Helicobacter pylori in Human Stomach: The Inconsistencies in Clinical Outcomes and the Probable Causes (original) (raw)
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The discovery of Helicobacter pylori (H. pylori) has greatly changed the approach to the management of peptic ulcer disease and gastric cancer. A sound knowledge of the basics of H. pylori is an important aid in the diagnosis and treatment of clinical conditions associated with this infection. Gastric carcinoma is estimated to be the world's second most common cancer as a cause of death. It is hoped that gastric cancer can be prevented by H. pylori eradication; however, this issue is still under investigation. Active research is ongoing to highlight the mechanisms by which H. pylori leads to severe gastric diseases as well as finding associations with extra-gastric diseases.
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Helicobacter pylori infection causes a broad spectrum of clinical diseases and the clinical manifestations of the infection depend on host, environmental, and bacterial factors. These factors have an impact on the pattern and severity of gastritis and ultimately determine the clinical outcome of H. pylori infection. Better staging of gastritis may help to identify patients at risk of gastric cancer. In this article we will examine the complex interaction between host, environmental, and bacterial factors in the pathogenesis of H. pylori infection.
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Helicobacter pylori (H. pylori) is one of the most common infectious diseases worldwide. There are data on the epidemiology, pathophysiology, and histology of this disease that show that H. pylori gastritis has an important role in gastric carcinogenesis. However, it has to be considered that only very few of those infected with H. pylori will develop gastric cancer. Hence, it will be a main target of future research to identify individuals who carry a greater risk for developing gastric cancer, and therefore may benefit from eradication of H. pylori in terms of gastric cancer prevention.
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Helicobacter pylori infection induces gastric inflammation, ulcer, and cancer. H. pylori infection is coordinated in a cascade manner that helps it to colonize in the host. Colonization of bacterium starts by adapting itself to the harsh acidic environment in the stomach. H. pylori has the necessary machinery to neutralise the pH of its surroundings. It also has the ability to sense the pH of its surroundings and move towards the less acidic region. H. pylori's next hurdle is gastric mucosal barrier in the stomach and it has the capability to overcome this gastric mucosal barrier. Once the gastric mucosal barrier is weakened, pathogen uses different adhesion molecules to adhere to the epithelial lining of the stomach. Pathogen then establishes interaction with the host using several toxins that indirectly leads to development of inflammation or gastritis. Prolonged inflammation damages epithelial cells leading to ulcers in the stomach. Genetic changes in the host cell due to H. pylori infection leads to development of gastric cancer. The present paper reviews in detail H. pylori induced gastritis, gastric ulcers and gastric cancer.
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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.
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Helicobacter pylori has been implicated in the pathogenesis of a number of digestive tract disorders, such as chronic active gastritis, peptic ulceration, gastric cancer, and mucosa-associated lymphoid tissue lymphoma. Disease outcome is dependent on many factors, including bacterial genotype, host physiology and genetics, and environmental factors such as diet. Researchers continue to explore the complexities of H. pylori infection, seeking to explain why some individuals have asymptomatic infection, whereas others experience clinical disease. The importance of treating H. pylori infection in patients with gastrointestinal problems has been confirmed in recent years, with clinical trials showing that cure of infection can prevent duodenal ulcer and, to a lesser extent, gastric ulcer recurrence; cure early stage mucosa-associated lymphoid tissue lymphoma; and reduce the chances of developing gastric cancer in high-risk individuals.
Gastric Cancer Risk in Helicobacter Pylori Infected Patients: A Systematic Overview
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Helicobacter pylori is a gastric pathogen that colonizes approximately 50% (over 3 billion) of the world's population, mainly in the developing countries. Infection with H. pylori leads to a chronic inflammatory condition called severe chronic atrophic gastritis (SCAG) and significantly increases the risk of developing duodenal and gastric ulcer disease and gastric cancer. Infection with H. pylori is the strongest known risk factor for gastric cancer. Gastric cancer ranks fourth in incidence and second in mortality among all cancers worldwide. People with SCAG have an increased risk of gastric adenomas in both the upper and lower parts of the stomach. Although H. pylori affects a large percentage of the population, only a small percentage of carriers develop this malignancy. Recent investigations have begun to identify the factors that lead to these complications. Such clinical diversities are caused by variations of H. pylori pathogenicity, host susceptibility, environmental fa...