• Contents

  1. 1. Abstract
  2. 2. Introduction
  3. 3. Helicobacter pylori
     1. 3.1 Definition, characteristic of helicobacter pylori
     2. 3.2 physiological background
     3. 3.3 pathophysiology and gastric pathology
     4. 3.4 clinical presentation
        1. 3.4.1 symptoms
        2. 3.4.2 diagnostics
        3. 3.4.3 treatments
        4. 3.4.4 virulence factors
  4. 4. Conclusion
  5. 5. References

1. Abstract

2. Introduction

3. Helicobacter pylori

3.1 Definition, characteristic of helicobacter pylori

3.2 physiological background

3.3 pathophysiology and gastric pathology

Helicobacter.pylori is presumed to be transmitted through the oral or fecal route, and for humans, it has a very high infection rate within the family. In the stomach of individuals infected with H.pylori, H.pylori produces urease, decomposes the urea component of the stomach and reduces the acidity of the surrounding area. H.pylori migrates in the stomach using flagella, and adheres to the gastric epithelial cells through adhesion factors such as BabA. H.pylori does not always cause acute non-specific digestive symptoms, however, it is reported that H.pylori leads to chronic gastrointestinal diseases around 10-20% of the case. The complex interaction between virulence factors such as CagA and VacA, which were secreted by Helicobacter. pylori, preservation of the mucous membrane of the body, and other environmental factors are implicated in causing H. pylori-borne diseases. The immune response of the body activates for H. pylori infection, but it is known to accelerate damage to the gastric mucosa rather than removing the source of infection(virulence factors). Helicobacter. pylori causes antrum-predominant gastritis, promotes gastrin secretion, inhibits somatostatin secretion, and leads duodenal ulcer. It is also reported that H. pylori inhibits gastric acid secretion, causes pangastritis or corpus predominant gastritis, and leads gastric ulcer and gastric cancer. Helicobacter. Pylori is known as the main factor to cause intestinal type gastric cancer through the sequential process of atrophic gastritis, intestinal meta-plasia and dysplasia. It is reported that H. pylori was the main factor of gastric cancers in 71-95% cases, but conversely, not all H. pylori-infected patients got gastric cancer (less than 1% of H. pylori-infected patients had gastric cancer). It is estimated that cancer occurs due to multifactorial etiology such as genetic factors, diet, and the characteristics of the bacteria themselves. Primary gastric displacement zone B-cell lymphoma accounts for 1-7% of malignant tumors in the stomach, but is known to be the most common type, accounting for 50-60% of all gastrointestinal lymphomas. Up to 98% of gastric B-cell lymphomas and 30% of H. pylori infections produce lymphoid follicles through the inflammatory reaction of the mucous membrane, which is presumed to be a precursor to marginal B-cell lymphoma. In about 60% of patients complaining of symptoms of functional dyspepsia are diagnosed as functional dyspepsia, it shows a prevalence rate of 11-14% and no organic diseases are found through endoscopy and/or radiological examination, etc. However, the diseases such as Postprandial discomfort, bloating, epigastric pain, heartburn, etc. occur chronically and recurrently. Research says that 40 to 70% of functional indigestion is caused by H. pylori infection, and chronic gastric inflammation by H. pylori infection was suggested as a mechanism of the functional dyspepsia occurrence. Inflammatory reaction activated by chronic infection causes abnormalities in gastrointestinal motility and awareness due to hyper hormones and changes in gastric acid secretion.

3.4 clinical presentation

3.4.1 symptoms

3.4.2 diagnostics

3.4.3 treatments

3.4.4 virulence factors

4. Conclusion

5. References

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