SERUM GASTRIN AND MUCOSAL SOMATOSTATIN IN HELICOBACTER-PYLORI-ASSOCIATED GASTRITIS

Citation
Jm. Gotz et al., SERUM GASTRIN AND MUCOSAL SOMATOSTATIN IN HELICOBACTER-PYLORI-ASSOCIATED GASTRITIS, Scandinavian journal of gastroenterology, 30(11), 1995, pp. 1064-1068
Citations number
34
Categorie Soggetti
Gastroenterology & Hepatology
ISSN journal
00365521
Volume
30
Issue
11
Year of publication
1995
Pages
1064 - 1068
Database
ISI
SICI code
0036-5521(1995)30:11<1064:SGAMSI>2.0.ZU;2-O
Abstract
The aims were to study serum gastrin concentrations and gastric mucosa l somatostatin and gastrin concentrations in relation to the extent of gastritis in Helicobacter pylori infection. Methods: We measured basa l serum gastrin concentrations and somatostatin and gastrin concentrat ions in antral mucosal biopsy specimens and somatostatin concentration s in corpus biopsy specimens in 88 consecutive dyspeptic subjects unde rgoing endoscopy. These subjects were divided into three categories on the basis of histology, serology, and culture: H. pylori-positive pan gastritis, H. pylori-positive antral gastritis with normal body histol ogy, and H. pylori-negative controls. Statistical evaluation was done with the Wilcoxon rank sum test. Results: Basal serum gastrin concentr ations were significantly increased only in subjects with pangastritis and not in those with antral gastritis only, as compared with control s (mean +/- SEM: 72 +/- 7, 46 +/- 10, and 42 +/- 7 ng/l, respectively) . Subjects with pangastritis or antral gastritis had significantly low er antral somatostatin concentrations than controls (mean +/- SEM: 0.8 0 +/- 0.07, 1.03 +/- 0.15, and 2.40 +/- 0.31 mu g/g(protein), respecti vely). We also found significantly lower antral mucosal gastrin concen trations in subjects with pangastritis and in those with antral gastri tis only as compared with controls (mean +/- SEM: 62 +/- 13, 78 +/- 16 , and 165 +/- 25 mu g/g(protein), respectively). In subjects with pang astritis a significantly lower concentration of somatostatin was found in the corpus biopsy specimens than in those with antral gastritis on ly and controls. Conclusion: These results suggest that hypergastrinem ia in H. pylori gastritis is not caused by antral gastritis and antral somatostatin deficiency alone but that corpus inflammation plays a ke y role in the origin of hypergastrinemia. Furthermore, in patients wit h pangastritis a corpus mucosal somatostatin deficiency was found.