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Published on: February 7, 2015
Helicobacter pylori-associated atrophic gastritis and carotid intima-media thickness: is there a link?
1Department of Gastroenterology, School of Medicine, Mersin University, Mersin, Turkey. enginaltintas@mersin.edu.tr
Insights
Helicobacter pylori (H. pylori)-induced atrophic gastritis does not significantly impact carotid intima-media thickness, a marker for cardiovascular disease risk. This study found no association between H. pylori infection and this specific measure of arterial health.
Area of Science:
- Gastroenterology
- Cardiology
- Infectious Diseases
Background:
- Chronic infections, including Helicobacter pylori (H. pylori), are linked to cardiovascular diseases.
- H. pylori infection can lead to chronic active gastritis and subsequent atrophic gastritis.
- Atrophic gastritis is a condition affecting the stomach lining.
Purpose of the Study:
- To investigate the relationship between H. pylori-induced atrophic gastritis and carotid intima-media thickness (CIMT).
- To determine if CIMT, a marker of subclinical atherosclerosis, is associated with H. pylori-induced atrophic gastritis.
Main Methods:
- Oesophagogastroduodenoscopy was performed on 123 patients.
- H. pylori status was confirmed via histological examination and rapid urease testing.
- Patients were categorized into H. pylori-positive non-atrophic gastritis and H. pylori-positive atrophic gastritis groups.
Main Results:
- Of 123 patients, 92 had H. pylori-positive non-atrophic gastritis and 31 had H. pylori-positive atrophic gastritis.
- No statistically significant difference was observed in carotid intima-media thickness between the two H. pylori-positive groups.
Conclusions:
- Carotid intima-media thickness is not associated with H. pylori-induced atrophic gastritis.
- The findings suggest that H. pylori-induced atrophic gastritis may not be a direct risk factor for increased CIMT.
Abstract:
Chronic infections are associated with cardiovascular diseases. Helicobacter pylori-induced chronic active gastritis results in atrophic gastritis. In this study, we attempted to determine carotid intima-media thickness in patients with and individuals without H. pylori-induced atrophic gastritis. Oesophagogastroduodenoscopy was performed on 123 patients for various reasons. Helicobacter pylori were considered positive when histological examination and rapid urease test showed H. pylori. Helicobacter pylori-positive cases were divided into two groups, namely atrophic gastritis and non-atrophic gastritis. Of 123 patients, 92 patients had H. pylori-positive non-atrophic gastritis and 31 had H. pylori-positive atrophic gastritis. There was no significant difference in carotid intima-media thickness between the two groups. Carotid intima-media thickness is not associated with H. pylori-induced atrophic gastritis.
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