Person:

Duggan, Christopher

Objective: The determinants of anemia during both pregnancy and postpartum recovery remain incompletely understood in sub-Saharan African women. Subjects/methods: In a prospective cohort study among pregnant women, we assessed dietary, biochemical, anthropometric, infectious and sociodemographic factors at baseline. In multivariate Cox proportional hazards models, we examined predictors of incident anemia (hemoglobin <11 g/dl) and iron deficiency anemia (anemia plus mean corpuscular volume <80fL), and recovery from anemia and iron deficiency anemia through 18 months postpartum at antenatal clinics in Dar es Salaam, Tanzania between 2001 and 2005. A total of 2364 non-anemic pregnant women and 4884 anemic women were enrolled between 12 and 27 weeks of gestation. Results: In total, 292 women developed anemia during the postpartum period and 165 developed iron deficiency anemia, whereas 2982 recovered from baseline anemia and 2044 from iron deficiency anemia. Risk factors for postpartum anemia were delivery complications (RR 1.6, 95% confidence interval (CI) 1.13, 2.22) and low postpartum CD4 cell count (RR 1.73, 95% CI 0.96, 3.17). Iron/folate supplementation during pregnancy had a protective relationship with the incidence of iron deficiency anemia. Absence of delivery complications, education status and iron/folate supplementation were positively associated with time to recovery from iron deficiency. Conclusion: Maternal nutritional status during pregnancy, prenatal iron/folate supplementation, perinatal care, and prevention and management of infections, such as malaria, are modifiable risk factors for the occurrence of, and recovery from, anemia.

Prenatal iron supplementation may improve pregnancy outcomes and decrease the risk of child mortality. However, little is known about the importance of postnatal maternal iron status for child health and survival, particularly in the context of HIV infection. We examined the association of maternal anemia and hypochromic microcytosis, an erythrocyte morphology consistent with iron deficiency, with child health and survival in the first two to five years of life. Repeated measures of maternal anemia and hypochromic microcytosis from 840 HIV-positive women enrolled in a clinical trial of vitamin supplementation were prospectively related to child mortality, HIV infection, and CD4 T-cell count. Median duration of follow-up for the endpoints of child mortality, HIV infection and CD4 cell count was 58, 17 and 23 months, respectively. Maternal anemia and hypochromic microcytosis were associated with greater risk of child mortality (HR for severe anemia=2.58, 95% CI: 1.66-4.01, P trend<0.0001; HR for severe hypochromic microcytosis=2.36, 95% CI: 1.27-4.38, P trend=0.001). Maternal anemia was not significantly associated with greater risk of child HIV infection (HR for severe anemia=1.46, 95% CI: 0.91, 2.33, P trend=0.08) but predicted lower CD4 T-cell counts among HIV-uninfected children (difference in CD4 T-cell count/μL for severe anemia:-93, 95% CI: -204-17, P trend=0.02). The potential child health risks associated with maternal anemia and iron deficiency may not be limited to the prenatal period. Efforts to reduce maternal anemia and iron deficiency during pregnancy may need to be expanded to include the postpartum period.

BACKGROUND Zinc supplementation adversely affects iron status in animal and adult human studies but few, trials have included young infants. OBJECTIVE To determine the effects of zinc and multivitamin supplementation on infant hematologic and iron status. METHODS In a double-blind RCT, Tanzanian infants were randomized to daily, oral zinc (Zn), multivitamins (MV), Zn and MV, or placebo treatment arms at age 6 wk. Hemoglobin concentration (Hb) and red blood cell indices were measured at baseline and at 6, 12, and 18 mo of age. Plasma samples from 589 infants were examined for iron deficiency (ID) at 6 mo. RESULTS In logistic regression models, Zn treatment was associated with greater odds of ID (OR 1.8 [95% CI 1.0–3.3]), and MV treatment was associated with lower odds (OR 0.49 [95% CI 0.3–0.9]). In Cox models, MV were associated with a 28% reduction in risk of severe anemia (HR=0.72 [95% Cl 0.56–0.94]) and a 26% reduction in risk of severe microcytic anemia (HR=0.74 [0.56–0.96]) through 18 months. No effects of Zn on risk of anemia were seen. Infants treated with MV alone had higher mean Hb (9.9 g/dL [95% CI 9.7–10.1]) than those given placebo (9.6 g/dL [9.4–9.8]) or Zn alone (9.6 g/dL [9.4–9.7]). CONCLUSIONS MV treatment improved iron status in infancy, whereas Zn worsened iron status but without an associated increase in risk for anemia. Infants in long-term zinc supplementation programs at risk for ID may benefit from screening and/or the addition of a multivitamin supplement.