Helicobacter pylori increases gastric antral juxtamucosal pH

In order to examine the effect ofHelicobacter pylori colonization on the gastric mucus microclimate, antral juxtamucosal pH was measured in 47 patients attending as out patients for upper gastrointestinal endoscopy. The mean pH in 28 patients negative forH. pylori was 6.40±0.24 compared to 6.88±0.16 in 19 patients who were positive (P< 0.0001). In six of seven patients who agreed to a second study,H. pylori was eradicated and the mean pH fell from 6.81±0.17 to 6.08±0.16 (P<0.001). The pH remained high in the one patient who remained positive (6.8 and 7.0). This study provides the firstin vivo evidence thatH. pylori can increase the antral juxtamucosal pH and suggests that ammonia production by the organism is capable of altering gastric mucus microclimate to impair the normal negative feedback controlling gastrin release. This observation may explain the coexistence of relative hypergastrinemia andH. pylori colonization in duodenal ulcer patients.     

Helicobacter pylori and gastric cancer

Infection with Helicobacter pylori is now recognized as the primary cause of peptic ulcers and their recurrence. Compelling evidence has also been found linking H. pylori infection to gastric cancer, the second most common cancer in the world. Given the high rate of patient morbidity and mortality associated with gastric cancer, any method by which one can reduce the occurrence of the disease or increase its early detection is desirable. The strong correlation with H. pylori infection and the current availability of easily administered tests for the detection of the pathogen argue for screening at least those individuals with a family history of gastric cancer or other risk factors. This article reviews the association between H. pylori and gastric cancer and the pathologic changes that the infection produces in the gastric mucosa, as well as the cost-effectiveness of universal testing and eradication of the infection in H. pylori-positive individuals to reduce gastric cancer.     

Helicobacter pylori and gastric cancer

Gastric cancer despite a declining incidence remains a significant cause of morbidity and mortality world wide. There is strong epidemiological and histological evidence to associate Helicobacter pylori infection with the subsequent development of gastric cancer. The exact pathophysiological mechanisms involved remain to be elucidated. There is evidence to relate Helicobacter pylori infection and subsequent inflammation with an increase in gastric epithelial cell proliferation and with the induction of apoptosis. Such alterations in cellular dynamics may promote the development of mitogenic cell lines by inducing DNA damage. Studies have shown that following successful treatment, proliferation rates return to normal. At what histological stage, eradication is of benefit is less clear. It is likely that following the development of atrophy or intestinal metaplasia eradication will only slow progression. It would, therefore, seem logical, that to establish any benefit for a population, treatment should be employed at an earlier stage. As yet, an at risk group has not been identified, and as such population screening cannot be advised, mainly as a result of financial implications and the risk of promoting the development of resistant strains. Recent studies have explored the rules of bacterial factors, CagA and VacA status, host factors, HLA type, and environmental factors as determinants of outcome. Results have been variable. The establishment of an at risk group would enable selective screening and treatment, and thus prevent the development of gastric carcinoma as a result of Helicobacter pylori infection in the long-term.     

Helicobacter pylori and gastric cancer

Abstract This review focuses on the similarities between the epidemiology of gastric cancer and the epidemiology of Helicobacter pylori. Their demographic patterns and the results of studies regarding familial and environmental risk factors are described. The association of gastric cancer and H. pylori infection with both gastric ulcer and chronic atrophic gastritis is also characterized and the possibility that a H. pylori infection could lead to gastric cancer is discussed.     

Helicobacter pylori and gastric acid secretion

Helicobacter pylori (H. pylori) infection leads to profound changes in gastric physiology. Several clinical and animal studies have been performed to clarify the influence of H. pylori on gastric acid secretion. Published data, however, are not consistent throughout. Infection of the gastric antrum, which can be observed mainly in duodenal ulcer patients, increases gastrin release and consecutively acid output. The net effect of corpus and antrum gastritis, such as in patients with gastric cancer, is to decrease acid secretion. Chronic H. pylori infection may finally promote gastric atrophy with irreversibly diminished acid secretion but in earlier stages of this infection eradication of H. pylori normalizes gastric secretory activity.     

