Endoscopic risk factors to inform early detection of gastric cancer after eradication: Meta-analysis and systematic review.

Objectives: eradication reduces but cannot eliminate the risk of gastric cancer (GC). The prevalence of post-eradication GC has been rising. Characterization of the endoscopic findings of post-eradication GC may facilitate its early detection.

Serodiagnosis and Bacterial Genome of Infection.

The infection caused by is associated with several diseases, including gastric cancer. Several methods for the diagnosis of infection exist, including endoscopy, the urea breath test, and the fecal antigen test, which is the serum antibody titer test that is often used since it is a simple and highly sensitive test. In this context, this study aims to find the association between different antibody reactivities and the organization of bacterial genomes.

Correction to: Risk of gastric cancer in the second decade of follow-up after Helicobacter pylori eradication.

In the original publication of the article, the figure 3 was published with errors. The corrected figure 3 should appear as in this correction.

Risk of gastric cancer in the second decade of follow-up after Helicobacter pylori eradication.

Background And Aims: Eradication of Helicobacter pylori reduces the risk of gastric cancer. In this study, we investigated the risk beyond 10 years after eradication of H. pylori.

DEC205 mediates local and systemic immune responses to infection in humans.

infections cause gastritis and affect systemic immune responses; however, no direct association between immune cells and stomach bacteria has yet been reported. The present study investigated DEC205-mediated phagocytosis of and the role of DEC205-positive macrophages in the human gastric mucosa. DEC205 mediated phagocytosis of was detected immunocytochemically in PMA-stimulated macrophages differentiated from NOMO1 cells.

[Slow progression of gastric adenocarcinoma of fundic gland type: a case report].

Here we report the case of a 73-year-old male who had undergone esophagogastroduodenoscopy (EGD) at a nearby hospital or at our hospital every year since 2006. In 2013, EGD results revealed a discolored lesion, measuring 6mm in diameter, on the anterior side of the upper body in the stomach. Helicobacter pylori (HP) was eradicated in 2010, and the background mucosa around the lesion was endoscopically diagnosed as non-atrophic.

[A Study to Determine the Optimum Antigens for the Serodiagnosis of Helicobacter Pylori Infection in Japanese Patients and the Association with IgG Subclass and Gastric Cancer].

Atrophic gastritis is caused by Helicobacter pylori infection, and is involved in gastric cancer. In this study, we investigated the association with total IgG and IgG subclass antibodies using several strains isolated from Japanese in H. pylori positive and negative individuals, and gastric atrophy using measuring pepsinogen I and II levels.

Seventeen-year effects of eradicating Helicobacter pylori on the prevention of gastric cancer in patients with peptic ulcer; a prospective cohort study.

Background: We previously reported that eradication of Helicobacter pylori in our cohort of patients with peptic ulcer disease reduced their risk of developing gastric cancer to approximately one-third after a mean follow-up period of 3.4 years (up to 8.6 years).

The genetic diversity of Helicobacter pylori virulence genes is not associated with gastric atrophy progression.

Atrophy of the gastric mucosa is a precursor of intestinal-type gastric cancer, and Helicobacter pylori infection causes atrophic gastritis. The aim of this study was to determine whether the genetic diversity of H. pylori virulence genes is associated with the development and progression of gastric atrophy in humans.

Multi-center randomized controlled study to establish the standard third-line regimen for Helicobacter pylori eradication in Japan.

Backgrounds: The present study sought to establish a standard third-line eradication regimen for Helicobacter pylori in Japan.

Methods: Subjects were 204 patients with H. pylori infection in whom the standard Japanese first- and second-line eradication therapies had proven unsuccessful.

Reinfection rate of Helicobacter pylori after eradication treatment: a long-term prospective study in Japan.

Background: We previously reported that the reinfection rate with Helicobacter pylori in Japan was low despite a high prevalence of infection. In the present study, we extended our previous work to more accurately determine the reinfection rate.

Methods: We enrolled 1625 patients (219 women and 1406 men, mean age 50.

[Helicobacter pylori eradication therapy does not prevent gastric cancer development in all patients].

We previously reported that eradication of Helicobacter pylori reduced the risk of gastric cancer developing in patients with peptic ulcer diseases. In the present study, we followed up with our patient group to investigate the occurrences and clinical features of gastric cancers that developed after cure of the infection. Prospective post-eradication evaluations were conducted on 1, 674 consecutive patients who had received successful H.

The long-term risk of gastric cancer after the successful eradication of Helicobacter pylori.

Background: We previously reported that eradication of Helicobacter pylori reduced the risk of developing gastric cancer in patients with peptic ulcer diseases. In the present study, we further followed up our patient group to investigate the occurrence and clinical features of gastric cancers that developed after cure of the infection.

Methods: Prospective post-eradication evaluations were conducted on 1674 consecutive patients who had received successful H.

Helicobacter pylori eradication may induce de novo, but transient and mild, reflux esophagitis: Prospective endoscopic evaluation.

Backgrounds And Aim: The effect on reflux esophagitis of eradicating Helicobacter pylori is variable and not fully defined. We previously reported that in patients who have reflux esophagitis associated with duodenal ulcer, a significant improvement in the pre-existing reflux esophagitis occurred after H. pylori was eradicated.

A better cure rate with 800 mg than with 400 mg clarithromycin regimens in one-week triple therapy for Helicobacter pylori infection in cigarette-smoking peptic ulcer patients.

Background/aims: In Helicobacter pylori eradication therapy, using a proton pump inhibitor plus amoxicillin and clarithromycin (PPI/AC regimen), the impact of the clarithromycin dose and smoking on efficacy is conflicting. Here, we compared the efficacy of 400 and 800 mg of clarithromycin in the regimen in relation to smoking in patients with peptic ulcer disease.

Methods: We studied 601 H.

Baseline gastric mucosal atrophy is a risk factor associated with the development of gastric cancer after Helicobacter pylori eradication therapy in patients with peptic ulcer diseases.

Background: We previously reported that eradication of Helicobacter pylori could reduce the risk of developing gastric cancer in patients with peptic ulcer diseases. In the present study, we further followed up our patient groups to identify factors associated with the development of gastric cancer.

Methods: Prospective posteradication evaluations were conducted in 1342 consecutive patients (1191 men and 151 women; mean age, 50 years) with peptic ulcer disease who had received H.

The effect of eradicating helicobacter pylori on the development of gastric cancer in patients with peptic ulcer disease.

Objectives: Infection with Helicobacter pylori is a risk factor for the development of gastric cancer. However, it is not known whether eradication therapy can prevent the development of gastric cancer in persons in whom the cancer is not yet established. In the present study, we investigated whether the eradication of H.

Helicobacter pylori eradication improves pre-existing reflux esophagitis in patients with duodenal ulcer disease.

Background & Aims: There has been significant controversy over the relationship between Helicobacter pylori infection and reflux esophagitis. We investigated the effects of eradicating H. pylori on the reflux esophagitis found in patients with peptic ulcers.

[Interluekin-1 beta genetic polymorphism influences the impact of cytochrome P 2C19 genotype on the cure rate of H. pylori eradication therapy].

Genetic polymorphism of interleukin(IL)-1 beta is associated with differences in gastric acid suppression in response to H. pylori infection. Thus, the polymorphism might affect H.