Iron Deficiency and IL1β Polymorphisms in Helicobacter pylori-infected Children
Carolina A Serrano1, Andrea Villagrán1, Héctor Toledo2
1Department of Pediatric Gastroenterology and Nutrition, School of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile.
Insights
Helicobacter pylori infection in children is linked to iron deficiency (ID). Increased gastric IL-1β may explain this association, potentially impacting iron absorption and leading to hypochlorhydria.
Area of Science:
- Pediatric Gastroenterology
- Infectious Diseases
- Human Genetics
Background:
- Helicobacter pylori infection is a known factor contributing to iron homeostasis imbalance.
- Interleukin-1 beta (IL-1β) is implicated in iron absorption disturbances.
- The study investigates the role of IL-1β in H. pylori-related iron deficiency (ID) in children.
Purpose of the Study:
- To evaluate IL-1β gene cluster polymorphisms and gastric IL-1β mRNA expression in H. pylori-infected children.
- To determine the relationship between these factors, hypochlorhydria, and iron deficiency (ID).
Main Methods:
- A prospective study involving 105 symptomatic children.
- Analysis of gastric biopsies for H. pylori and IL-1β mRNA expression via RT-PCR.
- Assessment of iron status (ferritin, transferrin, serum iron, TIBC) and IL-1β gene polymorphisms (PCR-RFLP).
Main Results:
- H. pylori positivity was significantly associated with iron deficiency (OR: 5.1).
- Increased gastric IL-1β mRNA was observed in H. pylori-infected children with ID compared to those without ID.
- A positive correlation was found between mucosal IL-1β mRNA and increased gastric pH in infected children with ID.
Conclusions:
- The association between H. pylori infection and iron deficiency in children may be mediated by elevated gastric IL-1β.
- Increased IL-1β may contribute to hypochlorhydria and impaired iron absorption in infected children.
Background:
Helicobacter pylori infection has been associated with an imbalance of iron homeostasis. IL-1β has been related with iron absorption disturbances through a variety of mechanisms. The aim of this study was to evaluate the presence of polymorphic variants for IL-1β cluster and gastric IL1β mRNA expression in H. pylori-infected children and their relationship with hypochlorhydria and iron deficiency (ID).
Patients And Methods:
Prospective study of 123 symptomatic children. At endoscopy, antral biopsies were taken for urease test, pathology and culture and blood for analysis of ferritin, transferrin, serum iron, and total iron-binding capacity. Polymorphisms in the IL-1β cluster (positions -511, -31, +3954, ILRN) were determined by PCR-RFLP. Gastric mucosal expression of IL-1β mRNA was determined by RT-PCR.
Results:
After exclusions, of 105 patients, 33 (31.4%) were H. pylori positive. Nine (8.6%) children were classified as iron deficient (ID). Helicobacter pylori positivity was associated with ID (OR: 5.1; 95% CI: 1.2-21.9) (p = .04). No significant differences were found in allele frequency for IL1β gene cluster polymorphisms between infected and uninfected children. Helicobacter pylori-infected children with ID had significantly increased gastric IL1β mRNA in comparison with infected children without ID. In addition, a significant positive correlation was observed between mucosal IL-1β mRNA and fasting gastric juice pH. Gastric pH values were significantly increased in H. pylori-infected patients with ID compared to uninfected children.
Conclusions:
The established association between H. pylori infection and ID in children may be mediated by increased gastric mucosal IL-1β.
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