G-cell hyperplasia of the stomach induces ECL-cell proliferation in the pyloric glands in a paracrinal manner.
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.
Department of Pathology, Tohoku University Hospital, Sendai, Japan.
Atsuko
A
Kasajima
Fumiyoshi
F
Fujishima
Takanori
T
Morikawa
Shuhei
S
Kawasaki
Sachiko
S
Konosu-Fukaya
Yukiko
Y
Shibahara
Tadaho
T
Nakamura
Takeo
T
Yoshikawa
Katsunori
K
Iijima
Tomoyuki
T
Koike
Mika
M
Watanabe
Chikashi
C
Shibata
Hironobu
H
Sasano
D000368:Aged; D002452:Cell Count; D049109:Cell Proliferation; D005260:Female; D005753:Gastric Mucosa / Q000473:pathology*; D005755:Gastrins / Q000378:metabolism*; D006801:Humans; D006965:Hyperplasia / Q000473:pathology; D013270:Stomach / Q000473:pathology*
D005755:Gastrins
ECL-cell hyperplasia; G-cell hyperplasia; hypergastrinemia; persistent ulcers