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1993 ; 8
(1
): 1-7
Nephropedia Template TP
gab.com Text
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G- and D-cell populations, serum and tissue concentrations of gastrin and
somatostatin in patients with peptic ulcer diseases
#MMPMID7903552
Park SM
; Park HS
Korean J Intern Med
1993[Jan]; 8
(1
): 1-7
PMID7903552
show ga
BACKGROUND: Gastric acid is the most important pathophysiologic determinant in
the development of peptic ulcer diseases, and gastrin and somatostatin are
believed to be physiologic hormonal regulators in gastric acid secretion. The aim
of this study is to investigate patterns of these peptides, both in serum and in
tissue, and to correlate with numbers of their secretory cells in the antral and
the duodenal bulb mucosa. METHODS: The study population was made up of 256
patients with peptic ulcer (duodenal ulcer, 127; gastric ulcer, 74) and 55
patients with non-ulcer control subjects. Serum and mucosal concentrations of
G17, G34 and somatostatin were measured by radioimmunoassay technique and
peptides producing cells were identified immunohistochemically using
peroxidase-antiperoxidase staining technique. RESULTS: Serum G17 concentration
was significantly decreased in duodenal ulcer patients (93.4 +/- 36.0 pg/ml) and
G34 were more than twice as high as G17 both in patients with gastric and
duodenal ulcer (210.6 +/- 50.6 pg/ml and 202.7 +/- 48.1 pg/ml vs 103.8 +/- 41.8
pg/ml and 93.4 +/- 36.0 pg/ml). Antral G17 (19.9 +/- 14.8 mcg/g, tissue) and G34
(26.6 +/- 18.5 mcg/g, tissue) were increased in duodenal ulcer patients and
duodenal G17 (12.5 +/- 9.5 mcg/g. tissue in Gu and 8.5 +/- 7.4 mcg/g. tissue in
DU) and G34 (15.7 +/- 12.6 mcg/g. tissue in GU and 13.9 +/- 12.0 mcg/g. tissue in
DU) concentrations were found to be increased in both gastric and duodenal ulcer
patients than in non-ulcer subjects (G17: 5.3 +/- 4.9 mcg/g. tissue. G34: 6.5 +/-
4.4 mcg/g. tissue). Only the antral somatostatin concentration was significantly
increased in duodenal ulcer patients (5.3 +/- 5.9 mcg/g. tissue). Numbers of the
antral G- and D-cell were lowest in GU patients (48.1 +/- 47.4 and 7.9 +/- 12.3)
and numbers of both cells decreased proportionately with the severity of atrophic
gastritis and/or intestinal metaplasia of the gastric mucosa. D/G cell ratio
between non-ulcer subjects and DU patients was similar (1:4 and 1:5) but slightly
increased in GU patients (1:7). There was no correlation between numbers of each
peptide-producing cells and serum or mucosal concentration of gastrin and
somatostatin. CONCLUSIONS: Patients with duodenal ulcer had decreased level of
serum G17 in the fasting state while mucosal concentrations of G17 and G34 were
increased in the antrum and the duodenal bulb. Patients with gastric ulcer had
increased levels of G17 and G34 only in the duodenal bulb mucosa. Only the antral
somatostatin concentration was significantly increased in duodenal ulcer
patients. Patients with gastric ulcer had lowest numbers of G- and D-cells in the
antrum and numbers of both cells decreased proportionately with the degree of
chronic atrophic gastritis and/or intestinal metaplasia of the gastric antrum.
Numbers of G- and D-cells were not correlated with the serum or mucosal
concentrations of each peptide.