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

In many African populations, the prevalences of both iron deficiency and malarial infection exceed 50%. The control of iron deficiency anemia is of urgent public health importance, but assessment of iron status in these contexts has been controversial because of the effects of malarial disease on common iron status indicators. We assessed iron status in 3605 school children in Zanzibar by measuring hemoglobin, erythrocyte protoporphyrin (EP) and serum ferritin concentrations. Malaria parasitemia was quantified by counting against leukocytes. Iron deficiency was highly prevalent: 62.4% of hemoglobin concentrations were <110 g/L, 59.7% of EP values were >80 micromol/mol heme, and 41.5% of ferritin concentrations were <12 microg/L. Prevalence of Plasmodium falciparum parasitemia was 60.6%, but <1% of children had densities above 5000 parasites/microL blood. Neither hemoglobin nor EP concentration was associated with malaria parasite density, but prevalence of abnormal values increased by < or = 25% with parasite density. Erythrocyte protoporphyrin and hemoglobin were strongly inversely related regardless of parasite density. The relationship of EP to hemoglobin was slightly attenuated when parasite density exceeded 1000 parasites/microL blood. Ferritin rose by 1.5 microg/L per 1000 parasites/microL for parasite densities >1000 parasites/microL, but the relationship of ferritin to hemoglobin or EP was strong even when parasite densities exceeded this cutoff. The population prevalences of iron deficiency were not significantly biased by malarial infection. In this population of school children, iron status assessment using these indicators was not seriously influenced by malarial infection. We hypothesize that these indicators perform reliably in populations in which malarial infection is infrequently associated with disease; namely older children and adults in holoendemic environments.
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PMID:Serum ferritin, erythrocyte protoporphyrin and hemoglobin are valid indicators of iron status of school children in a malaria-holoendemic population. 903 30

To define the etiology of anemia post-renal transplantation, we assessed hematologic parameters and EPO levels in 38 anemic and 16 non-anemic control renal transplant recipients (RTRs) with varying degrees of allograft function at periods > 3 months post-transplantation. Significant differences between the two groups were found for serum creatinine (Cr) 291.7 +/- 26.5 vs. 203.3 +/- 26.5 mumol/l, p < 0.01; iron 9.3 +/- 0.92 vs. 13.6 +/- 1.7 mumol/l, p < 0.05; and ferritin 345.5 +/- 90.8 vs. 91.1 +/- 18.5 micrograms/l, p < 0.01. Serum EPO levels were inappropriately low in anemic patients with no significant correlation between EPO and Cr or hematocrit (Hct) levels. Serum iron was the only predictive factor for anemia on regression analysis (p < 0.05). Ferritin levels did not correlate with serum iron or Hct, and may be falsely elevated in iron deficient RTRs. Iron deficiency, poor renal function and inappropriately low EPO levels are major contributors to the 12% of our outpatient renal transplant population who are anemic.
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PMID:Anemia following renal transplantation: erythropoietin response and iron deficiency. 926 20

Iron deficiency in young rats leads to a decrease in brain iron and ferritin concentrations, an increase in transferrin (Tf) concentration, and an increased rate of uptake of iron from the plasma pool. We conducted two experiments to determine whether brain iron, Tf and ferritin respond quickly to iron repletion and to determine whether brain regions respond heterogeneously. Weanling male Sprague-Dawley rats were fed an iron-deficient diet (<5 mg/kg Fe) for 2 wk followed by an iron-adequate diet (REPL group, 35 mg/kg Fe in Experiment 1 and 15 mg/kg Fe in Experiment 2) for 2 or 4 wks, respectively. Age-matched iron-deficient (ID) and control rats composed the other two groups. Fourteen days of repletion with 35 mg/kg Fe dietary treatment were adequate to normalize hematology, brain microsomal and cytosolic Fe and brain ferritin (Experiment 1). Brain transferrin concentrations in REPL rats, however, were significantly above the levels of controls. Regional brain iron decreased heterogeneously due to dietary iron deficiency (Experiment 2), with some regions having a propensity to keep iron (e.g., substantia nigra, pons, and thalamus) and others losing significant amounts of iron (cortex and hippocampus). Ferritin and Tf concentrations also varied significantly across brain regions in ID and control rats. The hippocampus had the most dramatic Tf response to iron deficiency with elevations of approximately 100%, whereas other regions, except striatum, were unaffected. The brain of developing rats thus distributes iron and iron regulatory proteins differently from the brain of adult rats and is quite avid in its reacquisition of iron during iron therapy.
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PMID:Regional brain iron, ferritin and transferrin concentrations during iron deficiency and iron repletion in developing rats. 931 61

