cagA-positive Helicobacter pylori strains and gastro-oesophageal reflux disease
2004; Lippincott Williams & Wilkins; Volume: 16; Issue: 7 Linguagem: Inglês
10.1097/01.meg.0000108354.41221.3e
ISSN1473-5687
Autores Tópico(s)Gastroesophageal reflux and treatments
Resumo• Gastro-oesophageal reflux disease (GORD) and Helicobacter pylori infection are both common in Western countries. • A recently published meta-analysis has shown an association between an absence of H. pylori infection and GORD symptoms. • Infection with cagA-positive H. pylori strains is a causative factor for the development of duodenal ulcer and is a risk factor for gastric cancer. • Data about a protective role of cagA-positive H. pylori strains against more severe reflux oesophagitis are documented in several studies, but questioned by some other studies. • There is a need for further studies to clear the definite role of cagA-positive H. pylori strains in severe reflux oesophagitis and their possible effect on the development of Barrett's adenocarcinoma. The role of Helicobacter pylori in gastro-oesophageal reflux disease (GORD) is still discussed controversially. Different factors might be responsible for the remarkably heterogeneous results of previously performed studies (e.g. location, environmental factors and different virulence factors of H. pylori strains). A very recently published meta-analysis has shown a significant association between the absence of H. pylori infection and GORD symptoms, and a positive correlation between anti-H. pylori therapy and the occurrence of both de-novo and rebound/exacerbated GORD. The results of this meta-analysis are questioned by some authors because of single larger trials and geographical variations of the studies analysed. Data on the role of the cytotoxic-associated antigen (cagA)-positive H. pylori strains are contradictory. Several studies have provided evidence supporting the protecting role of cagA-positive H. pylori strains against GORD, but these results were not confirmed by all studies. A multitude of patients suffer from H. pylori infection and GORD, simultaneously. Therefore, further studies are needed to clearly answer the question whether infection with cagA-positive H. pylori strains, which bear a well-documented risk for gastric cancer and gastro-duodenal ulcer, is really helpful against more severe reflux oesophagitis and, in consequence, perhaps protective against Barrett's oesophagus and Barrett's adenocarcinoma.
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