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

To evaluate storage iron deficiency and iron-deficient erythropoiesis we determined, in a cross-sectional study of 95 patients mainly including end-stage renal disease patients (ESRD) with (32) and without rh-EPO therapy (55), the following parameters: hemoglobin, mean corpuscular red cell volume, ferritin, transferrin saturation (TS), zinc protoporphyrin (ZPP) and soluble transferrin receptor (TfR). In the dialysis group the percentage of positive samples with each marker of tissue iron supply defined as TS < 20%, ZPP > 40 mumol/mol Heme and TfR > 3.05 microgram/ml was as follows: TS 43.7% and 32.2% at a diagnostic threshold level of < 16%, ZPP 33.3% and TfR 17.2%. Manifest storage iron deficiency defined as ferritin < 30 ng/ml was observed in 5.7% of the samples while the mean ferritin concentration of the rh-Epo treated dialysis patients was 509.3 ng/ml compared to 262.5 ng/ml in the group without rh-EPO therapy. These data reflect a generous iron substitution in our series taking a TS < 20% as an intervention criterion. Looking at the different results of the three markers the best correspondence was found between ZPP and TfR resulting in a weak positive correlation (+0.64). In conclusion, we found quite different results with different assays when evaluating endogenous iron availability in our series of mainly ESRD patients in a cross-sectional study. Because a gold-standard is not defined further firm conclusions cannot be drawn from this type of study. The adequacy of the different parameters of iron metabolism including threshold levels and, consequently, the decision and route of iron substitution deserve an evaluation in a longitudinal study to characterize the best marker or marker combination in this setting.
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PMID:Transferrin receptor assay and zinc protoporphyrin as markers of iron-deficient erythropoiesis in end-stage renal disease patients. 954 1

The concentration of soluble transferrin receptor (sTfR) in serum is reported to be useful in the diagnosis of iron deficiency, especially for patients with concurrent chronic disease, where routine tests of iron status are compromised by the inflammatory condition. A new diagnostic assay for sTfR is calibrated against natural plasma sTfR, thus minimizing calibration discrepancies that result from differences between the analyte and the cellular transferrin receptor used in other assays. Use of the new assay to measure sTfR concentrations in 225 healthy, hematologically normal adults provided a reference interval against which pathological samples could be compared. There was no difference in the reference intervals for men and women and no correlation of [sTfR] with the age of the subject. Black subjects had significantly higher concentrations than nonblacks, and people living at high altitude had higher concentrations than those living closer to sea level. These differences were additive.
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PMID:Measurement of soluble transferrin receptor in serum of healthy adults. 955 May 51

To test the hypothesis that the quantities of circulating transferrin receptors are reduced in iron overload, we studied serum transferrin receptors and indirect measures of iron status in 150 subjects from rural Zimbabwe. We found significant inverse correlations between serum concentrations of transferrin receptors and ferritin, the ratio of ferritin to aspartate aminotransferase, and transferrin saturation (r > or = 0.44; P < 0.001). The mean +/- SD concentration of serum transferrin receptors in 23 subjects classified as having iron overload (ferritin > 300 microg/L and transferrin saturation > 60%) was 1.55 +/- 0.61 mg/L, significantly lower than the 2.50 +/- 0.62 mg/L in 75 subjects with normal iron stores (ferritin 20-300 microg/L and transferrin saturation 15-55%; P < 0.0005) and the 2.83 +/- 1.14 mg/L in 8 subjects with iron deficiency (ferritin < 20 microg/L; P = 0.001). In keeping with the regulation of transferrin receptor expression at the cellular level, our findings suggest that serum transferrin receptors are decreased in the presence of iron overload.
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PMID:Serum transferrin receptors are decreased in the presence of iron overload. 955 May 56

