Consideration of Helicobacter pylori infection in childhood: immune response, endoscopic and morphological findings

Related Experiment Video

Updated: Aug 17, 2026

Establishment and Evaluation of a Risk Prediction Model for Pathological Escalation of Gastric Low-Grade Intraepithelial Neoplasia
03:05

Establishment and Evaluation of a Risk Prediction Model for Pathological Escalation of Gastric Low-Grade Intraepithelial Neoplasia

Published on: February 16, 2024

Studenikin MYa1, A A Nijevitch, A G Mutalov

  • 1Institute of Pediatrics, Russian Academy of Medical Sciences, Moscow, Russia.

Acta Paediatrica Japonica : Overseas Edition
|October 1, 1995
PubMed

Insights

Children infected with Helicobacter pylori showed increased IgG and IgE antibody levels, along with endoscopic signs of gastritis. These immune responses correlate with infection severity and endoscopic findings.

Area of Science:

  • Pediatric Gastroenterology
  • Immunology
  • Microbiology

Background:

  • Helicobacter pylori infection is a common cause of chronic gastritis in children.
  • Understanding the immune response in pediatric H. pylori infection is crucial for diagnosis and management.

Purpose of the Study:

  • To investigate the endoscopic and morphological signs of H. pylori infection in children.
  • To evaluate the specific immunoglobulin G (IgG) and total immunoglobulin E (IgE) responses in infected children.
  • To explore correlations between immune markers, endoscopic findings, and histology.

Main Methods:

  • Endoscopic examination and morphological analysis of gastric mucosa in 75 infected children and 36 controls.
  • ELISA technique to measure total IgE and specific IgG against H. pylori.
  • Histological confirmation of gastritis.

Main Results:

  • Endoscopic findings in infected children included erythema, erosions, lymphoid nodular hyperplasia, and ulcers.
  • Gastritis was histologically confirmed in 58 children, with 6% classified as active.
  • Significantly higher anti-H. pylori IgG and total IgE titers were observed in infected children compared to controls.
  • Correlations were noted between anti-H. pylori IgG titers, age, endoscopic signs, and histology.

Conclusions:

  • Pediatric H. pylori infection is associated with distinct endoscopic and histological changes.
  • Elevated IgG and IgE levels are indicative of H. pylori infection in children.
  • Immune responses correlate with disease presentation, suggesting a role in chronic gastroduodenal pathology.

More Related Videos

Gastric Mucosa Quantitative Polymerase Chain Reaction Analysis for Detecting Helicobacter pylori and Antibiotic Resistance05:23

Gastric Mucosa Quantitative Polymerase Chain Reaction Analysis for Detecting Helicobacter pylori and Antibiotic Resistance

Published on: March 7, 2025

Detection of Helicobacter pylori Infection and Antibiotic Resistance via Stool Quantitative Polymerase Chain Reaction Analysis04:56

Detection of Helicobacter pylori Infection and Antibiotic Resistance via Stool Quantitative Polymerase Chain Reaction Analysis

Published on: May 16, 2025

Related Concept Videos

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 I: Introduction01:30

Peptic Ulcer Disease I: Introduction

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...
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...