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Effect of iron deficiency on small intestinal permeability in infants and young children
M Berant1, M Khourie, I S Menzies
1Department of Pediatrics, Rambam Medical Center, Haifa, Israel.
Insights
Iron deficiency in young children can impair small intestinal permeability, specifically affecting transcellular absorption. Restoring iron levels normalizes this function, highlighting the importance of iron status in assessing gut health.
Area of Science:
- Pediatric Gastroenterology
- Nutritional Science
- Biochemistry
Background:
- Iron deficiency is common in infants and young children.
- Altered small intestinal absorptive function is a known complication of iron deficiency.
Purpose of the Study:
- To investigate the impact of iron deficiency on small intestinal permeability in healthy children.
- To assess the reversibility of these permeability changes upon iron repletion.
Main Methods:
- 26 iron-deficient children underwent oral sugar absorption tests (lactulose/rhamnose).
- Urinary excretion of lactulose and rhamnose was measured via gas-liquid chromatography/mass spectrometry.
- Tests were repeated after 3 months of iron supplementation.
Main Results:
- Iron deficiency significantly increased the lactulose/rhamnose permeability index compared to normal values.
- This increase was primarily due to reduced urinary recovery of rhamnose (transcellular route).
- Lactulose recovery (paracellular route) remained unaffected; permeability normalized after iron repletion.
Conclusions:
- Iron deficiency in young children alters small intestinal mucosal permeability.
- The transcellular pathway of absorption appears most affected.
- Iron status is a critical factor to consider when interpreting intestinal permeability tests in pediatric populations.
Abstract:
Small intestinal absorptive function can be disturbed in iron deficiency. We examined the permeability behavior of the small intestinal mucosa toward lactulose and rhamnose in 26 otherwise healthy children with iron deficiency. Their (mean +/- SD) age was 21 +/- 8.6 months; hemoglobin 7.9 +/- 0.9 g/dl, mean corpuscular volume (MCV) 60.1 +/- 3.4 fl, serum iron 2.72 +/- 0.66 mumol/L, serum ferritin 7.3 +/- 1.6 micrograms/L. After an isotonic oral load of both sugars, their 5-h urinary excretion was measured by gas-liquid chromatography/mass spectrometry. The ratio of the percentage of urinary recovery of the sugars [lactulose/rhamnose (%)] was determined as the permeability index. The tests were repeated in the same subjects after 3 months of iron supplementation, and achievement of an iron sufficient state. In the iron-deficient state, the permeability index was significantly higher than the standard normal value (0.15 +/- 0.05 versus less than 0.07; p less than 0.01), but was not different from normal when the children had attained a normal iron status. The major factor for the alteration of the permeability index in the children with iron deficiency was a significantly lower urinary recovery of rhamnose (which passes the small intestinal epithelium by a transcellular route); the recovery of lactulose (which passes through a paracellular route) was not affected by iron deficiency. Our study indicates that iron deficiency in infants and young children can alter permeability characteristics of the small intestinal mucosa. Iron status should therefore be considered when interpreting permeability tests in the young.