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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Food intake and dietary patterns in Kenyan households have been studied since the 1920s. Reports on breastfeeding, nutrient intake, micronutrient deficiencies and the impacts of malaria and intestinal parasites on nutritional status are reviewed. Diets are mainly cereal-based, with tubers and a variety of vegetables and fruits when available. White maize, sorghum and millet are high in phytate and fiber, which inhibit the absorption of micronutrients such as zinc and iron. Communities growing cash crops have little land for food crops. Although households may own cattle, goats and poultry, commonly these are not consumed. Adults in nomadic communities consume more meat than nonpastoralists. Lakeside and oceanside communities do not consume adequate amounts of fish. Poor households have a limited capacity to grow and purchase food, therefore they have more nutrient deficiencies. Early weaning to cereal porridge deprives the infant of protein and other nutrients from human milk. Other milk is consumed only in small amounts in sweetened tea. Older children eat adult diets, which are extremely bulky and hard to digest. Anemia is mainly due to iron deficiency, malaria and intestinal parasites. In general, Kenyan children have inadequate intakes of energy, fat and micronutrients such as calcium, zinc, iron, riboflavin and vitamins A and B-12. The multiple micronutrient deficiencies may contribute to early onset of stunting and poor child development, whereas lack of calcium together with vitamin D deficiency are responsible for the resurgence of rickets. There is an urgent need to increase the intake of animal source foods by Kenyan children.
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PMID:The need for animal source foods by Kenyan children. 1467 93

Low birth weight (LBW) remains a significant public health problem in many developing countries, and poor nutrition both before and during pregnancy is recognized as an important cause. Emerging evidence on the role of intergenerational effects in determining maternal preconceptual nutritional status indicates the need for continued investment in strategies that improve women's nutrition and health throughout the life cycle, especially during the early years. Controlled trials have shown that improving food intakes during pregnancy effectively reduces LBW, but programs have been less successful because these interventions are expensive and difficult to manage. Multivitamin-mineral supplements have been viewed as a simpler solution, but 2 of 3 controlled trials conducted to date failed to show that multivitamin-mineral supplements are more effective than are iron-folate supplements, which are already the standard of care during pregnancy. Emerging evidence indicating the benefits of iron supplements in improving birth weight illustrate the need for increased efforts to reduce iron deficiency by improving coverage of antenatal programs and promoting fortification. Other causes of LBW include environmental factors, such as smoking; indoor air pollution; and infections, such as malaria. However, little is known about the interactions between nutrition and infection. Underlying social factors, such as poverty and women's status, are also important, especially in South Asia, where more than one-half of the world's LBW infants are born. In summary, strategies that combine nutrition-based interventions, such as improving food intakes and micronutrient status, especially iron status, with approaches that improve women's status and reproductive health are needed to reduce LBW.
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PMID:Nutrition and low birth weight: from research to practice. 1468 92

Iron deficiency and helminth infections are two common conditions of children in developing countries. The consequences of helminth infection in young children are not well described, and the efficacy of low dose iron supplementation is not well documented in malaria-endemic settings. A 12-mo randomized, placebo controlled, double-blind trial of 10 mg daily iron and/or mebendazole (500 mg) every 3 mo was conducted in a community-based sample of 459 Zanzibari children age 6-71 mo with hemoglobin > 70 g/L at baseline. The trial was designed to examine treatment effects on growth, anemia and appetite in two age subgroups. Iron did not affect growth retardation, hemoglobin concentration or mild or moderate anemia (hemoglobin < 110 g/L or < 90 g/L, respectively), but iron significantly improved serum ferritin and erythrocyte protoporphyrin. Mebendazole significantly reduced wasting malnutrition. but only in children <30 mo old. The adjusted odds ratios (AORs) for mebendazole in this age group were 0.38 (95% CI: 0.16, 0.90) for weight-for-height less than -1 Z-score and 0.29 (0.09, 0.91) for small arm circumference. In children <24 mo old, mebendazole also reduced moderate anemia (AOR: 0.41, 0.18, 0.94). Both iron and mebendazole improved children's appetite, according to mothers' report. In this study, iron's effect on anemia was limited, likely constrained by infection, inflammation and perhaps other nutrient deficiencies. Mebendazole treatment caused unexpected and significant reductions in wasting malnutrition and anemia in very young children with light infections. We hypothesize that incident helminth infections may stimulate inflammatory immune responses in young children, with deleterious effects on protein metabolism and erythropoiesis.
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PMID:Low dose daily iron supplementation improves iron status and appetite but not anemia, whereas quarterly anthelminthic treatment improves growth, appetite and anemia in Zanzibari preschool children. 1474 71

