Helicobacter Pylori Infection
Conditions
Keywords
Helicobacter pylori, Interleukin-1 beta, Gastric H+, K+- APTase
Brief summary
We will evaluate the long-term changes of gastric H+, K+-adenosine triphosphatase (H+, K+-ATPase) and Interleukin-1B mRNA expression according to Helicobacter pylori (H.pylori) infection and intestinal metaplasia and investigate the long-term effect of H. pylori eradication
Detailed description
H. pylori suppresses gastric acid secretion by repressing gastric acid pump, H+, K+-ATPase, and stimulating Interleukin-1B. In this study, we will evaluate the expression of H+, K+-ATPase and Interleukin-1B mRNA according to H. pylori infection and intestinal metaplasia in controls and patients with gastric cancer. In addition, we observe the changes of H+, K+-ATPase and Interleukin-1B mRNA expression over 5 years after H. pylori eradication.
Interventions
None listed
Sponsors
Study design
Eligibility
Inclusion criteria
* Controls who did not have any evidence of gastric cancer, gastric dysplasia, esophageal tumor, peptic ulcer and lymphoma on esophagogastroduodenoscopy * Patients with gastric dysplasia or gastric cancer who diagnosed with gastric dysplasia or early gastric cancer in the final pathological report
Exclusion criteria
* Subjects with previous eradication treatment for H. pylori * Subjects with previous gastrectomy
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| Interleukin-1B and H+,K+-ATPase mRNA expression | 1 year | Gastric Interleukin-1B and H+,K+-ATPase mRNA expression in subjects with and without H. pylori infection at baseline, and changes of Interleukin-1B and H+,K+-ATPase mRNA expression with time in subjects without H. pylori infection and subjects who underwent H. pylori eradication successfully. Gastric Interleukin-1B and H+,K+-ATPase mRNA expression measured by reverse transcription polymerase chain reaction, using the gastric mucosa specimen obtained during esophagogastroduodenoscopy |
Countries
South Korea