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G ‐cell hyperplasia of the stomach induces ECL ‐cell proliferation in the pyloric glands in a paracrinal manner
Author(s) -
Kasajima Atsuko,
Fujishima Fumiyoshi,
Morikawa Takanori,
Kawasaki Shuhei,
KonosuFukaya Sachiko,
Shibahara Yukiko,
Nakamura Tadaho,
Yoshikawa Takeo,
Iijima Katsunori,
Koike Tomoyuki,
Watanabe Mika,
Shibata Chikashi,
Sasano Hironobu
Publication year - 2015
Publication title -
pathology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 74
eISSN - 1440-1827
pISSN - 1320-5463
DOI - 10.1111/pin.12276
Subject(s) - gastrin , hyperplasia , gastrinoma , somatostatin , enterochromaffin like cell , cell , medicine , cell growth , stomach , endocrinology , zollinger ellison syndrome , pathology , biology , secretion , biochemistry
An inhibitory mechanism toward gastrin hypersecretion is significantly different between G ‐cell hyperplasia and gastrinoma despite the common clinical manifestations; hypergastrinemia and its related persistent gastric ulcers. We recenlty studied the G ‐cell, d ‐cell and ECL ‐cell density in a case of G ‐cell hyperplasia. The 70‐year‐old patient has been treated for persistent gastric ulcers with a markedly increased plasma gastrin (5600 pg/mL). The stomach was surgically resected because of the obstruction associated with ulcer scars. The number of G ‐cells in the pyloric glands was quantified on the surgical specimens and G ‐cell hyperplasia was histolopathologically identified. Immunostainig of histidine decarboxylate revealed the presence of ECL ‐cell hyperplasia in the pyloric glands and its density was significantly and positively correlated with G ‐cell density. Somatostatin immunoreactive cells ( d ‐cells) increased in their number in the oxyntic glands. These results all indicated that hypersecretion of gastrin in G ‐cell hyperplasia could induce ECL ‐cell proliferation in a paracrinal manner. In addition, relatively non‐prominent endocrinological features in the G ‐cell hyperplasia compared to gastrinoma could be also related to the paracrinal somatostatin inhibitory effects upon ECL ‐cells in the pyloric glands.