HYPERPLASIA OF GASTRIC ANTRAL BETA-MICROSEMINOPROTEIN ENDOCRINE-LIKE CELLS AND INCREASED SERUM LEVELS OF BETA-MICROSEMINOPROTEIN IN ATROPHIC CORPUS GASTRITIS
H. Weiber et al., HYPERPLASIA OF GASTRIC ANTRAL BETA-MICROSEMINOPROTEIN ENDOCRINE-LIKE CELLS AND INCREASED SERUM LEVELS OF BETA-MICROSEMINOPROTEIN IN ATROPHIC CORPUS GASTRITIS, Scandinavian journal of gastroenterology, 33(9), 1998, pp. 911-915
Background: beta-Microseminoprotein is a 94-kDa protein present on mos
t mucosal surfaces in the body. It is produced in mucin cells but is a
lso found in a particular type of cells (E-cells) in the gastric antra
l mucosa. Most of these cells also contain gastrin. In atrophic corpus
gastritis the gastrin-producing cells become hyperplastic, and the pa
tients have hypergastrinemia. We wanted to ascertain whether there is
a similar effect on the E-cells and on the concentration of beta-micro
seminoprotein in serum. Methods: Antral biopsy specimens from 10 patie
nts with atrophic corpus gastritis and 10 controls were stained immuno
histochemically for beta-microseminoprotein and gastrin. beta-Microsem
inoprotein and gastrin were measured by radioimmunoassay in serum from
15 women with atrophic corpus gastritis and 31 healthy female blood d
onors. Results: There was a 3.5-fold increase of the number of E-cells
(which also were hypertrophic) and a 2.1 times higher serum concentra
tion of beta-microseminoprotein in the patients with atrophic corpus g
astritis than in the control subjects. Gastrin was seen in 28% of the
E-cells in patients with atrophic corpus gastritis, compared with 87%
in normal antral mucosa. There was no correlation between the serum co
ncentrations of beta-microseminoprotein and gastrin. Conclusions: in a
trophic corpus gastritis antrum E-cells undergo hyperplasia and hypert
rophy, and the proportion of E-cells containing gastrin decreases. Inc
reased amounts of beta-microseminoprotein are secreted to the blood bu
t uncorrelated with gastrin.