Related Experiment Video
Updated: Jan 3, 2026

Retinal and Choroidal Thickness Changes in Populations with Helicobacter pylori Infection by Swept-Source Optical Coherence Tomography
Published on: November 1, 2024
Fundic gland polyp prevalence according to Helicobacter pylori infection status
Takumi Notsu1, Kyoichi Adachi1, Tomoko Mishiro1
1Health Center, Shimane Environment and Health Public Corporation, Matsue, Japan.
Background And Aim:
The prevalence of fundic gland polyp (FGP) occurrence has not been clarified in individuals with Helicobacter pylori infection post-eradicated status. This study was performed to examine the relationship between FGP prevalence and H. pylori infection status.
Methods:
We enrolled 3400 subjects (2185 male subjects and 1215 female subjects; mean age 54.7 ± 9.5 years) with known H. pylori infection status and who underwent an upper gastrointestinal endoscopy examination as part of an annual check-up. Subjects without and with H. pylori infection numbered 1617 and 239, respectively, while 1544 had a post-eradication status. The presence of FGP and degree of gastric mucosal atrophy were determined in each subject using an endoscopic method.
Results:
Endoscopy findings showed FGPs in 1029 (30.3%) of all subjects. The prevalence ratio of FGP positivity in H. pylori-negative, H. pylori-positive, and post-eradicated subjects was 51.9%, 1.7%, and 12.0%, respectively. Multiple logistic regression analysis revealed that female gender, older age, milder gastric mucosal atrophy, and anti-secretory therapy were significant risk factors for FGP occurrence. As compared with H. pylori-positive subjects, the odds ratios for H. pylori-negative and post-eradication status were 48.3 and 6.6, respectively (P < 0.001). In the post-eradication status subjects, longer duration following bacterial eradication was a significant risk factor for occurrence of FGPs.
Conclusion:
The risk of FGP occurrence in individuals who have undergone H. pylori eradication treatment is lower as compared with those who have never been infected. However, that risk increases over time following eradication.
More Related Videos
03:33Rapid Detection of Fecal Antigen of Helicobacter pylori Infection Based on Double Antibody Sandwich Detection Technology
Published on: May 23, 2025
04:56Detection of Helicobacter pylori Infection and Antibiotic Resistance via Stool Quantitative Polymerase Chain Reaction Analysis
Published on: May 16, 2025
Related Concept Videos
Peptic Ulcer Disease III: Clinical Manifestations and Diagnostic Studies
Few clinical manifestations differentiate gastric ulcers from duodenal ulcers. Distinctions in the location, timing, and pain relief are crucial for healthcare providers in differentiating between gastric and duodenal ulcers during clinical assessments.
Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy
Peptic Ulcer Disease I: Introduction
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...
Pathophysiology of Peptic Ulcer Disease: Injurious Factors
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors
Gastritis-II: Pathophysiology
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...