Related Experiment Video
Updated: Mar 13, 2026

Retinal and Choroidal Thickness Changes in Populations with Helicobacter pylori Infection by Swept-Source Optical Coherence Tomography
Published on: November 1, 2024
RELATIONSHIP BETWEEN THE PRESENCE OF HELICOBACTER PYLORI WITH INFLAMMATORY ENDOSCOPIC CHANGES IN GASTRODUODENAL
Irma Cláudia Saboya Ribeiro1,2, Luiz Fernandao Kubrusly1, Paulo Afonso Nunes Nassif1
1Postgraduate Program in Principles of Surgery, Evangelic Faculty of Paraná/University Evangelic Hospital of Curitiba/Medical Research Institute, Curitiba, PR, Brazil.
Background:
The influence of Helicobacter pylori (HP) in inflammatory disorders of the digestive mucosa has been the subject of several studies since socioeconomic, personal and environmental factors were implicated in the bacteria transmission.
Aim:
To correlate the inflammatory endoscopic findings with HP infection and the onset of mucosal diseases mucous of the upper digestive tract.
Method:
Comparative observational study, in which were collected data from 2247 patients who underwent upper endoscopy and biopsies for HP with urease test. The patients were divided into two groups: HP+ and HP- (control) in which endoscopic findings were observed for the following changes: esophagitis, esophageal ulcer, gastritis, erosive gastritis, gastric ulcer, bulboduodenitis, bulbar ulcer and without disease.
Results:
As for esophagitis, there was little disparity in the distribution favorable to HP+ group (HP+ =67.11% and HP- =69.89%) and esophageal ulcer (HP+ =0% and HP- =0, 21%). Gastritis was favorable to HP- group (HP+ =78.34% and HP- =73.63%), as well as erosive gastritis (HP+ = 67,11% and HP- = 64,55%), in bulboduodenitis (HP+ =1,87% and HP- 1,23%), in gastric ulcer (HP+ =2,14% and HP- =2,03%) and in the absence of alterations in the HP+ group (4.81%) with the HP- control group (6,30%), in which there was little disproportion in favor of HP- group, but without statistical significance. As for the bulbar ulcer (HP +=10.16% and HP- =4.48%), there was statistically significant (p=0.00001).
Conclusion:
There is no difference between HP+ and HP- groups in inflammatory changes in endoscopic gastroduodenal mucosa, except for the relationship between HP and bulbar ulcer.
More Related Videos
03:05Author Spotlight: Advancing Early Detection and Treatment of Gastrointestinal Tumors
Published on: February 16, 2024
09:05High Resolution Electron Microscopy of the Helicobacter pylori Cag Type IV Secretion System Pili Produced in Varying Conditions of Iron Availability
Published on: November 21, 2014
Related Concept Videos
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...
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.
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...
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: Mucosal Defense Factors
Peptic Ulcer Disease II: Pathophysiology
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.