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Plasma Concentrations of Hepcidin in Anemic Zimbabwean Infants
Tatenda G Mupfudze1, Rebecca J Stoltzfus2, Sandra Rukobo3
1Department of International Health, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, United States of America; Zvitambo Institute for Maternal and Child Health Research, Harare, Zimbabwe.
Insights
Infant anemia in Zimbabwe is linked to inflammation early on and iron deficiency later. Plasma hepcidin levels indicate the cause, but more research is needed on hepcidin drivers in developing nations.
Area of Science:
- Pediatric Health
- Nutritional Immunology
- Global Public Health
Background:
- Infant anemia presents a significant global public health challenge.
- Understanding the distinct roles of iron deficiency and inflammation is crucial for effective interventions.
Purpose of the Study:
- To evaluate the relative contributions of iron deficiency and inflammation to anemia in Zimbabwean infants.
- To analyze the relationship between plasma hepcidin concentrations and anemia status.
Main Methods:
- Plasma samples from 289 infants (3, 6, and 12 months) were analyzed for hepcidin, ferritin, sTfR, AGP, and CRP.
- Iron-deficiency anemia (IDA) and anemia of inflammation (AI) were determined in anemic infants.
- Regression analyses assessed hepcidin levels in relation to anemia, adjusting for covariates.
Main Results:
- Early infancy anemia (3-6 months) showed higher CRP and hepcidin, with later anemia (12 months) showing lower hepcidin and ferritin.
- Proportions of IDA and AI varied by age, with IDA being more prevalent later in infancy.
- Plasma hepcidin levels demonstrated age- and sex-dependent changes, reflecting differing anemia etiologies.
Conclusions:
- Anemia in infancy is influenced by inflammation in early life and iron deficiency later.
- Plasma hepcidin concentrations serve as an indicator of the dominant etiological factor (inflammation vs. iron deficiency).
- Further research is required to fully elucidate the drivers of hepcidin during infancy in resource-limited settings.
Objective:
Anemia in infancy is a global public health problem. We evaluated the relative contributions of iron deficiency and inflammation to infant anemia.
Methods:
We measured plasma hepcidin, ferritin, soluble transferrin receptor (sTfR), alpha-1-acid glycoprotein and C-reactive protein (CRP) by ELISA on archived plasma from 289 HIV-unexposed anemic or non-anemic Zimbabwean infants at ages 3 mo, 6 mo and 12 mo. Among anemic infants, we determined the proportion with iron-deficiency anemia (IDA) and anemia of inflammation (AI). We undertook regression analyses of plasma hepcidin and anemia status, adjusting for sex, age and birthweight.
Results:
Anemic infants at 3 mo were more stunted and had higher CRP (median 0.45 vs 0.21 mg/L; P = 0.037) and hepcidin (median 14.7 vs 9.7 ng/mL; P = 0.022) than non-anemic infants, but similar levels of ferritin and sTfR; 11% infants had IDA and 15% had AI. Anemic infants at 6 mo had higher hepcidin (median 7.9 vs 4.5 ng/mL; P = 0.016) and CRP (median 2.33 vs 0.32 mg/L; P<0.001), but lower ferritin (median 13.2 vs 25.1 microg/L; P<0.001) than non-anemic infants; 56% infants had IDA and 12% had AI. Anemic infants at 12 mo had lower ferritin (median 3.2 vs 22.2 microg/L; P<0.001) and hepcidin (median 0.9 vs 1.9 ng/mL; P = 0.019), but similar CRP levels; 48% infants had IDA and 8% had AI. Comparing anemic with non-anemic infants, plasma hepcidin was 568% higher, 405% higher and 64% lower at 3 mo, 6 mo and 12 mo, respectively, after adjusting for sex and birthweight (all p<0.01). Plasma hepcidin declined significantly with age among anemic but not non-anemic infants. Girls had 61% higher hepcidin than boys, after adjusting for age, anemia and birthweight (p<0.001).
Conclusion:
Anemia is driven partly by inflammation early in infancy, and by iron deficiency later in infancy, with plasma hepcidin concentrations reflecting the relative contribution of each. However, there is need to better characterize the drivers of hepcidin during infancy in developing countries.
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