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Updated: Aug 20, 2026

A Point-of-Care Method with Integrated Decision Support Tool to Estimate Anemia at Population Level
Published on: January 19, 2024
Infection and anemia in Canadian aboriginal infants
Noreen D Willows1, Katherine Gray-Donald
1Department of Agricultural, Food and Nutritional Science, University of Alberta, Edmonton.
Insights
High rates of anemia in Aboriginal infants are linked to both infection and iron deficiency. This study highlights the challenge in distinguishing between these two causes in young children.
Area of Science:
- Pediatrics
- Nutritional Science
- Public Health
Background:
- Anemia prevalence is high in Aboriginal children.
- The roles of infection and iron deficiency in causing anemia are unclear in this population.
Purpose of the Study:
- To determine the contribution of iron deficiency to anemia in Aboriginal infants.
- To differentiate the effects of infection from dietary iron deficiency on anemia.
Main Methods:
- Screened 144 Aboriginal infants for anemia (hemoglobin <105 g/L) and iron deficiency.
- Assessed infection history in the two weeks prior to screening.
- Measured serum iron and serum ferritin concentrations to assess iron status.
Main Results:
- Anemia prevalence was 18.8% in the screened infants.
- Anemic infants were significantly more likely to have had a recent infection (74.1% vs. 48.7%).
- Iron deficiency, indicated by low serum iron, was more prevalent in anemic infants (73.7% vs. 38.3%).
- Serum ferritin levels, a marker for iron deficiency, were paradoxically lower in infants with recent infections, likely due to ferritin's acute-phase response.
Conclusions:
- Both infection and iron deficiency contribute to anemia in Aboriginal infants.
- Distinguishing between anemia caused by infection and that caused by dietary iron deficiency is challenging.
- Further research is needed to understand the interplay between infection and iron status in pediatric anemia.
Abstract:
The prevalence of anemia in Aboriginal children is high, but, given the high burden of infection in these children, the extent to which anemia is due to iron deficiency and/or infection is unclear. To determine the contribution of iron deficiency to anemia, we screened 144 Aboriginal infants (70 boys, 74 girls) who were free from infection. The prevalence of anemia (hemoglobin <105 g/L) was 18.8%; caregivers reported that 53.5% of infants had had an infection in the two weeks before screening. Anemic infants were more likely than non-anemic infants to have had an infection before screening (74.1% versus 48.7%, p = 0.02), and anemic infants had a higher prevalence of iron deficiency revealed by low serum iron concentrations (<7 micromol/L) (73.7% versus 38.3%, p <0.01). Iron deficiency measured using serum ferritin concentration tended to be less marked in infants who had had an infection (13% versus 30.3%, p = 0.06); this is probably because serum ferritin is a positive acute-phase protein. This study indicates the difficulty of isolating the contribution of infection to anemia from the separate effects of dietary iron deficiency.
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