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

Recombinant human erythropoietin (EPO; epoetin) has been shown to be effective in improving anemia in a proportion of cancer patients. The response rate is approximately 60%, but varies considerably according to baseline hematocrit and transfusion needs, as well as the response criteria used. Response is not greatly influenced by the type of tumor, except in situations of major marrow involvement and limited residual hematopoiesis, or in the presence of specific mechanisms of anemia, such as hemolysis, splenomegaly, bleeding, hemodilution, or ineffective erythropoiesis. Stem cell damage by previous therapy as well as marrow suppression by current intensive chemotherapy can impair response. Besides its intensity, the type of chemotherapy may not be critical, although patients undergoing platinum-based chemotherapy may respond faster than those receiving non-platinum regimens. Complications, such as infections, bleeding, or nutritional deficiencies, may have a major negative impact on outcome. An important response-limiting factor is functional iron deficiency (ie, an imbalance between iron needs in the erythropoietic marrow and iron supply), which depends on the level of iron stores and its rate of mobilization. Functional iron deficiency is best monitored by the percentage of hypochromic red blood cells, and oral or intravenous iron supplements should be given when this percentage increases above 10%. All these factors explain why the response rate to epoetin is only approximately 60%. Therefore, it would be interesting to develop models that could help predict response to epoetin to help select the most appropriate cancer patients for this therapy. Few baseline parameters have been shown to be highly predictive of response in patients with solid tumors, although most studies in patients with myeloma or lymphoma have indicated that patients with a low baseline serum EPO level will respond better. Early changes after 2 to 4 weeks of treatment are also of great interest. Among these early changes, increments of soluble transferrin receptor, reticulocytes, and hemoglobin, as well as the persistence of elevated ferritin or EPO levels, have all shown some predictive value. Combination of baseline serum EPO and the 2-week increment of soluble transferrin receptor or hemoglobin may provide the best prediction of response.
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PMID:Prediction of response to optimize outcome of treatment with erythropoietin. 967 27

Genetic haemochromatosis is a common iron overload disorder of unknown aetiology. To characterize the defect of iron metabolism responsible for this disease, this study localized and semi-quantified the mRNA and protein expression of transferrin, transferrin receptor and ferritin in the liver and duodenum of patients with genetic haemochromatosis. Biopsies were obtained from iron-loaded non-cirrhotic patients with genetic haemochromatotic and control patients with normal iron stores. Additional duodenal biopsies were obtained from patients with iron deficiency. Immunohistochemical and in situ hybridization analysis for transferrin, transferrin receptor and ferritin was performed. Hepatic transferrin, transferrin receptor and ferritin protein expression was localized predominantly to hepatocytes and was increased in patients with genetic haemochromatosis when compared with normal controls. Interestingly, hepatic ferritin mRNA expression was not increased in these same patients. In the genetic haemochromatotic duodenum, ferritin mRNA and protein was localized mainly to crypt and villus epithelial cells and the level of expression was decreased compared with normal controls, but similar to iron deficiency. Duodenal transferrin receptor mRNA and protein levels colocalized to epithelial cells of the crypt and villus were similar to normal controls. Early in the course of genetic haemochromatosis and before the onset of hepatic fibrosis, transferrin receptor-mediated iron uptake by hepatocytes contributes to hepatic iron overload. Increased hepatic ferritin expression suggests this is the major iron storage protein. While persisting duodenal transferrin receptor expression may be a normal response to increased body iron stores in patients with genetic haemochromatosis, decreased duodenal ferritin levels suggest that duodenal mucosa is regulated as if the patient were iron deficient.
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PMID:Cellular expression and regulation of iron transport and storage proteins in genetic haemochromatosis. 971 7

The present study was undertaken to assess the feasibility of using ferritin and transferrin receptor measurements on dried capillary blood spots to identify iron deficiency (ID) in public health surveys. Measurements on serum and blood spots prepared from venous blood were performed in 71 healthy subjects, 41 of whom were iron-replete and 30 who had ID, either without (n = 20) or with (n = 10) anemia. Parallel measurements were performed on hemolyzed whole blood and washed hemolyzed red blood cells to assess the erythrocyte contribution of ferritin and transferrin receptor to dried blood samples. The concentration of ferritin in dried blood samples was threefold higher than serum assays due to the release of ferritin from hemolyzed erythrocytes, which diminished the usefulness of ferritin measurements for detecting ID. On the other hand, there was negligible erythrocyte contribution to the measurement of transferrin receptor in dried blood spots. The most sensitive parameter in dried blood spots was the ratio of receptor/ferritin, which was suitable for identifying iron-deficiency anemia (IDA), but less reliable than serum assays for detecting milder ID without anemia. We conclude that tandem measurements of serum ferritin and transferrin receptor in dried blood spots can be used to facilitate the identification of IDA in epidemiologic studies.
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PMID:An assessment of dried blood-spot technology for identifying iron deficiency. 971 12

