Literature DB >> 8420745

Helicobacter pylori in duodenal ulcer patients with idiopathic gastric acid hypersecretion.

M J Collen1, R M Strong.   

Abstract

Thirty-three consecutive patients with idiopathic gastric acid hypersecretion (defined as a basal acid output > 10.0 meq/hr with a normal fasting serum gastrin level and negative secretin stimulation test) who were being treated for duodenal ulcer disease and other acid-peptic disorders were evaluated for the presence of Helicobacter pylori by means of a rapid urease test. Fourteen patients had duodenal ulcer and 19 had other acid-peptic disorders (gastroesophageal reflux in 14, including six with Barrett's esophagus; four with nonulcer dyspepsia; and one with erosive gastritis). Helicobacter pylori was present in 12 of the 14 ulcer patients (86%) compared to only two of the 19 nonulcer patients (11%) (P < 0.0001). The distribution of basal acid output for patients with duodenal ulcer was similar to that for nonulcer patients, and no significant difference in the mean basal acid output was found among Helicobacter pylori-positive compared to Helicobacter pylori-negative patients. Seven of the duodenal ulcer patients with a basal acid output greater than 15.0 meq/hr were Helicobacter pylori-positive, suggesting that the organism can withstand even extreme levels of gastric acidity. In conclusion, this study demonstrates that the prevalence of Helicobacter pylori infection in patients with duodenal ulcer disease associated with idiopathic gastric acid hypersecretion is not different from a majority of ulcer patients with normal acid secretory profiles and offers additional evidence that extreme levels of gastric acid are not bactericidal for the organism.

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Mesh:

Year:  1993        PMID: 8420745     DOI: 10.1007/bf01296785

Source DB:  PubMed          Journal:  Dig Dis Sci        ISSN: 0163-2116            Impact factor:   3.199


  30 in total

1.  Effect of acid inhibition on Campylobacter pylori.

Authors:  M Blanco; J M Pajares; M L Jimenez; M Lopez-Brea
Journal:  Scand J Gastroenterol Suppl       Date:  1988

2.  Comparison of different tests for Campylobacter pylori.

Authors:  F Mégraud
Journal:  Scand J Gastroenterol Suppl       Date:  1988

3.  Refractory duodenal ulcers (nonhealing duodenal ulcers with standard doses of antisecretory medication).

Authors:  M J Collen; V J Stanczak; C A Ciarleglio
Journal:  Dig Dis Sci       Date:  1989-02       Impact factor: 3.199

4.  Four hour rapid urease test (RUT) for detecting Campylobacter pylori: is it reliable enough to start treatment?

Authors:  D Vaira; J Holton; S Cairns; M Falzon; P Salmon
Journal:  J Clin Pathol       Date:  1988-03       Impact factor: 3.411

5.  The susceptibility of Campylobacter pylori to antiulcer agents and antibiotics.

Authors:  T Nagate; K Numata; K Hanada; I Kondo
Journal:  J Clin Gastroenterol       Date:  1990       Impact factor: 3.062

Review 6.  Helicobacter pylori and the pathogenesis of gastroduodenal inflammation.

Authors:  M J Blaser
Journal:  J Infect Dis       Date:  1990-04       Impact factor: 5.226

7.  Iatrogenic Campylobacter pylori infection is a cause of epidemic achlorhydria.

Authors:  D Y Graham; L C Alpert; J L Smith; H H Yoshimura
Journal:  Am J Gastroenterol       Date:  1988-09       Impact factor: 10.864

8.  Zollinger-Ellison syndrome. Relation to Helicobacter pylori-associated chronic gastritis and gastric acid secretion.

Authors:  A Fich; N J Talley; R G Shorter; S F Phillips
Journal:  Dig Dis Sci       Date:  1991-01       Impact factor: 3.199

Review 9.  Gastric Campylobacter-like organisms, gastritis, and peptic ulcer disease.

Authors:  M J Blaser
Journal:  Gastroenterology       Date:  1987-08       Impact factor: 22.682

10.  Comparison of ranitidine and cimetidine in the treatment of gastric hypersecretion.

Authors:  M J Collen; J M Howard; K E McArthur; J P Raufman; M J Cornelius; C A Ciarleglio; J D Gardner; R T Jensen
Journal:  Ann Intern Med       Date:  1984-01       Impact factor: 25.391

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