Literature DB >> 8722380

Helicobacter pylori and disturbance of gastric function associated with duodenal ulcer disease and gastric cancer.

K E McColl1, E el-Omar.   

Abstract

Helicobacter pylori is now recognized as the major acquired factor in the pathogenesis of duodenal ulcer disease (DU). There is also an association between H. pylori infection and the subsequent development of gastric cancer. The mechanisms by which such infection predisposes the host to these diseases are incompletely understood, but disorders induced by the bacterium in gastric function play a pivotal role. In most patients, H. pylori infection stimulates acid secretion, leading to a predisposition to DU development. However, in some patients, the infection is associated with a significant decrease in acid secretion, a predisposition to gastric cancer. These divergent effects of H. pylori on gastric acid secretion explain the early conflicting reports on changes in acid secretion associated with the infection. The reason why H. pylori infection produces divergent effects on gastric acid secretion is unclear, but may be related to differences in bacterial strains or genetic, dietary or other environmental factors.

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Year:  1996        PMID: 8722380     DOI: 10.3109/00365529609094531

Source DB:  PubMed          Journal:  Scand J Gastroenterol Suppl        ISSN: 0085-5928


  9 in total

Review 1.  Clinical outcome of patients with Helicobacter pylori infection: the bug, the host, or the environment?

Authors:  S N Sgouros; C Bergele
Journal:  Postgrad Med J       Date:  2006-05       Impact factor: 2.401

2.  13C urea breath test for (Helicobacter pylori): determination of the optimal cut-off point in a Canadian community population.

Authors:  Marina Mauro; Vladimir Radovic; Pengfei Zhou; Melanie Wolfe; Markad Kamath; Premsyl Bercik; Ken Croitoru; David Armstrong
Journal:  Can J Gastroenterol       Date:  2006-12       Impact factor: 3.522

3.  Long-term follow-up study of gastric emptying and Helicobacter pylori eradication among patients with functional dyspepsia.

Authors:  J Koskenpato; T Korppi-Tommola; K Kairemo; M Färkkilä
Journal:  Dig Dis Sci       Date:  2000-09       Impact factor: 3.199

Review 4.  [Peptic ulcer disease. Clinical evaluation in 2006].

Authors:  P Malfertheiner; M Bellutti
Journal:  Internist (Berl)       Date:  2006-06       Impact factor: 0.743

5.  Polymorphisms in the intermediate region of VacA impact Helicobacter pylori-induced disease development.

Authors:  Kathleen R Jones; Sungil Jang; Jennifer Y Chang; Jinmoon Kim; In-Sik Chung; Cara H Olsen; D Scott Merrell; Jeong-Heon Cha
Journal:  J Clin Microbiol       Date:  2010-11-17       Impact factor: 5.948

6.  H pylori stimulates proliferation of gastric cancer cells through activating mitogen-activated protein kinase cascade.

Authors:  Yong-Chang Chen; Ying Wang; Jing-Yan Li; Wen-Rong Xu; You-Li Zhang
Journal:  World J Gastroenterol       Date:  2006-10-07       Impact factor: 5.742

7.  Variations in Helicobacter pylori lipopolysaccharide to evade the innate immune component surfactant protein D.

Authors:  Wafa Khamri; Anthony P Moran; Mulugeta L Worku; Q Najma Karim; Marjorie M Walker; Heidi Annuk; John A Ferris; Ben J Appelmelk; Paul Eggleton; Kenneth B M Reid; Mark R Thursz
Journal:  Infect Immun       Date:  2005-11       Impact factor: 3.441

8.  homB status of Helicobacter pylori as a novel marker to distinguish gastric cancer from duodenal ulcer.

Authors:  Sung Woo Jung; Mitsushige Sugimoto; David Y Graham; Yoshio Yamaoka
Journal:  J Clin Microbiol       Date:  2009-08-26       Impact factor: 5.948

9.  Helicobacter pylori stimulates dendritic cells to induce interleukin-17 expression from CD4+ T lymphocytes.

Authors:  Wafa Khamri; Marjorie M Walker; Peter Clark; John C Atherton; Mark R Thursz; Kathleen B Bamford; Robert I Lechler; Giovanna Lombardi
Journal:  Infect Immun       Date:  2009-11-16       Impact factor: 3.441

  9 in total

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