Management of major sickle hemoglobinopathies in industrialized countries has improved significantly over the last few years thanks to strict application of the preventive and curative measures developed as a result of a better understanding of the underlying pathophysiological mechanisms. However patients in Africa have benefited little from progress in the field due to the lack of human and physical resources in sharp contrast with the high prevalence of the disease. The purpose of this study was to analyze problems involved in management of childhood sickle cell disease in Africa based on our experience in a cohort of 556 cases treated over a period of 12 years. The main problems were the same as those encountered in other black African nations, i.e., delayed diagnosis due to a lack of routine neonatal diagnostic screening, difficulty implementing anti-infectious prophylaxis due not only to the high cost of recommended vaccinations not covered by the Expanded Program on Immunization but also to poor compliance with antiobioprophylaxis, and insufficient transfusion facilities hindering application of long-term transfusion protocols when indicated. In addition the high prevalence of digestive-tract parasitosis and malaria raise the need to combine standard preventive measures with routine parasiticidal treatment and malarial prophylaxis adapted to each geographical area. The high frequency of associated iron deficiency requires systematic laboratory testing to identify and treat resulting manifestations during follow-up. An important prerequisite for widespread implementation of appropriate preventive and curative measures in Africa is recognition of sickle cell disease as a priority in public health care policy.
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PMID:[Management of children with sickle cell disease in Africa: experience in a cohort of children at the Royal Albert Hospital in Dakar]. 1476 8

Both iron deficiency and malaria are common in much of sub-Saharan Africa, and the interaction between these conditions is complex. To investigate the association between nutritional iron status, immunoglobulins, and clinical Plasmodium falciparum malaria, we determined the incidence of malaria in a cohort of children between the ages of 8 months and 8 years who were living on the Kenyan coast. Biochemical iron status and malaria-specific immune responses were determined during 2 cross-sectional surveys. We found that the incidence of clinical malaria was significantly lower among iron-deficient children (incidence-rate ratio [IRR], 0.70; 95% confidence interval [CI], 0.51-0.99; P<.05), that the incidence of malaria was significantly associated with plasma ferritin concentration (IRR for log ferritin concentration, 1.48; 95% CI, 1.01-2.17; P<.05), and that iron status was strongly associated with a range of malaria-specific immunoglobulins. We conclude that iron deficiency was associated with protection from mild clinical malaria in our cohort of children in coastal Kenya and discuss possible mechanisms for this protection.
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PMID:Iron deficiency and malaria among children living on the coast of Kenya. 1565 90

Iron deficiency is common in the developing world; consequently, programmes of presumptive therapy and mass supplementation have been introduced in several countries. In this article Stephen Oppenheimer suggests caution, as recent evidence suggests that these practices may actually increase the likelihood of the subject developing patent malaria in endemic areas. This may be especially significant in infants, who are less likely to be immune to malaria, and in pregnant women, who are often routinely given iron supplements and in whom malaria may damage the foetus.
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PMID:Iron and malaria. 1546 83

