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Effect of maternal and neonatal vitamin A supplementation and other postnatal factors on anemia in Zimbabwean infants: a prospective, randomized study^1,2,3

¹ From the Cancer Prevention Fellowship Program, Division of Cancer Prevention, National Cancer Institute, Bethesda, MD (MFM); the Department of International Health, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD (JHH); Paediatrics and Child Health (PJI) and the Division of Nutrition, Institute of Food, Nutrition and Family Sciences (LCM), University of Zimbabwe, Harare, Zimbabwe; and the Division of Nutritional Sciences, Cornell University, Ithaca, NY (RJS and NVM)

Background: Anemia is prevalent in infants in developing countries. Its etiology is multifactorial and includes vitamin A deficiency.

Objective: Our primary aim was to measure the effect of maternal or neonatal vitamin A supplementation (or both) on hemoglobin and anemia in Zimbabwean infants. Our secondary aim was to identify the underlying causes of postnatal anemia.

Design: A randomized, placebo-controlled trial was conducted in 14 110 mothers and their infants; 2854 infants were randomly selected for the anemia substudy, of whom 1592 were successfully observed for 8–14 mo and formed the study sample. Infants were randomly assigned within 96 h of delivery to 1 of 4 treatment groups: mothers and infants received vitamin A; mothers received vitamin A and infants received placebo; mothers received placebo and infants received vitamin A; and mothers and infants received placebo. The vitamin A doses were 400 000 and 50 000 IU in the mothers and infants, respectively.

Results: Vitamin A supplementation had no effect on hemoglobin or anemia (hemoglobin <105 g/L) in unadjusted or adjusted analyses. Infant HIV infection independently increased anemia risk >6-fold. Additional predictors of anemia in HIV-negative and -positive infants were male sex and lower total body iron at birth. In addition, in HIV-positive infants, the risk of anemia increased with early infection, low maternal CD4⁺ lymphocyte count at recruitment, and frequent morbidity. Six-month plasma ferritin concentrations <12 µg/L were a risk factor in HIV-negative but not in HIV-positive infants. Maternal HIV infection alone did not cause anemia.

Conclusion: Prevention of infantile anemia should include efforts to increase the birth endowment of iron and prevent HIV infection.

Key Words: Vitamin A • infants • hemoglobin • HIV • supplementation • Zimbabwe

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				Minerva BMJ, August 5, 2006; 333(7562): 310 - 310. [Full Text] [PDF]