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Clinicopathological Study of G-cell Area and Antral Gastritis Takumi Nanbu 1 , Toshiyuki Matsui 1 , Mitsuo Iida 1 , Tsuneyoshi Yao 2 1The Second Department of Internal Medicine, Faculty of Medicine, Kyushu University 2The First Department of lnternal Medicine, School of Medicine, Fukuoka University pp.625-633
Published Date 1985/6/25
DOI https://doi.org/10.11477/mf.1403109875
  • Abstract
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 To determine the effect of varying degrees of chronic gastritis on the gastric secretion, five factors were analyzed in 44 patients (duodenal ulcer 16, gastric ulcer 8, gastric cancer 20); gastric acid output, postprandial gastrin response (percent peak gastrin responce, %PGR), degree of pyloric gland atrophy and intestinal metaplasia in the pyloric antrum, and total G-cell number (TGCN). G-cells were studied by the specific immunoperoxidase method. There was a significant positive correlation between TGCN and %PGR. TGCN was inversely related to degree of pyloric gland atrophy and intestinal metaplasia. There was a fall in postprandial gastrin response with increasing grade of pyloric gland atrophy and intestinal metaplasia. It is concluded that chronic gastritis causes a reduction in gastrin secretion associated with a decrease in G-cell population. No correlation was found between gastric acid output and postprandial gastrin response.

 G-cell distribution (G-cell area) was also studied. The size of G-cell area was estimated in 38 cases without extremely diffuse intestinal metaplasia, and it was not related toage, and degree of pyloric gland atrophy and intestinal metaplasia. There was no case with the proximal border of pseudopyloric gland distribution corresponding completely with that of G-cell area. Nakamura's F boundary line was not associated with G-cell area. It issuggested that G-cell area remains unchanged, although distribution of pseudopyloric gland and intestinal metaplasia extends with advancing age.


Copyright © 1985, Igaku-Shoin Ltd. All rights reserved.

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電子版ISSN 1882-1219 印刷版ISSN 0536-2180 医学書院

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