Iron deficiency and Plasmodium falciparum malaria are the two main causes of anemia in young children in region endemic for this disease. The impact on iron status of prophylactic oral iron supplementation (2 mg/kg/day from two to six months of age) and the duration of this effect were assessed in a group of 832 Tanzanian infants exposed to P. falciparum malaria. Iron parameters and red blood cell indices were assessed at 2, 5, 8, and 12 months of age. Infants who received iron supplements had a significantly lower prevalence of iron deficiency (P < 0.01 at 5 months and P < 0.001 at 8 and 12 months). Red blood cell indices (mean corpuscular volume, mean cell hemoglobin, and mean cell hemoglobin concentration) were increased in children receiving iron supplementation and they did not differ between those protected and unprotected against malaria. The prevalence of ferropenia was similar in children protected against malaria and in those who were not protected and did not receive iron supplements (34.7% versus 37.3% at 12 months of age). We concluded that iron supplementation between the ages of 2-6 months improves iron status at least up to 12 months of age. Malaria infection does not contribute to iron deficiency.
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PMID:The effects of short-term iron supplementation on iron status in infants in malaria-endemic areas. 1551 39

Iron deficiency has been reported to affect both malaria pathogenesis and cell-mediated immune responses; however, it is unclear whether the protection afforded by iron deficiency is mediated through direct effects on the parasite, through immune effector functions or through both. We have determined cytokine mRNA expression levels in 59 children living in a malaria endemic area on the coast of Kenya who we selected on the basis of their biochemical iron status. Real-time quantitative reverse transcriptase polymerase chain reaction analysis of cytokine mRNA levels of peripheral blood mononuclear cells (PBMC) obtained from these children showed an association between interleukin-4 (IL-4) mRNA levels and all the biochemical indices of iron that we measured. Furthermore, IL-10 mRNA was higher in parasite blood smear-positive children than in blood smear-negative children irrespective of their iron status. This study suggests that IL-4 expression by PBMC may be affected by iron status.
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PMID:Cytokine mRNA expression and iron status in children living in a malaria endemic area. 1585 21

Severe anaemia is a common presentation in non-pregnant adults admitted to hospital in southern Africa. Standard syndromic treatment based on data from the pre-HIV era is for iron deficiency, worms and malaria. We prospectively investigated 105 adults admitted consecutively to medical wards with haemoglobin < 7 g/dl. Those with acute blood loss were excluded. Patients were investigated for possible parasitic, bacterial, mycobacterial and nutritional causes of anaemia, including bone marrow aspiration, to identify potentially treatable causes. Seventy-nine per cent of patients were HIV-positive. One-third of patients had tuberculosis, which was diagnosed only by bone marrow culture in 8% of HIV-positive patients. In 21% of individuals bacteria were cultured, with non-typhi salmonella predominating and Streptococcus pneumoniae rare. Iron deficiency, hookworm infection and malaria were not common in HIV-positive anaemic adults, although heavy hookworm infections were found in 6 (27%) of the 22 HIV-negative anaemic adults. In conclusion, conventional treatment for severe anaemia in adults is not appropriate in an area of high HIV prevalence. Occult mycobacterial disease and bacteraemia are common, but iron deficiency is not common in HIV-positive patients. In addition to iron supplements, management of severe anaemia should include investigation for tuberculosis, and consideration of antibiotics active against enterobacteria.
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PMID:Treatable factors associated with severe anaemia in adults admitted to medical wards in Blantyre, Malawi, an area of high HIV seroprevalence. 1589 81

Malnutrition and infectious diseases in infancy and early childhood have an impact on the cognitive development of children in developing countries. The long-term effects of these diseases are less well understood. A number of studies relate early malnutrition, iron deficiency, and malaria infection to poor cognitive abilities in the school-age years. The long-term effect of randomized interventions in early childhood has been evaluated for nutrition supplementation and psychosocial stimulation of malnourished children and for malaria prevention in a community cohort. The evidence suggests that improving the health and nutrition of young children can improve their subsequent chances of attending school, the gender equity of education access, and performance of children once at school.
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PMID:The long-term impact of preschool health and nutrition on education. 1607 69


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