Low rates of Helicobacter pylori reinfection in children

M Rowland1, D Kumar, L Daly

  • 1Department of Paediatrics, University College, Dublin, Ireland.

Gastroenterology
|July 27, 1999
PubMed

Insights

Children over 5 rarely get reinfected with Helicobacter pylori after treatment. Age is the main factor, not family infections or socioeconomic status, suggesting family-wide treatment isn't always needed.

Area of Science:

  • Pediatric Infectious Diseases
  • Gastroenterology
  • Microbiology

Background:

  • Reinfection with Helicobacter pylori (H. pylori) is uncommon in adults but more frequent in children.
  • Understanding reinfection patterns in children is crucial for effective treatment strategies.

Purpose of the Study:

  • To investigate the likelihood of H. pylori reinfection in children post-treatment.
  • To identify potential risk factors associated with H. pylori reinfection in pediatric populations.

Main Methods:

  • A prospective study followed 52 children with documented successful H. pylori treatment.
  • [(13)C]urea breath tests were used for children, parents, and siblings.
  • Cox logistic regression analysis identified risk factors for reinfection.

Main Results:

  • Only 11.5% of children were reinfected during a mean follow-up of 24 months.
  • Age was the sole significant risk factor; children reinfected were younger (mean 5.8 years) than those who remained clear (mean 12.3 years).
  • Reinfection was rare (4.3%) in children over 5, irrespective of infected family members or socioeconomic status.

Conclusions:

  • H. pylori reinfection is infrequent in children over 5 years old.
  • Age is the primary determinant of reinfection risk in children.
  • Treating all family members for H. pylori may not be necessary for long-term eradication 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.
Pharmacokinetics in Pediatric Patients: Overview and Drug Absorption01:23

Pharmacokinetics in Pediatric Patients: Overview and Drug Absorption

Understanding the physiological differences in the pediatric population is crucial for effective pharmacotherapy. Neonates, infants, and children exhibit significant variations in gastric pH, gastric emptying time, intestinal transit time, and biliary function. These variations profoundly affect oral drug absorption, necessitating a nuanced approach to pediatric dosing.Neonates present with a unique physiological profile, having a gastric pH greater than 4 and faster and more irregular gastric...
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...