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Helicobacter pylori infection, gastric acid secretion, and infant growth
A Dale1, J E Thomas, M K Darboe
1Department of Child Health, University of Newcastle-upon-Tyne, United Kingdom.
Insights
Helicobacter pylori infection in Gambian infants is linked to reduced stomach acid and poorer growth. This early infection may increase susceptibility to childhood enteric infections, diarrhea, and malnutrition.
Area of Science:
- Pediatric Infectious Diseases
- Gastroenterology
- Global Health
Background:
- Helicobacter pylori (H. pylori) infection is prevalent in Gambian infants.
- These infants are also susceptible to chronic diarrhea and undernutrition.
- H. pylori infection can impair gastric acid secretion, potentially increasing vulnerability to enteric infections.
Purpose of the Study:
- To investigate the relationship between H. pylori infection and gastric acid output in Gambian infants.
- To assess the impact of H. pylori infection on infant growth and nutritional status.
Main Methods:
- A prospective study involving 101 Gambian infants aged 3-12 months.
- Noninvasive gastric acid output measurement using urine acid output changes.
- 13C urea breath test for H. pylori prevalence and serial anthropometry for growth monitoring.
Main Results:
- A significant association was found between H. pylori infection and reduced urine acid output in 6-month-old infants during weaning.
- Infants with persistent H. pylori infection exhibited significantly poorer growth compared to uninfected infants.
- The findings highlight a critical period during weaning for H. pylori's impact on growth.
Conclusions:
- Infantile H. pylori acquisition may predispose children to enteric infections.
- This can lead to recurrent diarrhea, malnutrition, and impaired growth.
- H. pylori infection in infancy could be a critical factor in childhood growth failure.
Background:
Helicobacter pylori infection is very common in Gambian infants and children, who are also at risk of chronic diarrhoea and undernutrition. Acute H. pylori infection is associated with depressed gastric acid secretion, and loss of the gastric acid barrier may predispose to enteric infections.
Methods:
In a prospective study a noninvasive test of gastric acid output (measurement of change in urine acid output before and after a feed) was performed on a population of Gambian infants at high risk of H. pylori infection. The 13C urea breath tests was used to measure the prevalence of H. pylori infection and growth was measured by serial anthropometry.
Results:
In 101 infants aged 3 to 12 months, there was a significant relation between H. pylori infection and depressed urine acid output in those aged 6 months, during weaning when growth failure and malnutrition begin. Those infants with sustained H. pylori infection grew less well than those without.
Conclusions:
We speculate that H. pylori, acquired in infancy, could be a "key that opens the door" to enteric infection in childhood, leading to recurrent diarrhoea, malnutrition, and growth failure.