Related Experiment Video
Updated: Mar 23, 2026
Author Spotlight: Gastric Epithelial Cell Responses in Helicobacter pylori infection
Published on: July 5, 2024
Reduced secretion of epidermal growth factor in duodenal ulcer patients with Helicobacter pylori infection
X Q Chen1, W D Zhang1, B Jiang1
1Xue-Qing Chen, Wan-Dai Zhang, Bo Jiang, Yu-Gang Song, Ri-Zi Reng, Dian-Yuan Zhou, PLA Institute for Digestive Diseases and Department of Gastroenterology, Nanfang Hospital, First Military Medical University, Gangzhou 510515, Guangdong Province, China.
Aim:
To investigate the concentration changes of epidermal growth factor (EGF) in duodenal ulcer patients with Helicobacter pylori (H. pylori) infection.
Methods:
Immunoreactive concentration of somatostatin, gastrin and epidermal growth factor of gastric and saliva juice in healthy volunteers, and chronic gastritis and duodenal ulcer patients with H. pylori infection were measured by radioimmunoassay.
Results:
Gastrin concentration of gastric juice in H. pylori-positive chronic gastritis (P > 0.05) and duodenal ulcer patients (P < 0.01) was higher than that of healthy volunteers (P < 0.05), whereas som atostatin concentration of gastric juice in chronic gastritis (P < 0.05) and duodenal ulcer patients (P < 0.01) was lower than that in healthy volunteers. Furthermore, EGF levels of gastric and saliva juice in duodenal ulcer patients with H. pylori infection (n = 10, 272.0 ng/L ± 96.3 ng/L and 8.3 ng/L ± 2.4 ng/L, respectively) were significantly lower than that in healthy volunteers (n = 12, 405.6 ng/L ± 35.6 ng/mL and 22.0 ng/L ± 17.0 ng/L, respectively) and in H. pylori-positive chronic gastritis patients (n = 25, 423.0 ng/L ± 104.0 ng/L and 22.0 ng/L ± 11.1 ng/L, respectively (P < 0.05).
Conclusion:
A lower secretion of EGF may be a causative factor in the pathogenesis of H. pylori-positive duodenal ulcer.
Related Concept Videos
01:22Pathophysiology 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...
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.
01:27Peptic Ulcer
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...