Related Experiment Video
Updated: Oct 20, 2025
Retinal and Choroidal Thickness Changes in Populations with Helicobacter pylori Infection by Swept-Source Optical Coherence Tomography
Published on: November 1, 2024
Long-term risk of upper gastrointestinal bleeding after Helicobacter pylori eradication: a population-based cohort
Fang Jiang1, Chuan-Guo Guo1, Ka Shing Cheung1
1Department of Medicine, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong, China.
Background:
The long-term effects of H. pylori eradication in preventing upper GI bleeding (UGIB) remains unknown.
Aim:
To determine the long-term risks of UGIB after H. pylori eradication METHODS: We included all patients who had received clarithromycin-containing triple therapy for the treatment of H. pyliori infection between 2003 and 2012, without subsequent need for re-treatment. We included a propensity score (PS)-matched endoscopy cohort of H. pylori-negative patients as controls. The primary endpoint was the risk of subsequent UGIB. A multivariable Cox model was used to compute the hazard ratio (HR) of UGIB.
Results:
We included 62 738 H. pylori-eradicated and 62 738 PS-matched H. pylori-negative patients, with a median follow-up of 8.1 years (IQR 5.5-10.6). The incidence of UGIB was 20.8 (95% CI 19.5-22.1) and 13.6 (95% CI 12.7-14.7) per 10 000 person-years in H. pylori-eradicated and H. pylori-negative patients, respectively. Compared to controls, H. pylori-eradicated patients had a significantly higher risk of UGIB (HR: 1.65, 95% CI 1.49-1.83). The risk of UGIB in H. pylori-eradicated patients increased after the first 2 years of follow up (HR: 2.18, 95% CI 1.91-2.49). Age-stratified analysis showed that patients >45 years had higher UGIB risk, even after eradication.
Conclusions:
Despite H. pylori eradication, the long-term risk of UGIB was still higher than in H. pylori-negative control subjects. The protective effects of eradication therapy in preventing UGIB appeared to be limited to younger patients, and to within the first 2 years after eradication.
More Related Videos
Related Concept Videos
01:16Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy
01:30Peptic 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...
01:28Peptic 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.
01:26Peptic Ulcer Disease IV: Management
The therapeutic approach involves ensuring adequate rest, implementing drug therapy, promoting smoking cessation, making dietary modifications, and emphasizing long-term follow-up care.
Pharmacological management
The prevailing therapy for peptic ulcers involves a combination of managing the patient's current...
01:24Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors
01:28Peptic 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.