Soluble transferrin receptor (sTfR) and ferritin concentrations were measured in a variety of clinical settings to compare the ability of these two tests to identify iron deficiency. Among 62 anemic patients who either had a bone marrow aspirate performed or had a documented response to iron therapy, the diagnostic sensitivity and specificity of sTfR (at a diagnostic cutoff of > 2.8 mg/L) were 92% and 84%, respectively, with a positive predictive value of 42% in this population. Ferritin (< or = 12 microg/L) had a sensitivity of 25% and a specificity of 98%. However, the sensitivity and specificity of ferritin could be improved to 92% and 98%, respectively, by using a diagnostic cutoff value of < or = 30 microg/L, resulting in a positive predictive value of 92%. Ferritin and sTfR were also measured in 267 outpatient samples and 112 medical students. In the outpatient group, the two tests agreed in 73% of the samples; however, 25% of the samples had ferritin values > 12 microg/L and increased sTfR. Among the medical students, there was 91% agreement between the two tests, but 7% of the samples had ferritin < or = 12 microg/L and normal sTfR. Together, these data suggest that measurement of sTfR does not provide sufficient additional information to ferritin to warrant routine use. However, sTfR may be useful as an adjunct in the evaluation of anemic patients, whose ferritin values may be increased as the result of an acute-phase reaction.
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PMID:Clinical utility of the soluble transferrin receptor and comparison with serum ferritin in several populations. 955 May 57

A number of factors have been shown to limit the response to recombinant human erythropoietin (r-HuEPO). One major factor appears to be an inadequate iron supply to the bone marrow. Erythropoiesis is dependent upon a continuous supply of iron to the bone marrow. The rate at which iron can be drawn from existing stores may easily limit the rate of delivery for haemoglobin synthesis. This results in 'functional iron deficiency' which is distinct from 'absolute iron deficiency' caused by depletion of iron stores. At present there are three main parameters available to clinicians wishing to monitor iron status in their patients: serum ferritin and transferrin saturation (TFS), which are indirect measurements, and the percentage of hypochromic red cells, which directly reflects marrow iron status. Ferritin levels should be measured before starting r-HuEPO therapy to ensure adequate iron stores (>200 microg/l), and when patients move from the correction phase to the maintenance phase of therapy (have stores become depleted during the correction phase?). In addition, ferritin levels can give an indication of iron overload following excess parenteral iron administration. The TFS represents a balance between iron supply by stores and demand by bone marrow. A saturation below 20% probably indicates iron-deficient erythropoiesis. However, this is an indirect measure of marrow iron supply and wide fluctuations have been observed when determined at different time points. The percentage of hypochromic red blood cells is measured by flow cytometry and a hypochromic subpopulation of more than 10% (normal percentage <2.5%) indicates iron-deficient erythropoiesis. However, not all departments may have access to the required equipment. The aim of iron supplementation is to provide sufficient iron for the correction phase and to replace iron losses (1500-2000 mg/year in haemodialysis patients) during the maintenance phase of r-HuEPO therapy. This amounts to a daily iron need in the range of 5 7 mg, which is well above the normal dietary intake and absorptive capacity of the human intestine. Therefore, there is a need for intravenous iron, in particular when the patient has absolute or functional iron deficiency, is intolerant of oral iron, or is not complying well with the oral regimen.
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PMID:Iron monitoring and supplementation: how do we achieve the best results? 956 84

Reference values for two ferritin assays (Tina-quanta Ferritin, Enzymun, both Roche Diagnostics, Mannheim, Germany) were established (136 males and 139 females). To rule out inflammation as well as iron deficiency in the reference population, subjects with the C-reactive protein concentration < 5 mg/l, and zinc protoporphyrin < 40 micromol/mol heme and the soluble transferrin receptor < 3 mg/l were selected. Taking into account latent iron deficiency as well as hereditary hemochromatosis the 5-95 percentile range was as follows: male, 27-365 microg/l; female, 13-148 microg/l for Tina-quanta and 12-151 microg/l for Enzymun. The Tina-quanta Ferritin assay showed a very good correlation (r > or = 0.990) to Enzymun ferritin, Ferritin Abbott (Abbott Diagnostics, Delkenheim, Germany), N Latex Ferritin (Dade Behring, Marburg, Germany) and the Ferritin Chiron (Chiron Diagnostics, Fernwald, Germany). However, the slopes of the standard principal component method analysis were calculated to be between 1.03 (Enzymun) and 1.41 (N Latex Ferritin). For four assays the median recovery of the 3rd International Recombinant Ferritin Standard (NIBSC 94/572) measured by serial dilution was 89-109%. The N Latex Ferritin assay recovered half of the target values. Because of the good correlation with other assays, a matrix effect is likely. The question arises whether the manufacturers' agreement on the recombinant ferritin standard would harmonize ferritin measurement.
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PMID:Reference values for a homogeneous Ferritin assay and traceability to the 3rd International Recombinant Standard for Ferritin (NIBSC code 94/572). 1053 31

