Anaemia in African children: malaria or iron deficiency?
Explore the source record for details and available documents.
Africa↗
Biomedical subjects
Hans Verhoef
Publications and source records attributed to Hans Verhoef.
Factors associated with stunting in infants aged 5-11 months in the Dodota-Sire District, rural Ethiopia.
The contribution of various factors to malnutrition, particularly stunting, may differ among areas and communities. This cross-sectional study aimed to estimate the level of malnutrition and identify factors associated with the high level of stunting in breast-fed infants aged 5-11 mo living in Dodota-Sire District, Ethiopia. Infants (n = 305) and their mothers were examined physically, and anthropometric and demographic data were collected. The content of zinc, calcium and copper in breast milk was measured, and data collected on the type, frequency of consumption, and time of introduction of supplementary feeding. Overall, 36% were stunted, 41% underweight and 13% wasted. The highest prevalence of malnutrition was seen in infants aged 9-11 mo. Among mothers, 27% had chronic energy deficiency (body mass index, <18.5 kg/m(2)) and 20% were night blind, indicating that vitamin A deficiency was a serious problem. Infants fed >3 times/d, consuming >600 mL/d or consuming cow's milk in addition to cereals and/or legumes had markedly higher length-for-age Z-scores than their peers fed less frequently, consuming less food or not consuming cow's milk [differences: 0.39, 95% confidence interval (CI): 0.04-0.74; 0.17, 95% CI: 0.02-0.32; 0.40, 95% CI: 0.07-0.72, respectively). Infants of mothers with low concentrations of zinc in their breast milk were more stunted. In conclusion, the quality and quantity of foods consumed by infants is insufficient to prevent stunting. Thus it is necessary to increase the nutrient supply to infants by increasing intake and nutrient concentration of breast milk and of supplementary foods they consume, and by providing supplements to infants where appropriate.
Developmental Disabilities↗
Intermittent administration of iron and sulfadoxine-pyrimethamine to control anaemia in Kenyan children: a randomised controlled trial.
BACKGROUND: Iron supplementation is recommended for children at high risk of anaemia, but its benefits may not outweigh the associated risk of malaria in areas of seasonal transmission. We investigated the effect on haemoglobin concentrations of intermittent administration of iron supplements and sulfadoxine-pyrimethamine in symptom-free children under intense health surveillance. METHODS: In a trial of two by two factorial design, 328 anaemic Kenyan children were randomly assigned either iron or placebo and sulfadoxine-pyrimethamine or placebo (82 to each group). Primary outcomes were haemological indicators of iron status and inflammation at the end of the follow-up, and occurrence of malaria attacks. Morbidity surveillance consisted of medical examinations every 4 weeks, continuous passive case detection, and visits twice a week to community health-workers. Analyses were by intention to treat. FINDINGS: After 12 weeks, the groups assigned iron plus sulfadoxine-pyrimethamine, iron alone, or sulfadoxine-pyrimethamine alone had higher haemoglobin concentrations than the group assigned placebo (treatment effect adjusted for prognostic factors at baseline: 11.1 g/L [95% CI 7.5 to 14.7]; 10.7 g/L [7.1 to 14.3]; and 3.1 g/L [-0.5 to 6.7]). Administration of iron plus sulfadoxine-pyrimethamine also lowered the proportion with anaemia from 100% at baseline to 36% at 12 weeks, and of iron deficiency from 66% at baseline to 8% at 12 weeks. Survival analysis showed no evidence of substantially increased risk of malaria after iron supplementation. INTERPRETATION: Iron supplementation gives substantial health benefits, which may outweigh possible inherent risks caused by malaria. A larger study than ours is needed to assess benefits and risks of intermittent administration of sulfadoxine-pyrimethamine in reducing the incidence of malaria attacks in areas of seasonal malaria transmission.
Anemia↗
Malarial anemia leads to adequately increased erythropoiesis in asymptomatic Kenyan children.
