Normal gastric histology in Helicobacter pylori-infected children

F Gottrand1, F Cullu, D Turck

  • 1Service de Pédiatrie, Hôpital Huriez, Lille, France.

Insights

Helicobacter pylori (H. pylori) infection in children can present with normal gastric histology, unlike in adults where it typically causes gastritis or ulcers. This study found H. pylori in children with both normal and abnormal gastric findings.

Area of Science:

  • Pediatric Gastroenterology
  • Infectious Diseases
  • Microbiology

Background:

  • Helicobacter pylori (H. pylori) infection is consistently linked to gastritis or ulcers in adults.
  • Gastritis and ulcers are infrequently observed in children with H. pylori infection.
  • Understanding H. pylori's impact on pediatric gastric mucosa is crucial.

Purpose of the Study:

  • To investigate the association between H. pylori infection and the condition of gastric mucosa in pediatric patients.
  • To determine if H. pylori infection in children always leads to visible gastric pathology.

Main Methods:

  • Retrospective study of 80 children and adolescents (2 months-22 years) with H. pylori infection.
  • Inclusion of 48 institutionalized, neurologically impaired patients (60%).
  • Gastroscopy with antral and fundic biopsies for histological and bacteriological analysis.

Main Results:

  • A normal gastric mucosa was observed in 27.5% (22/80) of infected children.
  • Gastritis was present in 72.5% (58/80) of the study cohort.
  • No significant differences in age, sex, ethnicity, symptoms, or bacterial colonization levels were found between groups with normal versus abnormal histology.

Conclusions:

  • H. pylori infection in children can coexist with normal gastric histology.
  • The findings challenge the assumption that H. pylori always causes significant gastric pathology in pediatric populations.
  • Further research is needed to understand the implications of H. pylori in children with normal histology.
Abstract

Related Concept Videos

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 to M3...
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...
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.
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 mucus...
Gastritis II: Pathophysiology01:26

Gastritis II: Pathophysiology

The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...
Peptic Ulcer Disease II: Pathophysiology01:24

Peptic Ulcer Disease II: Pathophysiology

Peptic ulcer disease develops when protective mechanisms of the gastrointestinal mucosa are overwhelmed by harmful factors, leading to localized erosions in the stomach or proximal duodenum. The main causes are Helicobacter pylori infection and chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs).Helicobacter pylori–Induced InjuryBacterial Adaptation and Colonization:H. pylori is a spiral, Gram-negative bacterium adapted to the acidic stomach. and transmitted through oral-oral or...