietal cells, stained cytoplasm is less uniform and appears granular or contains several vacuole-like clear areas which are negatively stained for H+,K+-ATPase (arrows). Original magnification × 210. 

Figure 2  .

Figure 2  

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Semithin plastic sections of gastric mucosa stained with toluidine blue. (A) Gastric mucosal tissue from an H pylori negative patient without enlarged folds. Parietal cells appear large and pyramidal or spherical with central nuclei (arrow). Original magnification × 210. (B) Gastric mucosal tissue from an H pylori positive patient with enlarged fold gastritis. Extensive infiltration of inflammatory cells in the lamina propria is visible. Numerous parietal cells show abnormally dilated canaliculi (arrow) and sometimes vacuole-like structures which are different from canaliculi (arrowhead). Original magnification × 210. 

Figure 3  .

Figure 3  

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Low magnification electron micrograph of the gastric mucosal lumen in an H pylori positive patient with enlarged fold gastritis. N, nucleus. Numerous bacteria (arrowheads) are observed in the mucous layer and close to gastric epithelial cells. There is considerable superficial vacuolation (*), evidence of loss of microvilli, and depletion of mucin granules. The organisms are also observed in the foveolar and intercellular spaces (arrows). Original magnification × 2000 (bar = 5 µm).

Figure 4  .

Figure 4  

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Electron micrographs of parietal cells in an H pylori positive patient with enlarged fold gastritis before (A, B) and after (C) H pylori eradication. N, nucleus; C, intracellular canaliculus. (A) This parietal cell is classified as an altered parietal cell with dilated canaliculi. It has dilated canaliculi containing few short microvilli (bar = 3 µm). (B) This parietal cell is classified as an altered parietal cell with vacuoles. Three large spherical electron lucent structures interpreted to be a vacuole-like structure (VL) are present in the cytoplasm, and microvilli at the luminal surface have completely disappeared (bar = 3 µm). (C) After eradication of H pylori in patients with enlarged fold gastritis, the parietal cell has almost reverted to a normal appearance as seen in H pylori negative patients. Most of the cytoplasm is occupied by tubulovesicles and mitochondria, and canaliculi with developed microvilli can be recognised (arrows) (bar = 3µm). Original magnification: A, × 4000; B, × 4000; C, × 4000. 

Figure 5  .

Figure 5  

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Semiquantitative analysis of parietal cell morphology before and after eradication of H pylori in six patients with enlarged fold gastritis and 12 patients without enlarged folds (six H pylori positive and six H pylori negative). Electron micrographs of gastric mucosa were scored according to parietal cell morphology as being normal, altered with dilated canaliculi, altered with vacuoles, or degenerated. The mean of the percentage of each class is represented by bars. Standard errors are represented by vertical lines.

Figure 6  .

Figure 6  

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Basal acid output (A), 4 µg/kg tetragastrin stimulated maximal acid output (B), and fasting serum gastrin concentrations (C) before and after eradication of H pylori in six patients with enlarged fold gastritis, in six H pylori positive patients without enlarged folds, and six H pylori negative patients.

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