Malarial anemia is associated with a shift in iron distribution from functional to storage compartments. This suggests a relative deficit in erythropoietin production or action similar to that observed in other infections. Our study in Kenyan children with asymptomatic malaria aimed at investigating whether malaria causes increased erythropoiesis, and whether the erythropoietic response appeared appropriate for the degree of resulting anemia. Longitudinal and baseline data were used from a trial with a 2 x 2 factorial design, in which 328 anemic Kenyan children were randomly assigned to receive either iron or placebo, and sulfadoxine-pyrimethamine or placebo. Erythropoiesis was evaluated by serum concentrations of erythropoietin and soluble transferrin receptor. Prospectively collected data showed that malarial infection resulted in decreased hemoglobin concentrations, and increased serum concentrations of erythropoietin and transferrin receptor. Conversely, disappearance of malarial antigenemia resulted in increased hemoglobin concentrations, and decreased concentrations of these serum indicators. Additionally, our baseline data showed that current or recent malarial infection is associated with increased serum concentrations of erythropoietin and transferrin receptor, and that these were as high as or perhaps even higher than values of children without malarial infection and without inflammation. Our findings indicate that in asymptomatic malaria, the erythropoietic response is adequate for the degree of anemia, and that inflammation probably plays no or only a minor role in the pathogenesis of the resulting anemia. Further research is needed to demonstrate the role of deficient erythropoietin production or action in the pathogenesis of the anemia of symptomatic malaria.
Adaptation, Physiological↗
Decreased plasma leptin concentrations in tuberculosis patients are associated with wasting and inflammation.
Tuberculosis patients often suffer from severe weight loss, which is considered to be immunosuppressive and a major determinant of severity and outcome of disease. Because leptin is involved in weight regulation and cellular immunity, its possible role in tuberculosis-associated wasting was investigated. In an urban clinic in Indonesia, plasma leptin concentrations, indicators of adipocyte mass, appetite, C-reactive protein (CRP), tuberculin reactivity, and cytokine response were measured in tuberculosis patients and healthy controls. Plasma leptin concentrations were lower in patients than in controls (615 vs. 2,550 ng/liter; P < 0.001). Multivariate regression analysis showed that body fat mass and inflammation were two independent factors determining plasma leptin concentrations; there was a positive correlation between fat and leptin, whereas, unexpectedly, leptin was inversely associated with CRP and tumor necrosis factor-alpha production. Concentrations of both CRP and leptin were independently associated with loss of appetite. Our results do not support the concept that weight loss in tuberculosis is caused by enhanced production of leptin. Rather, loss of body fat leads to low plasma leptin concentrations, and prolonged inflammation may further suppress leptin production. Because leptin is important for cell-mediated immunity, low leptin production during active tuberculosis may contribute to increased disease severity, especially in cachectic patients.
Adipose Tissue↗
Stunting may determine the severity of malaria-associated anemia in African children.
OBJECTIVE: Evidence from previous studies that malnourished children are protected against malaria is controversial. In individuals repeatedly exposed to malaria, immunity may develop first against severe disease, then against pyrogens, and last, against parasites. If this is true, this would suggest that reduced immune function that may exist in stunted children exacerbates the severity of malarial signs and symptoms, rather than the occurrence of parasitemia. On the other hand, several studies have suggested that malnourished children are protected to some degree against malaria. Our aim was to evaluate whether observational data support the hypothesis that nutritional inadequacies that cause stunting modify the associations between malaria and hematologic indicators such as hemoglobin concentration and serum concentrations of C-reactive protein and soluble transferrin receptor (sTfR). We showed earlier that increased serum concentrations of these receptors in asymptomatic malaria may be explained, at least in part, by increased erythropoiesis to compensate for malaria-induced hemolysis. METHODOLOGY: Community-based cluster survey among Kenyan children aged 2 to 36 months asymptomatic for malaria or anemia (n = 318). RESULTS: When adjusted for age and wasting, the malaria-associated decrease in mean hemoglobin concentration was 8.5 g/L and 15.8 g/L in nonstunted and stunted children, respectively. The malaria-associated increase in geometric mean serum concentrations of sTfR was 1.1-fold and 1.8-fold in nonstunted and stunted children, respectively. The malaria-associated increase in geometric mean serum concentrations of C-reactive protein was 1.4-fold and 2.3-fold in nonstunted and stunted children, respectively. Thus, children with malaria and those who were stunted suffered from more severe anemia and had higher serum concentrations of C-reactive protein and sTfR than would be expected from the combined effect of the 2 working independently. CONCLUSIONS: Our results are consistent with the notion that the nutritional inadequacies causing stunting also impair host immunity, thus increasing the degree to which malaria is associated with decreased concentrations of hemoglobin, with increased inflammation, and with increased iron demand in developing erythroblasts. Increased intake of micronutrients may not only reduce stunting and nutritional anemia, but also reduce malaria-associated anemia.
Anemia, Iron-Deficiency↗