Progression of gastric enterochromaffin-like cells growth in Zollinger-Ellison syndrome and atrophic body gastritis patients.
BACKGROUND
Enterochromaffin-like cell hyperplasia of the gastric body mucosa occurs in hypergastrinaemic conditions such as atrophic body gastritis and Zollinger-Ellison syndrome. However, the time course of change or factors involved are not known.


OBJECTIVE
To compare the rate of change of enterochromaffin-like cell proliferation in patients with atrophic body gastritis and Zollinger-Ellison syndrome.


METHODS
From a consecutive series of atrophic body gastritis and Zollinger-Ellison syndrome patients, studied at the time of first diagnosis, 10 atrophic body gastritis (4 with pernicious anaemia) and 14 Zollinger-Ellison syndrome (4 with multiple endocrine neoplasia type 1) patients were followed-up for a median time of 48 months.


METHODS
At entry and during follow-up patients underwent: plasma gastrin determination, endoscopic sampling of body mucosa for qualitative assessment of enterochromaffin-like cell hyperplasia pattern and degree of glandular atrophy, qualitative and morphometric analyses of body mucosa endocrine cells.


RESULTS
At time of diagnosis, enterochromaffin-like cell lesions were more severe in atrophic body gastritis than in Zollinger-Ellison syndrome. During follow-up, no significant variations were observed in gastrin values, enterochromaffin-like cell patterns and grade of body mucosa atrophy in atrophic body gastritis. In contrast, gastrin levels were significantly increased [median 1200 (235-2625) vs 1947 (225-5200) pg/ml; p<0.001)] as was total volume density of enterochromaffin-like cells [median 1.60 (0.53-4.06) vs 3.18 (1.35-21.13)% of mucosal epithelial component; (p<0.005)] in Zollinger-Ellison syndrome. Micronodular hyperplasia of enterochromaffin-like cells, present in only one patient at diagnosis, was observed in 8 Zollinger-Ellison syndrome patients at follow-up.


CONCLUSIONS
These data suggest that the progression of enterochromaffin-like cell growth in human gastric mucosa requires an increase of and/or a prolonged exposure to severe hypergastrinaemia.
Delle Fave
G
G
Division of Digestive and Liver Diseases, 2nd School of Medicine, University La Sapienza, Rome, Italy. gianfranco.dellefave@uniroma1.it
Marignani
M
M
Corleto
V D
VD
Angeletti
S
S
D'Ambra
G
G
Ferraro
G
G
D'Adda
T
T
Azzoni
C
C
Jensen
R T
RT
Annibale
B
B
Bordi
C
C
D000328:Adult; D000368:Aged; D018450:Disease Progression; D019861:Enterochromaffin-like Cells / Q000473:pathology*; D005260:Female; D005753:Gastric Mucosa / Q000473:pathology; D005755:Gastrins / Q000097:blood; D005757:Gastritis, Atrophic / Q000473:pathology*; D006801:Humans; D006965:Hyperplasia; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D015043:Zollinger-Ellison Syndrome / Q000473:pathology*
D005755:Gastrins