The role of Helicobacter pylori in the development of peptic ulcers
Helicobacter pylori infection occurs in about half of the world's population and prevalence varies greatly in Western and developing countries. The prevalence of H. pylori infection in Swedish people aged 30-50 years is about 30% and is higher in older age groups. Several studies have investigated the transmission of H. pylori infection within the family. A 2003 study of gastroenterologists in the families of Hp-infected children found that all families had one or more family members infected with the H. pylori bacterium. This supports the hypothesis that transmission/spread of the bacterium occurs within the family. A review article also shows that Hp-infected mothers and siblings pose a risk for the newborn child to develop Hp infection before the age of 4 years.
The infection is thought to cause up to 95% of duodenal ulcers, up to 70% of gastric ulcers and at least up to 70% of gastric cancers.
Several studies show an association between Hp infection and atrophic gastritis. Studies using biomarkers to detect and grade atrophic gastritis have been published. The biomarkers can be a tool to detect and offer anti-Hp treatment to people with atrophic gastritis in order to prevent progression to gastric cancer. Characteristics of the infected person, so-called host factors, may be of importance for how an infection with H. pylori develops in the individual. Future research focusing on genetic information from the human genome may identify new genetic host factors and thus increase the chance of identifying potential risk markers for ulcer and gastric cancer.
The starting point for this study is a patient and study material from the Swedish Dyspepsia Study conducted in 1990 with follow-up in 2008. There are limited longitudinal data describing how a long-term infection with H. pylori affects the gastric mucosa of the individual. This study aims to elucidate the possible progression to atrophic gastritis which appears to be a precursor to pernicious anemia and gastric cancer.
Objectives/questions
The study aims to investigate how a chronic infection of the peptic ulcer bacterium H. pylori develops and how it has affected the gastric mucosa over 17-19 years.
Questions:
- How does the H. pylori bacterium change after at least 17 years of chronic infection in the stomach?
- Are there multiple H. pylori strains in the same stomach?
- Are there aggressive H. pylori strains that should be treated even if they are not associated with a serious condition such as peptic ulcer disease or atrophic gastritis at first examination?
- Is it possible to identify virulence markers in certain H. pylori strains that indicate a more aggressive variant of the bacterium?
- What is the macroscopic and histological picture of the gastric mucosa?
Methodology
Subjects from the Swedish Dyspepsia Study 1990 who were infected with H. pylori bacteria have participated in a gastroscopy study.
Biopsy taking and handling of biopsy material
Two biopsies were taken from the corpus and two from the antrum. The biopsies are analyzed at the Swedish Institute for Communicable Diseases. The H. pylori bacteria are cultured and DNA from these is prepared. The entire bacterial mass is analyzed at SMI with so-called 454 pyrosequencing.
The analysis results will then provide a certain picture of what has happened to the development of H. pylori infection over an 18-year period in terms of the pathogenicity of the strain and possible infection with another strain. Biopsies have also been taken for histopathologic examination to be compared with the 1990 results.
Collaborators
Kerstin Stake-Nilsson, University of Gävle
Peter Unge, Vice President, Head of FSCO, Novartis, Basel
Rolf Hultcrantz, Professor, Unit of Gastroenterology and Hepatology, Karolinska University Hospital
Lars Engstrand, Professor and Head of Department, Department of Bacteriology, Swedish Institute for Communicable Diseases, Solna
This page was last updated 2025-01-13