ISSN:
1573-2568
Keywords:
Campylobacter pylori
;
Helicobacter pylori
;
Zollinger-Ellison syndrome
;
peptic ulcer
;
gastric acid secretion
;
gastrin
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract Helicobacter pylori (previouslyCampylobacter pylori) is almost invariably associated with chronic duodenal ulcer disease. The relationship betweenH. pylori infection and duodenal ulcer in Zollinger-Ellison syndrome is unknown. We investigated the frequency ofH. pylori infection in Zollinger-Ellison syndrome and also what effectH. pylori infection had on gastric function in patients with Zollinger-Ellison syndrome.H. pylori infection was diagnosed based on a specific serologic (ELISA) assay based on high-molecular-weight cell-associated proteins ofH. pylori. We studied 20 patients with Zollinger-Ellison syndrome; 15 men and 5 women ranging in age from 24 to 71 years, median age 51. Six Zollinger-Ellison syndrome patients hadH. pylori infection compared to 100 consecutive patients with chronic recurrent duodenal ulcer disease (P〈0.05). Pretreatment basal acid output in Zollinger-Ellison syndrome patients ranged from 7.9 to 95.0 mmol/hr, median 35.2. Pentagastrin-stimulated maximal acid output ranged from 8.5 to 132 mmol/hr, median 52.7. Acid secretion was lower in theH. pylori-infected patients than the uninfected patients (BAO 24.5±6.5 vs 45.4±6.6, and MAO 44.3±11.8 vs 67.9±10.7, forH. pylori infected vs uninfected patients, respectively). The difference in BAO was statistically significant (P〈0.05). The present results indicate thatH. pylori is not a major contributing factor in duodenal ulcer associated with Zollinger-Ellison syndrome. The association of a reduced BAO withH. pylori suggests that these findings may be related.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF01300080