Helicobacter pylori infection and gastric cancer

Gastric cancer remains a major health burden on many societies claiming hundreds of thousands of lives every year. The discovery of Helicobacter pylori has no doubt revolutionised our understanding of this malignancy, which is now regarded as a paradigm for infection-induced chronic inflammation-mediated cancer. In this paper, we discuss the evidence for the association between H. pylori and gastric adenocarcinoma and MALT lymphoma. We also discuss the pathogenesis of these two forms of cancer and the factors that determine their outcome. There is no doubt that the knowledge accumulated over the past two decades will be translated into eventual victory over this killer cancer, largely because we now appreciate that the best way to prevent the cancer is by preventing acquisition of the infection in the first place, or by eradicating the infection in infected subjects. Defining the optimal timing of intervention is going to be the challenge facing us over the next two decades.     

Helicobacter pylori gastritis and gastric physiology

It is now recognized that Helicobacter pylori infection exerts profound and diverse effects on gastric acid secretory function and that the alterations in acid secretion depend on the pattern of gastritis caused by the infection. In patients with an antral predominant nonatrophic gastritis, there is acid hypersecretion leading to duodenal ulcer disease. In patients with an atrophic pangastritis, there is markedly reduced acid secretion and increased risk for gastric cancer. It is now recognized that acid secretion also modifies H. pylori gastritis and a person's premorbid acid secretory status may be an important factor in determining the pattern of gastritis that an individual develops. This two-way interaction between H. pylori gastritis and gastric acid secretion is important in understanding the role of H. pylori infection in the response to proton-pump inhibitor therapy: It explains the more profound control of gastric acid secretion in H. pylori-positive patients and why rebound acid hypersecretion is confined to H. pylori-negative subjects.     

Helicobacter pylori and the gastric microbiota

The human microbiota along the gastrointestinal tract is currently extensively studied and a number of studies focuses on elucidating the association between a more or less diverse intestinal microbial community and health and disease. The human stomach is considered to be exclusively inhabited by Helicobacter pylori and further lacks a colonizing non-H. pylori bacterial flora due to the acidic environment. However, recently a limited number of studies using molecular-based methods have provided a broader picture of the stomach microbiota. The question is whether changes in gastric pH or antibiotic treatment can lead to significant shifts in the stomach microbiota that may be involved in disease development such as gastric cancer.     

Helicobacter pylori and other gastric bacteria

The discovery of Helicobacter pylori opened a new field for extensive research on the interactions of this bacterium with the gastric mucosa in the past decades. Basic principles of infection, virulence factors, and treatment options have been identified and recognized. New questions have emerged concerning possible interactions of H. pylori with other bacteria in the human stomach. Herein we discuss hallmark findings in relation to H. pylori infection and the new evidence on other bacteria in the human stomach. Probiotic bacteria seem to interfere with colonizing H. pylori bacteria and thus influence the inflammatory response of the gastric mucosa to H. pylori infection.     

Helicobacter pylori infection and gastric cancer

According to several prospective controlled epidemiologic studies, the positive rate of H. pylori antibody was shown to be higher in the patients with gastric cancer than in the control group. Retrospective studies on the association between gastric cancer and H. pylori have been conducted in a large number of subjects and the results can be classified broadly into two categories, i.e., findings affirming an association and others denying it. Research concerning the association between gastric cancer and H. pylori has achieved great progress over time, leading to the recognition of this relationship by the WHO. One of the greatest concerns is to ascertain whether the final outcome of H. pylori-induced gastritis may lead to gastric cancer. The onset of gastric cancer can be explained as being caused not only by H. pylori infection, but also by a combination of various factors such as food and the environment. However, the possibility that the occurrence of gastric cancer, like the recurrence of peptic ulcer, can be prevented by eradication of H. pylori has also been suggested. Further progress in clinical research is needed to resolve this issue.     

Gastroduodenal mucosal surface and luminal pH in gastric ulcer

Gastroduodenal mucosal surface pH was measuredin situ by electrode in endoscopically normal and gastric ulcer patients. With the exception of the antrum, mucosal surface pH in the ulcer group (GU) resembled that of the endoscopically normal group. In contrast, the antral mucosal surface pH of the GU group of 7.06±0.11 (22) was significantly (P<0.001) higher than that of 5.46±0.36 (34) for the endoscopically normal group. This difference was also evident when comparison was restricted to subjects in both groups having a fundal luminal fluid pH of less than 3. When the fundal luminal pH was below pH 3, antral mucosal surface pH was 4.79±0.41 (24) in endoscopically normal subjects and significantly less (P<0.001) than the value of 6.98±0.18 (12) for gastric ulcer patients. Mucosal surface alkalinity of the GU antrum may be a response to damage but seems inappropriate in view of the likelihood of acid dependent inhibition of gastric acid secretion.