Mini-Symposium
Helicobacter pylori infection: A clinical overview

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Abstract

Background

Helicobcater pylori colonizes the stomach of more than half of the world's population, and the infection continues to play a key role in the pathogenesis of a number of gastroduodenal diseases. Colonization of the gastric mucosa with Helicobcater pylori results in the development of chronic gastritis in all infected individuals and in a subset of patients chronic gastritis progresses to complications (i.e. ulcer disease, gastric neoplasias, some distinct extragastric disorders). The clinical outcome of the disease is dependent on many variables, including Helicobcater pylori genotype, innate host physiology, genetic predisposition and environmental factors. Helicobcater pylori eradication decreases the incidence of gastroduodenal ulcer and prevents its recurrence. Helicobcater pylori eradication for gastric cancer prevention has been suggested by preclinical research and clinical trials, showing even reversibility of precancerous lesions (atrophic gastritis and intestinal metaplasia) after Helicobcater pylori eradication.

Aims

To review the current literature about H. pylori and its related pathologies.

Conclusion

At present, several clinical manifestations are recognized to be causally linked to Helicobcater pylori infection, and most of them can be cured by Helicobcater pylori eradication. Besides the relationship of Helicobcater pylori and gastroduodenal diseases, it has been well established that Helicobcater pylori infection is also involved in some extragastrointestinal diseases.

Introduction

More than 20 years after its discovery, H. pylori infection remains the main cause of gastric and duodenal diseases. Epidemiologic and clinical studies have provided convincing evidence that H. pylori infection is the cause of chronic gastritis, peptic ulcer disease, low grade gastric mucosa associated lymphoid tissue (MALT) lymphoma and gastric adenocarcinoma [1], [2], [3].

This review focuses on the role of H. pylori in gastrointestinal diseases including functional dyspepsia, peptic ulcer disease and nonsteroidal anti-inflammatory drug (NSAID) associated ulcers, GERD, gastric adenocarcinoma and MALT lymphoma, as well as in some extragastrointestinal diseases such as idiopathic thrombocytic purpura, iron deficiency anaemia and allergic diseases.

Section snippets

H. pylori and dyspepsia

Dyspepsia is a frequent disorder that at least sporadically affects up to 25% of the population. The cause can be organic (i.e. ulcer) but most of the time the nature of the disease is functional. Dyspepsia is defined as epigastric pain or discomfort in the upper abdomen. Patients who undergo endoscopy for upper gastrointestinal complaints with no abnormalities detected (and no organ pathologies in the ultrasound as well) are defined as functional dyspepsia. For the clinical management, the

Non-NSAID-related peptic ulcer disease

The strong correlation between the colonization of H. pylori and peptic ulcer disease is well established by an abundance of studies. The clinical outcome of H. pylori infection is highly variable and depends on host, environmental and bacterial virulence factors. The pattern of colonization and distribution of gastritis strongly correlates with the clinical manifestation. Antral-predominant gastritis shows a strong correlation to the development of duodenal ulcers, whereas patients with

H. pylori and gastroesophageal reflux disease (GERD)

The interaction between colonization of H. pylori and GERD is another topic of dispute over the past years. The prevalence of H. pylori was found to be lower among patients suffering from GERD [33], [34]. The falling prevalence of H. pylori and related diseases in developed countries over the past decades with the inverse correlation to an increase of GERD has prompted the speculation of H. pylori as a protecting factor for the esophagus, while others argued that [35], [36], [37], [38], [39],

H. pylori and MALT lymphoma

H. pylori has been clearly defined as a causative agent for the development of MALT lymphoma. MALT lymphoma is a unique and distinct form of marginal zone B-cell-non-Hodgkin's lymphoma. MALT lymphomas account for approximately 7–8% of all non-Hodgkin's lymphomas, and the gastrointestinal tract is the most common site of the disease [45]. The association between H. pylori infection and MALT lymphoma has been provided by various studies and a pathogenic link has been confirmed. MALT lymphoma

Gastric adenocarcinoma

Despite a decline of the incidence of gastric cancer in developed countries, gastric cancer remains the fifth most common cancer and shows responsibility for the death of more than 100,000 each year in Europe [50]. The etiology of gastric carcinogenesis has been demonstrated to be multifactorial. The most important risk factor is the infection with H. pylori. Host genetic elements, such as a pro-inflammatory cytokine profile and/or a positive family history as well as bacterial virulence

H. pylori and extragastric diseases

As of today, among the long list of possible associations, H. pylori infection is confirmed to play an important role in three extragastroduodenal diseases.

Conclusion

H. pylori is the key pathogen in gastroduodenal diseases. All infected individuals develop chronic gastritis, and in a subset of patients a progression to severe complications occurs. The cure of H. pylori represents a change in the paradigm of peptic ulcer disease treatment. The challenge now is to prevent H. pylori infection and in particular to prevent gastric cancer by H. pylori eradication.

Practice points

  • •

    H. pylori eradication is recommended in infected patients with different gastroduodenal pathologies.

  • •

Conflict of interest statement

None declared.

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