Related Experiment Video
Updated: Sep 2, 2025
Retinal and Choroidal Thickness Changes in Populations with Helicobacter pylori Infection by Swept-Source Optical Coherence Tomography
Published on: November 1, 2024
A Comprehensive Survey of the Relationship between Helicobacter pylori Infection and Atherosclerosis in the Iranian
Masoud Keikha1,2, Mohsen Karbalaei3
1Antimicrobial Resistance Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Background:
Helicobacter pylori is a gram-negative, spiral-shaped, and microaerophilic bacterium that inhabits the human gastric mucosa and is considered to be the most important etiologic agent for gastrointestinal disorders. Recently, however, there is ample evidence to suggest an association between H. pylori infection and extragastric complications, particularly atherosclerosis. The aim of this study was to evaluate the rate of H. pylori infection and the risk of atherosclerosis in an Iranian population.
Methods:
We conducted a comprehensive electronic search on PubMed, Scopus, Google scholar, IranMedex, SID, ISC, and Magiran to find the main published documents related to the relationship between H. pylori and atherosclerosis in Iran. A summary odds ratio with 95% confidence interval was used to investigate the potential association between H. pylori and atherosclerosis. In addition, the heterogeneity between studies was assessed by the I2 index and the Cochrane Q-test. Publication bias was determined using a funnel plot.
Results:
A total of 12 studies met our inclusion criteria and were included in the present study. The results showed that there is a significant positive relationship between infection with this bacterium and the two-fold risk of developing atherosclerosis in the Iranian population (OR: 1.44; 95% CI: 1.07-1.95). However, the heterogeneity was significant and we observed a slight publication bias.
Conclusion:
We confirmed a positive relationship between H. pylori infection and atherosclerosis in the Iranian population, which is similar to other reports from Western countries. Most likely, H. pylori infection can increase the risk of developing atherosclerosis.
More Related Videos
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
05:23Gastric Mucosa Quantitative Polymerase Chain Reaction Analysis for Detecting Helicobacter pylori and Antibiotic Resistance
Published on: March 7, 2025
Related Concept Videos
01:16Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy
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.
01:30Peptic 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...
01:23Gastritis III: Clinical Manifestations and Management
Clinical manifestations of acute gastritis
The patient with acute gastritis may have a rapid onset of symptoms, such as epigastric pain or discomfort, dyspepsia, anorexia, hiccups, or nausea and vomiting, which can last from a few hours to a few days. Erosive or hemorrhagic gastritis may cause bleeding, which may manifest as blood in vomit or as...
01:17Gastritis-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...
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.