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

Malnutrition and respiratory disease commonly occur together, and the immunologic defects caused by malnutrition may affect clinical responses and the impact of vaccines. These defects include impaired maturation and function of T lymphocytes, diminished secretory immune responses, poor humoral antibody responses to polysaccharide antigens, deficient complement activity (especially the alternative pathway), and impaired antimicrobial mechanisms by phagocytic cells. In addition, protein-energy malnutrition often leads to very high serum levels of IgE as a result of altered T cell regulation of IgE production and may contribute to IgE-mediated pathologic responses to respiratory syncytial virus or parainfluenza virus infection. Correction of these deficits may improve host response to infection and enhance vaccine-related protection. Both vitamin A and iron deficiency states have been epidemiologically associated with increased morbidity due to respiratory infection. The impact of preventive therapy with either vitamin A or iron is still uncertain, but such therapy has the potential for diminishing the incidence of respiratory infections and their consequences.
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PMID:Nutritional effects on response of children in developing countries to respiratory tract pathogens: implications for vaccine development. 190 99

Iron deficiency is prevalent in childhood in the developed and developing countries. Programs of presumptive therapy, mass supplementation and food fortification have been introduced in many countries. The unresolved debate over the interaction of iron and infection in the clinical setting prompts re-evaluation of these practices. Situations of iron overload are associated with increased susceptibility to certain infections, although the exact mechanisms may vary with the main pathology. Iron treatment has been associated with acute exacerbations of infection, in particular malaria. In most instances parenteral iron was used. In the neonate parenteral iron is associated with serious E. coli sepsis. In one country, with endemic malaria, parenteral iron was associated with increased rates of malaria and increased morbidity due to respiratory disease in infants. In contrast in non-malarious countries studies of oral iron supplementation have if anything shown a reduction in infectious morbidity. Methodological problems in the latter reports indicate the need for further controlled prospective studies with accurate morbidity recording if informed recommendations are to be made.
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PMID:Iron and infection: the clinical evidence. 187 85

Iron deficiency is prevalent in children worldwide. Programmes of presumptive therapy, mass supplementation and food fortification have been introduced in many countries. The continuing unresolved debate over the interaction of iron and infection in the clinical setting indicates the need for firm guidelines for these practices. Iron overload is associated with increased susceptibility to certain infections, although the exact mechanisms may vary with the main pathology. Iron treatment has been associated with acute exacerbations of infection, in particular malaria. In Papua New Guinea parenteral iron was associated with increased rates of malaria and increased morbidity due to respiratory disease in infants but not in school children. Several subsequent studies in Africa using oral iron showed deleterious effects. In most instances cited, immunity was compromised, and therapeutic doses of oral iron were used. Knowledge of malarial endemicity, immunity with respect to age and the prevalence of haemoglobinopathies is important in planning interventions. A fine balance needs to be struck in the timing and dose of oral iron if informed recommendations are to be made. In parallel with supplementation studies, the effects of iron chelation on infection are being reported increasingly. Such therapy is clearly protective against malaria and some other infections but may predispose to fungal and Yersinia infections.
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PMID:Iron and infection in the tropics: paediatric clinical correlates. 987 73

The continuing unresolved debate over the interaction of iron and infection indicates a need for quantitative review of clinical morbidity outcomes. Iron deficiency is associated with reversible abnormalities of immune function, but it is difficult to demonstrate the severity and relevance of these in observational studies. Iron treatment has been associated with acute exacerbations of infection, in particular, malaria. Oral iron has been associated with increased rates of clinical malaria (5 of 9 studies) and increased morbidity from other infectious disease (4 of 8 studies). In most instances, therapeutic doses of oral iron were used. No studies in malarial regions showed benefits. Knowledge of local prevalence of causes of anemia including iron deficiency, seasonal malarial endemicity, protective hemoglobinopathies and age-specific immunity is essential in planning interventions. A balance must be struck in dose of oral iron and the timing of intervention with respect to age and malaria transmission. Antimalarial intervention is important. No studies of oral iron supplementation clearly show deleterious effects in nonmalarious areas. Milk fortification reduced morbidity due to respiratory disease in two very early studies in nonmalarious regions, but this was not confirmed in three later fortification studies, and better morbidity rates could be achieved by breast-feeding alone. One study in a nonmalarious area of Indonesia showed reduced infectious outcome after oral iron supplementation of anemic schoolchildren. No systematic studies report oral iron supplementation and infectious morbidity in breast-fed infants in nonmalarious regions.
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PMID:Iron and its relation to immunity and infectious disease. 1116 May 94

Anemia due to iron deficiency is the most prevalent form of micronutrient malnutrition in the world, however, the causal relationship between anemia and infection remains unclear. We examined prospectively, the association between anemia and infection among Bedouin infants. We recruited 293 families and newborns from the Bedouin population, which is ongoing major lifestyle changes, during the periods of 1989-1992 and 1994-1997 and followed them to age 18 months. The number of diarrhea and respiratory disease episodes as well as total days of diarrhea were ascertained weekly. Hemoglobin levels were obtained at age 6 months. Additional data on feeding practices, environmental, household and demographic characteristics were obtained throughout the 18 months. Diarrhea before 6 months of age was found to be a risk factor for diarrhea after that age. After controlling for early morbidity < 6 months, anemia (Hb < 11 g/dl) at 6 months was an independent risk factor for diarrhea and respiratory illness from 7 to 18 months of age. This associations remained significant even after controlling, in addition, for environmental and socio-economic factors. In the multivariable models, anemia at age 6 months increased the risk for diarrhea after that age by 2.9-fold (95% confidence interval 1.6 - 5.3; p = 0.001) and that of respiratory disease by 2-fold (1.1 - 3.7; p = 0.03). Our findings suggest that anemia may increase the rates of infections in toddlers. The possibility that reducing anemia in infants may be a preventive measure to lower disease burden from infectious disease in this and other vulnerable populations should be tested in further studies.
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PMID:Anemia as a risk factor for infectious diseases in infants and toddlers: results from a prospective study. 1592 Oct 46