Symptom and Gastritis Severity in Pediatric Duodenogastric Reflux: Interaction with Helicobacter pylori Infection

Melike Arslan1, Coşkun Fırat Özkeçeci2, Meryem İlkay Eren Karanis3

  • 1Division of Pediatric Gastroenterology, Department of Pediatrics, Konya City Hospital, 42090 Konya, Türkiye.

Insights

Duodenogastric reflux (DGR) in children significantly increases dyspeptic symptom severity, independent of gastritis. Helicobacter pylori (H. pylori) infection worsens gastritis and symptoms, with combined DGR and H. pylori causing the most severe symptoms.

Area of Science:

  • Pediatric Gastroenterology
  • Digestive Diseases
  • Clinical Research

Background:

  • Duodenogastric reflux (DGR) is increasingly recognized in children with dyspeptic complaints.
  • The association between DGR, symptom severity, and histopathological gastritis in pediatric patients is not well understood.
  • Helicobacter pylori (H. pylori) infection is a common comorbidity that may influence these relationships.

Purpose of the Study:

  • To evaluate the relationship between dyspeptic symptom severity and gastric histopathological findings in children with DGR.
  • To assess the contribution of concomitant H. pylori infection to symptom severity and gastritis.
  • To determine if DGR is an independent predictor of symptom severity in pediatric dyspepsia.

Main Methods:

  • Multicenter observational cross-sectional study of 180 children (aged 5-18) undergoing upper gastrointestinal endoscopy for dyspeptic symptoms.
  • Symptom severity assessed using a standardized Likert dyspepsia scale.
  • Patients categorized into four groups based on DGR and H. pylori infection status.

Main Results:

  • Children with DGR, with or without H. pylori, exhibited significantly higher symptom severity scores compared to controls.
  • The highest symptom severity scores were observed in the H. pylori-positive/DGR-positive group.
  • H. pylori infection was strongly associated with severe gastritis and inflammatory activity (p < 0.001), while DGR correlated with mild gastritis despite increased symptoms.

Conclusions:

  • DGR is independently linked to increased dyspeptic symptom severity in children, irrespective of histopathological gastritis.
  • H. pylori infection contributes to more severe gastritis and symptom burden.
  • The combination of DGR and H. pylori infection leads to the greatest symptom severity, indicating DGR's clinical significance in pediatric dyspepsia.

Related Concept Videos

Peptic Ulcer01:27

Peptic Ulcer

Peptic ulcers are erosive lesions of the gastric or duodenal lining, most commonly caused by Helicobacter pylori infection. This Gram-negative, helical bacterium has adapted to survive the stomach’s acidic environment by producing urease, which converts urea into ammonia and carbon dioxide. The ammonia neutralizes gastric acid in the bacterium’s immediate environment, allowing colonization of the gastric mucosa. H. pylori attaches to mucus-secreting epithelial cells, penetrates the...
30
Gastritis III: Clinical Manifestations and Management01:23

Gastritis III: Clinical Manifestations and Management

The clinical manifestations of gastritis can vary depending on the cause and type of gastritis, but some common symptoms may include the following.
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...
1.7K
Pathophysiology of Peptic Ulcer Disease: Injurious Factors01:22

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

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...
1.5K
Gastritis-II: Pathophysiology01:17

Gastritis-II: Pathophysiology

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...
1.7K
Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy01:16

Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy

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...
2.0K
Peptic Ulcer Disease III: Clinical Manifestations and Diagnostic Studies01:28

Peptic Ulcer Disease III: Clinical Manifestations and Diagnostic Studies

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.
782