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Correlation between plasma or mucosal ghrelin levels and chronic gastritis
Keisei Ikeda1, Toshimi Chiba, Tamotsu Sugai
1Department of Internal Medicine, Iwate Medical University, Iwate, Japan.
Hepato-Gastroenterology
|September 24, 2011
Summary
Plasma and mucosal ghrelin levels correlate with stomach atrophy in chronic gastritis. These ghrelin levels may indicate the extent of atrophy, regardless of Helicobacter pylori infection status.
Area of Science:
- Gastroenterology
- Endocrinology
- Oncology
Background:
- Chronic gastritis is a common condition often associated with Helicobacter pylori infection.
- Ghrelin, a hormone involved in appetite regulation, has been implicated in gastrointestinal pathophysiology.
- The relationship between ghrelin levels and the severity of chronic gastritis requires further elucidation.
Purpose of the Study:
- To investigate the association between plasma and mucosal ghrelin levels and the endoscopic and histological severity of chronic gastritis.
- To explore the correlation between ghrelin levels and acid secretion, and H. pylori infection status.
Main Methods:
- Plasma and mucosal ghrelin levels were measured in 80 individuals with chronic gastritis.
- Histological parameters (activity, inflammation, atrophy, metaplasia) were assessed using the updated Sydney System.
- H. pylori infection, serum pepsinogen I and II, and gastrin levels were also measured.
Main Results:
- H. pylori-positive patients exhibited significantly higher histological parameters and serum pepsinogen levels compared to H. pylori-negative patients.
- Plasma and mucosal ghrelin levels showed a strong correlation with the topographic distribution of gastritis.
- Ghrelin levels were also associated with histological parameters of glandular atrophy in the stomach.
Conclusions:
- Plasma and mucosal ghrelin levels may serve as indicators of glandular atrophy in the stomach.
- Ghrelin's potential role in reflecting atrophy extent is independent of H. pylori infection status.
- Ghrelin warrants further investigation in the context of chronic gastritis pathogenesis.
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