EFFECT OF HELICOBACTER-PYLORI ERADICATION ON ANTRAL SOMATOSTATIN CELL-DENSITY IN HUMANS

Citation
Tck. Tham et al., EFFECT OF HELICOBACTER-PYLORI ERADICATION ON ANTRAL SOMATOSTATIN CELL-DENSITY IN HUMANS, European journal of gastroenterology & hepatology, 10(4), 1998, pp. 289-291
Citations number
17
Categorie Soggetti
Gastroenterology & Hepatology
ISSN journal
0954691X
Volume
10
Issue
4
Year of publication
1998
Pages
289 - 291
Database
ISI
SICI code
0954-691X(1998)10:4<289:EOHEOA>2.0.ZU;2-Q
Abstract
Objective As Helicobacter pylori infection is associated with an eleva tion in plasma gastrin with normal antral gastrin cell counts, an abno rmality in antral somatostatin cells may be associated with the infect ion. We evaluated the effect of eradication of H. pylori on antral som atostatin cell density in the light of antral gastrin cell density and plasma gastrin levels, Design Prospective study, Methods Of 25 dyspep tic patients with H. pylori infection, nine had H. pylori successfully eradicated and the rest remained infected, Antral biopsies were immun ostained for somatostatin cells and plasma gastrin measured before and 4 weeks after ii. pylori eradication therapy. Ten other dyspeptic pat ients without H, pylori infection had their somatostatin cell density evaluated as controls, Results Somatostatin cell density in the patien ts without H. pylori infection at the outset was significantly higher than that in the patients with H. pylori infection at the outset (medi an 57 [18-83] vs. 37 [6-80] cells/mm) respectively (P <0.05). Somatost atin cell density increased after ii. pylori eradication (before treat ment median 50 [15-72]; after treatment 71 [39-107] cells/mm) (P < 0.0 5) but was unchanged with persistent ii. pylori infection. Plasma gast rin decreased after H. pylori eradication (before treatment, median 70 [45-100]; after treatment 30 [10-100] ng/l) (P < 0.05) but was unchan ged with persistent H. pylori infection, Conclusions Following eradica tion of ii. pylori, there is an increase in somatostatin cell density with a fall in plasma gastrin. This supports the theory that H. pylori infection results in a decrease in somatostatin cell density and, as the latter is an inhibitor of gastrin cells, this results in an increa sed plasma gastrin. (C) 1998 Lippincott-Raven Publishers.