Serum ferritin levels were determined in 85 Healthy Ghanaian adults (45 men and 39 women) with a Ciba Corning 125I-Ferritin procedure. Concentrations showed a non-guassian distribution. Values for males ranged from 5.6-273 ng/ml and from 0.74-135 ng/ml for females. The non-guassian nature of the distribution necessitated a logarithmic transformation of the data in order to calculate the serum ferritin reference range (Mean +/- 2SD) for the subjects. The reference range for the males (antilogarithm) was 8.5-306.5 ng/ml (mean = 51.0 ng/ml). The reference range for the Ghanaian women was 3-112 ng/ml (mean = 18.0 ng/ml). The reported reference range for the Caucasian male is 7-350 ng/ml (mean -51.0 ng/ml) and for the Caucasian female, 5-135 ng/ml (mean = 22.0 ng/ml). These Ghanaian reference ranges agree closely with the caucasian values. Data from this preliminary study suggest serum ferritin values of < 8.5 ng/ml and < 3 ng/ml could serve as cut-off points below which iron deficiency may be said to be present in the adult Ghanaian male and female respectively when the same method of analysis is used. A further study of ferritin levels in the Ghanaian is recommended. Pending further work, continued use of the conventional cut-off points of 20 ng/ml for males and 10 ng/ml for females to identify iron-deficient individuals is in order. These conventional cut-off points enhance chances for identifying iron-deficient individuals.
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PMID:A preliminary study of serum ferritin reference range in the adult Ghanaian. 1073 86

A number of factors have been shown to limit the response to recombinant human erythropoietin (rhEPO). One major factor appears to be an inadequate iron supply to the bone marrow. Erythropoiesis is dependent upon a continuous supply of iron to the bone marrow. The rate at which iron can be drawn from existing stores may easily limit the rate of delivery for hemoglobin synthesis. This may result in "functional iron deficiency" which is distinct from "absolute iron deficiency" caused by depletion of iron stores. At present there are three main parameters available to clinicians wishing to monitor iron status in their patients: serum ferritin and transferrin saturation (TFS), which are indirect measurements, and the percentage of hypochromic red cells, which directly reflects marrow iron status. Ferritin levels should be measured before starting rhEPO therapy to ensure adequate iron stores (> 200 microg/l), and when patients move from the correction phase to the maintenance phase of therapy (have stores become depleted during the correction phase?). In addition, ferritin levels can give an indication of iron overload following excess parenteral iron administration. The TFS represents a balance between iron supply by the stores and demand by bone marrow. A saturation below 20% probably indicates iron-deficient erythropoiesis. However, this is an indirect measure of marrow iron supply and wide fluctuations have been observed when determined at different time points. The percentage of hypochromic red blood cells is measured by flow cytometry and a hypochromic subpopulation of more than 10% (normal percentage > 2.5%) indicates iron-deficient erythropoiesis. However, not all departments have access to the required equipment. The aim of iron supplementation is to provide sufficient iron for the correction phase and replace iron losses (1,500 - 3,000 mg/year in hemodialysis patients) during the maintenance phase of rhEPO therapy. This amounts to a daily iron need in the range of 5-7 mg, which is well above the normal dietary intake and absorptive capacity of the human intestine. Therefore there is a need for intravenous iron, in particular when the patient ha absolute or functional iron deficiency, is in tolerant of oral iron, or is not complying we with the oral regimen.
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PMID:Iron metabolism in rhEPO-treated hemodialysis patients. 1074 9

Ferritin is the principal iron storage protein participating in iron metabolism. As serum ferritin levels often reflect the amount of storage iron in the body, physicians have measured serum ferritin in order to evaluate iron deficiency or overload. Although a rise in serum ferritin concentration occurs in iron overload, hyperferritinemia without it has been reported in some inflammatory diseases and malignancies. Some cytokines have been reported to be responsible for the elevation of ferritin production. Studies on serum isoferritin in adult Still's disease and other diseases, especially measurements of the proportion of glycosylated ferritin, have been widely accepted. Pathophysiological properties of the increased serum ferritin are not clear. However, we should be aware that the hyperferritinemia is not a result, but is profoundly participating in the disease process.
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PMID:[Hyperferritinemia and diseases]. 1086 14

Ferritin (Ft) H and L subunits are independently regulated proteins with both transcriptional and translational regulation in response to cellular iron levels. While the heterogeneous distribution of ferritin and iron in the brain is now well established, the relative response of each subunit to iron deficiency and iron supplementation, is not well defined. Weanling male Sprague-Dawley rats (n=12 per group) were randomly assigned to an iron deficient (3.5 mg Fe/kg diet), control (35 mg Fe/kg diet) or supplemented (350 mg Fe/kg diet) diet for six weeks. The H-/L-ferritin subunit ratio and mRNA levels were determined. Overall, the protein ratio in control rats of H to L was approximately 45:1 compared to a ratio >60:1 in iron deficiency but the absolute amounts of each subunit varied greatly from one brain region to another. The ratio of H-:L-ferritin mRNA was 6:1 and was not affected by dietary iron deficiency in contrast to a potent effect on mRNA levels in liver. Severe iron deficiency reduced brain ferritin H protein levels significantly in all regions, whereas only ferritin L levels in striatum, substantia nigra and pons were affected by iron deficiency. Supplemental dietary iron increased both ferritin subunits, with the largest increase (50%) in the hippocampus. These data indicate that ferritin H and L subunits within the brain respond differently to iron status and suggest post transcription regulation as a key event.
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PMID:Iron deficiency alters H- and L-ferritin expression in rat brain. 1087 39


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