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

Because of its essentiality, iron occurs in tissues of all living matter especially aerobes. Iron compounds have been utilized in various aspects of argo-industry. Iron-binding proteins and their vital role in intestinal uptake, distribution and storage of iron are concisely examined. Ceruloplasmin (cuproenzyme) is imperative for iron mobilization from storage sites for hemoglobin synthesis. There is evidence of relationship between enhance susceptibility to infection and iron deficiency. The extent to which behavioral abnormalities and iron depletion are related remains to be established. The efficacy of chelating agents such as desferroxamine, bicarbonates and ethylene diamine tetraacetic acid (EDTA) against iron overload has been tested.
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PMID:A review of the biochemical roles, toxicity and interactions of zinc, copper and iron: III. Iron. 220 45

We have used the monoclonal antibodies 2A4 (specific for the H subunit of human ferritin) and LO3 (specific for the L subunit) for immunocytochemical detection of ferritin in bone marrow and peripheral blood cells from normal subjects and patients with various haematological disorders. Formalin-fixed slides were stained by the immunoalkaline phosphatase procedure (APAAP). In normal subjects, ferritin could be found only in bone marrow smears and appeared to be largely confined to erythroid precursors and reticuloendothelial cells. The more immature erythroid precursors contained higher concentrations of cellular ferritin. Although evaluation could be only semiquantitative, erythroblast ferritin appeared to be more reactive with the monoclonal 2A4 (15 +/- 7% positive erythroblasts) than with the monoclonal LO3 (6 +/- 5% positive erythroblasts), indicating that H-type ferritin was predominant, particularly in proerythroblasts and basophilic erythroblasts. By contrast, the ferritin present in reticuloendothelial cells appeared to be predominantly of L-type. Patients with iron deficiency showed low levels of positive erythroblast, whereas the reverse was true in patients with transfusional iron overload. Intense positivity for reticuloendothelial cell ferritin was found in patients with anaemia of chronic disease. In myelodysplastic syndromes and acute myeloid leukaemia (AML), ferritin positivity was generally very strong at any stage of erythroblast development, particularly with the monoclonal antibody 2A4. Perls-positive perinuclear granules of ring sideroblasts were not stained, confirming that mitochondrial iron deposition is not in the form of ferritin. In AML and myelodysplastic syndromes with excess of blasts, ferritin could be detected also in immature myeloid cells. These data indicate that: (a) in normal conditions ferritin is mainly expressed in red cell precursors and reticuloendothelial cells, and this is in keeping with the peculiar role of these cells in iron metabolism; (b) abnormal cell ferritin contents can be observed in both iron overload and malignancy.
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PMID:Immunocytochemical detection of ferritin in human bone marrow and peripheral blood cells using monoclonal antibodies specific for the H and L subunit. 226 53

This paper describes the status of iron stores, the incidence and the hematological characteristics of iron deficiency anemia in children heterozygous for beta-thalassemia. In beta-thalassemia heterozygotes, iron stores were similar to the controls in infancy and tended to increase with age, reaching levels of moderate iron overload solely in adult males. Iron deficiency anemia occurred less frequently in children heterozygous for beta-thalassemia as compared to normal controls, while no difference between the two groups was observed in the incidence of iron deficiency. Ineffective erythropoiesis, typical of heterozygous beta-thalassemia, by causing an increase of iron absorption may limit the effect of iron shortage. At similar levels of iron depletion, however, children heterozygous for beta-thalassemia develop a more severe anemia as compared to non beta-thalassemic children. With the exception of two children, HbA2 levels in the presence of iron deficiency anemia remain in the range of heterozygous beta-thalassemia. In conclusion, our results indicate that children heterozygous for beta-thalassemia have normal iron stores but are relatively protected against the development of iron deficiency. When iron deficiency anemia develops, its clinical expression is usually more severe than in non beta-thalassemic children.
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PMID:Iron stores and iron deficiency anemia in children heterozygous for beta-thalassemia. 227 77

Even with uncomplicated iron overload, serum ferritin which can be identified in the circulating blood by sensitive immunochemical methods has a direct and quantitative correlation to the iron stored in the organism. The relation of stored iron and serum ferritin is not linear, but has an exponential character. The diagnostic function of serum ferritin as an indicator of stored iron, however, is virtually not influenced by it. The indications listed in Tab. 3 can be demarcated for diagnostic application in cases of iron overload. Hitherto, the molecular microheterogenicity of serum ferritin has exercised no essential impact on its diagnostic application. High ferritin concentrations may arise in the circulating blood by a number of disease processes listed in Tab. 4, without the simultaneous existence of a respective iron overload of the tissue. These correlations have to be observed in the diagnostic application of determining serum ferritin as well as in methodical possibilities of fault (high dose hook effect), thus limiting the use of serum ferritin as an indicator of stored iron both in case of iron overload and iron deficiency. As in all isolated laboratory investigations, all other clinical and chemical laboratory information available about the individual patient has to be taken into account in each case for interpreting the serum ferritin concentration.
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PMID:[Serum ferritin in iron overload]. 244 6

