Helicobacter pylori infection in children of Texas

A R Opekun1, M A Gilger, S M Denyes

  • 1Department of Pediatrics, Baylor College of Medicine, Texas Children's Hospital and Veterans Affairs Medical Center, Houston 77030-2399, USA. aopekun@bcm.tmc.edu

Insights

Socioeconomic status, not ethnicity, is the primary risk factor for childhood Helicobacter pylori infection. Acute H. pylori infection is a common cause of abdominal pain in children.

Area of Science:

  • Pediatric Infectious Diseases
  • Gastroenterology
  • Epidemiology

Background:

  • Helicobacter pylori infection is typically acquired in childhood.
  • Prevalence varies by ethnicity and is inversely related to childhood socioeconomic status.
  • This study examines H. pylori seroprevalence in children across ethnic and socioeconomic groups.

Purpose of the Study:

  • To investigate H. pylori seroprevalence in children of diverse ethnic backgrounds.
  • To assess the relationship between socioeconomic status and H. pylori infection in children.
  • To determine the prevalence of acute H. pylori infection in children with recent abdominal pain.

Main Methods:

  • Collected serum samples from 797 children (6 months to 18 years).
  • Determined H. pylori status using a validated pediatric IgG enzyme-linked immunosorbent assay (ELISA).
  • Evaluated acute infection in emergency center patients using 13C-urea breath test and serology.

Main Results:

  • Overall H. pylori seroprevalence was 12.2%, increasing with age.
  • Prevalence was higher in lower socioeconomic status groups (15%) compared to moderate/high (6.6%).
  • Ethnic differences in seroprevalence were explained by socioeconomic status; acute infection found in 18% of children with abdominal pain.

Conclusions:

  • Socioeconomic status is a more significant risk factor than ethnicity for childhood H. pylori acquisition.
  • Acute H. pylori infection is a frequent cause of recent-onset, non-surgical abdominal pain in children.
Abstract

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 II: Pathophysiology01:28

Peptic Ulcer Disease II: Pathophysiology

Peptic Ulcer Disease (PUD) is characterized by the development of ulcers in the stomach or duodenal mucosa. Its pathophysiology is complex, involving a balance between damaging and protective elements.
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.
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...