Gastric luminal somatostatin secretion of normals and patients with pernicious anemia and with Zollinger-Ellison syndrome

We studied the release of gastric luminal somatostatin-like immunoreactivity (SLI) in response to a pentagastrin infusion (0.9 microgram/kg/hr, intravenous) in five normal volunteers, five patients with pernicious anemia, and two patients with Zollinger-Ellison syndrome. In addition, we studied the...

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Veröffentlicht in:Digestive diseases and sciences 1988-12, Vol.33 (12), p.1596-1600
Hauptverfasser: ERTAN, A, OZDEN, A, GOLODNER, E, DEGERTEKIN, H, ARIMURA, A
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container_end_page 1600
container_issue 12
container_start_page 1596
container_title Digestive diseases and sciences
container_volume 33
creator ERTAN, A
OZDEN, A
GOLODNER, E
DEGERTEKIN, H
ARIMURA, A
description We studied the release of gastric luminal somatostatin-like immunoreactivity (SLI) in response to a pentagastrin infusion (0.9 microgram/kg/hr, intravenous) in five normal volunteers, five patients with pernicious anemia, and two patients with Zollinger-Ellison syndrome. In addition, we studied the gastric luminal SLI secretion in response to a gastric luminal acid perfusion in two patients with pernicious anemia. Our results have shown that: (1) pentagastrin caused a parallel increase in luminal hydrogen ions and SLI release in normal volunteers; (2) Zollinger-Ellison patients had elevated basal acid and SLI levels that did not increase further with pentagastrin; (3) pentagastrin did not increase gastric acid or luminal SLI secretion in pernicious anemia patients; and (4) in pernicious anemia patients, a gastric luminal acid perfusion caused a significant increase in gastric luminal SLI over baseline values. In conclusion, gastric luminal hydrochloric acid appears to be a factor which stimulates the secretion of luminal SLI in human beings.
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In addition, we studied the gastric luminal SLI secretion in response to a gastric luminal acid perfusion in two patients with pernicious anemia. Our results have shown that: (1) pentagastrin caused a parallel increase in luminal hydrogen ions and SLI release in normal volunteers; (2) Zollinger-Ellison patients had elevated basal acid and SLI levels that did not increase further with pentagastrin; (3) pentagastrin did not increase gastric acid or luminal SLI secretion in pernicious anemia patients; and (4) in pernicious anemia patients, a gastric luminal acid perfusion caused a significant increase in gastric luminal SLI over baseline values. 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In addition, we studied the gastric luminal SLI secretion in response to a gastric luminal acid perfusion in two patients with pernicious anemia. Our results have shown that: (1) pentagastrin caused a parallel increase in luminal hydrogen ions and SLI release in normal volunteers; (2) Zollinger-Ellison patients had elevated basal acid and SLI levels that did not increase further with pentagastrin; (3) pentagastrin did not increase gastric acid or luminal SLI secretion in pernicious anemia patients; and (4) in pernicious anemia patients, a gastric luminal acid perfusion caused a significant increase in gastric luminal SLI over baseline values. 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subjects Adult
Anemia, Pernicious - metabolism
Biological and medical sciences
Female
Gastric Acid - metabolism
Gastric Mucosa - metabolism
Gastroenterology. Liver. Pancreas. Abdomen
Humans
Male
Medical sciences
Middle Aged
Other diseases. Semiology
Pentagastrin
Somatostatin - metabolism
Stomach. Duodenum. Small intestine. Colon. Rectum. Anus
Zollinger-Ellison Syndrome - metabolism
title Gastric luminal somatostatin secretion of normals and patients with pernicious anemia and with Zollinger-Ellison syndrome
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