The state of a child's iron nutrition depends on his genetic endowment, the stage of development he has reached and the environment in which he lives. Genetic disorders lead more commonly to iron overload than to deficiency. Generally interplay between genes and environment is apparently of little importance when considering iron deficiency; are we missing something? The greatest demands for iron are at the time of most rapid growth, i.e. during infancy and puberty, but during early infancy body stores can meet the demand without a need for dietary iron. Oxygen, diet and microbes are the important environmental factors related to iron nutrition. The relationship of oxygen toxicity to iron nutrition in the newborn has received only fleeting study, the availability of iron from many foods is unclear; the clinical significance of iron overload and deficiency in the evolution of an infection is also unclear despite a wealth of in vitro observation. I am not convinced that the bottle fed baby should receive iron in his diet during the first 4-6 months of life. Thereafter, while the concept of universal unselective supplementation causes some uneasiness there are considerable epidemiological arguments for fortification of food with iron.
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PMID:Iron nutrition in childhood: the interplay of genes, development and environment. 248 84

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

The prevalence of probable homozygous alpha+ thalassaemia in Zimbabwe was found to be 3.25 percent in a survey of hospital patients (n = 2,000), 7.6 percent in a Batonga village (n = 66), and 5.3 percent in 16 kindreds (n = 94) investigated for iron overload. The diagnosis was based on finding a reduced mean cell volume (MCV), reduced mean cell haemoglobin (MCH), increased red cell count (RBC), and a normal Haemoglobin. These cases usually had a normal red cell distribution width (RDW), and of three discriminant functions tested the MCV2 x MCH was the most useful. Iron deficiency was excluded in the community based surveys. The importance of recognizing these changes is emphasized so that inappropriate iron therapy is not given.
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PMID:Homozygous alpha+ thalassaemia in Zimbabwe: an unrecognized cause of hypochromia and microcytosis. 261 73

The baseline hematologic status of 27 patients with modest degrees of aluminum overload was examined. In addition, hematologic data were evaluated in 19 of these patients during and after treatment with DFO. Although neither severe anemia nor microcytosis was observed pretreatment, there was a significant correlation between hemoglobin level and degree of aluminum burden as determined by bone surface aluminum staining (r = -0.58; P less than 0.007). Following treatment with DFO, hemoglobin concentration increased dramatically by 1.3 to 4.4 g/dl in eight patients but did not change in the remaining eleven. Responders and nonresponders were similar with regard to the degree of aluminum overload both before and after chelation therapy but differed with regard to baseline levels of erythropoietin (higher in responders) and degree of iron overload (greater in nonresponders). Pretherapy levels of red cell ALA dehydratase were depressed in all patients (32 +/- 4 vs. 56 +/- 5 U/g Hb in normals) but did not correlate with the degree of aluminum overload and did not change with chelation therapy. Pretherapy levels of red cell protoporphyrin were elevated in 15 of 24 patients (62%) and were higher in responders than in nonresponders. Following DFO therapy, levels fell by 25 to 50% in 7 of 8 patients with elevated pretherapy values, despite the tendency in several patients to develop iron deficiency with treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Aluminum induced anemia: pathogenesis and treatment in patients on chronic hemodialysis. 261 92

The distribution of transferrin receptor (TfR)-positive cells and their staining intensity were examined in the liver, duodenum, pancreas, spleen, kidney and brain of iron-deficient, iron-overloaded and normal Wistar rats to elucidate the regulatory effects of iron on TfR expression in vivo. Iron deficiency was produced by an iron-deficient food and water regimen, and iron overload by repeated intraperitoneal injections of ferric nitrilotriacetate (Fe3(+)- NTA) for 12 weeks. In iron-deficient rats, levels of hemoglobin (Hb = 5.9 +/- 0.7) and serum iron (SI = 29.9 +/- 4.4) were lower, and total iron-binding capacity (TIBC = 624.4 +/- 72.7) was higher than in normal rats (Hb = 15.6 +/- 0.9, SI = 206.5 +/- 20.5, TIBC = 416.0 +/- 56.0), and vice versa for SI (217.7 +/- 15.5) and TIBC (307.1 +/- 45.4) in iron-overloaded rats. In normal rats, TfR-positive granules were observed in hepatocytes and Kupffer cells of the liver, absorptive epithelium of the duodenum, acinar and Langerhans islet cells of the pancreas, macrophages and red pulp erythroblast of the spleen, and distal convoluted tubular epithelium of the kidney. Although the tissue distribution pattern of TfR-positive cells was similar in normal, iron-deficient and iron-overloaded rats, the staining intensity and number of TfR-positive cells were obviously higher in iron-deficient, and lower in iron-overloaded rats. We conclude that TfR expression is negatively regulated by the tissue concentration of iron.
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PMID:Transferrin receptor expression in normal, iron-deficient and iron-overloaded rats. 262 2

The traditional options available for the correction of hemodialysis-related anemia are blood transfusions and androgen therapy to stimulate erythropoiesis. A new therapeutic option, recombinant human erythropoietin (r-HuEPO; EPOGEN, AMGEN Inc, Thousand Oaks, CA), is currently undergoing clinical trials. Each treatment alternative has certain attendant adverse effects. The adverse effects of transfusion include transmission of infections such as hepatitis or acquired immunodeficiency syndrome, iron overload, and sensitization to histocompatibility antigens. Androgen therapy can cause masculinization of women and children and, in some forms, is associated with a high incidence of abnormal liver function. Treatment with r-HuEPO has some potential adverse effects, including hypertension, thrombosis of arteriovenous fistulae, prolonged duration of dialysis, hyperkalemia, and iron deficiency. Gradual and careful introduction of r-HuEPO should prevent hypertension from becoming problematic.
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PMID:Adverse effects of therapy for the correction of anemia in hemodialysis patients. 264 19


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