Related Experiment Video
Updated: Sep 30, 2025
08:24
Author Spotlight: Gastric Epithelial Cell Responses in Helicobacter pylori infection
Published on: July 5, 2024
817
Does bile reflux reduce Helicobacter pylori gastritis?
Ezgi Kıran Taşcı1, Miray Karakoyun1, Murat Sezak2
1Departments of Pediatric Gastroenterology, Hepatology and Nutrition, Ege University Faculty of Medicine, İzmir, Turkey.
The Turkish Journal of Pediatrics
|March 14, 2022
Summary
Bile reflux, linked to dietary changes, is associated with a lower incidence of Helicobacter pylori gastritis in children. This suggests bile acids may inhibit H. pylori infection.
Area of Science:
- Pediatric Gastroenterology
- Microbiology
- Public Health Nutrition
Background:
- Chronic abdominal pain is common in children.
- Packaged food consumption is rising due to industry changes.
- Bile reflux is increasingly observed in pediatric patients.
Purpose of the Study:
- To investigate the relationship between bile reflux and Helicobacter pylori gastritis in children.
- To assess the impact of changing dietary patterns on these conditions.
Main Methods:
- Retrospective study of 804 pediatric patients undergoing endoscopy for abdominal pain.
- Analysis of endoscopic findings, patient demographics, and H. pylori status.
- Exclusion of patients with chronic diseases.
Main Results:
- Helicobacter pylori gastritis was present in 22.3% of patients.
- Bile reflux was observed in 23.9% of patients.
- A significantly lower rate of H. pylori positivity (14.1%) was found in patients with bile reflux (p=0.002).
Conclusions:
- Helicobacter pylori gastritis is less frequent in children with bile reflux.
- The rise in bile reflux may contribute to the observed decline in H. pylori gastritis rates since 2000.
- Bile acids likely possess bactericidal properties against H. pylori.
Related Concept Videos
01:16Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy
598
Helicobacter pylori, a resilient gram-negative bacterium, can thrive in the stomach's harsh, acidic environment. Infection with H. pylori leads to a cascade of events within the stomach lining. One of the critical disruptions caused by this bacterium is the interference with somatostatin production, a hormone responsible for regulating acid secretion. This interference tips the balance, escalating acid secretion and diminishing bicarbonate levels. This imbalance compromises the defensive...
598
01:17Gastritis-II: Pathophysiology
662
Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
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...
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...
662
01:22Pathophysiology of Peptic Ulcer Disease: Injurious Factors
759
Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
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...
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...
759
01:24Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors
636
Peptic ulcer disease, commonly called PUD, represents a multifaceted condition characterized by disruptions in the lining of the gastrointestinal (GI) tract. Central to the protection of the gastrointestinal lining is the mucosal-bicarbonate barrier. This physiological defense mechanism is a formidable shield against the corrosive effects of gastric acid and pepsin secretion in the stomach. Its role is pivotal in maintaining the structural integrity of the stomach's inner lining.
636
01:30Peptic Ulcer Disease I: Introduction
316
Peptic Ulcer Disease (PUD) is characterized by mucosal excavation in the esophagus, stomach, pylorus, or duodenum. It can manifest as acute or chronic based on the extent and duration of mucosal involvement.
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...
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...
316
01:28Peptic Ulcer Disease III: Clinical Manifestations and Diagnostic Studies
219
Peptic ulcer disease (PUD) presents with diverse symptoms depending on the location and severity of the ulcer. Clinical manifestations of peptic ulcer include dull pain and a burning sensation in the mid-epigastric region.
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.
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.
219