Despite the established utility of serum transferrin receptor (sTfR), serum ferritin, and the sTfR/log ferritin ratio (TfR-F Index) in the diagnosis of iron deficiency (ID) anemia, the numeric values of these parameters, which are indicative of subclinical ID, remain to be clearly defined. In this study, 65 apparently healthy nonanemic adults (22 men and 43 women) were treated with 3 months of oral iron supplementation to evaluate its effect on parameters reflecting iron status and to determine the prevalence of subclinical iron deficiency in apparently healthy adults. Significant supplementation-induced changes were observed in sTfR, ferritin, and TfR-F Index values in women, whereas in men, none of the studied parameters showed any significant change. Iron-deficient erythropoiesis (IDE) was not observed in men, but was found in 17 women (40%). Although individuals with a compromised iron status may be represented in substantial numbers in conventional reference populations, they can be readily identified using sTfR, ferritin, and TfR-F Index determinations.
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PMID:Serum transferrin receptor and transferrin receptor-ferritin index identify healthy subjects with subclinical iron deficits. 976 80

The anaemia associated with cancer can be effectively treated with recombinant human erythropoietin (rHuEpo) in about 60% of the patients. However, the response rate varies according to treatment modalities as well as the response criteria used. A number of disease- or chemotherapy-related factors determines the probability of response. Several specific mechanisms of anaemia, such as haemolysis, splenomegaly, bleeding, haemodilution, or ineffective erythropoiesis can seriously interfere with response. However, the type of tumor, in particular haematologic versus non-haematologic, is not critical, except in situations of major marrow involvement and limited residual haematopoiesis. Stem cell damage by previous therapy, reflected by low platelet counts or high transfusion needs, will impair response. In addition, marrow suppression by current intensive chemotherapy will also have a negative impact. Besides its intensity, the type of chemotherapy may not be critical, although patients undergoing platinum-based chemotherapy may respond faster than those receiving non-platinum regimens. Complications such as infections, bleeding or nutritional deficiencies may have a major negative impact on outcome. An important response-limiting factor is functional iron deficiency, i.e. an imbalance between iron needs in the erythropoietic marrow and iron supply, which depends on the level of iron stores and its rate of mobilisation. Therefore, oral or preferably intravenous iron supplements should be given when serum ferritin is below 40-100 micrograms/l, reflecting the absence of iron stores, or when the percentage of hypochromic red cells rises above 10%, indicating functional iron deficiency even in the presence of adequate storage iron. Because up to 40% of the patients will not respond to rHuEpo, it is of utmost importance to develop models that could help predict response to rHuEpo and thus select the most appropriate cancer patients for this therapy. Most studies of patients with myeloma or lymphoma have indicated that patients with a low baseline serum Epo level will respond better, but this is not true of patients with solid tumors. Also of considerable interest are early changes of erythropoietic parameters after 2 to 4 weeks of treatment, including increments of serum transferrin receptor (sTfR), reticulocytes and haemoglobin, as well as the persistence of elevated ferritin or Epo levels. Combination of baseline serum Epo and the 2-week increment of sTfR or haemoglobin may provide the best prediction of response.
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PMID:Prediction of response to treatment with recombinant human erythropoietin in anaemia associated with cancer. 978 36

Cell culture in vitro, ABC-ELISA,RNA dot blot and atom absorption spectrum analysis were used to study biological effects of low concentration of iron citrate (Fe-cit) on the expression of transferrin receptor (TfR) in healthy human peripheral lymphocytes. Results showed that TfR increased by 36%, 50%, and 67% in groups with 1.25 x 10(-5), 5 x 10(-6) Fe-cit and without it, respectively as compared with a control group with 2.5 x 10(-5) mol/L Fe-cit. Levels of TfR-mRNA also increased with decrease of iron in substrate. Iron concentration within cells correlated inversely to the change in the number of TfR. It indicated that iron deficiency could regulate the number of TfR in lymphocytes and its gene expression.
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PMID:[Effects of iron deficiency on expression of transferrin receptor in human lymphocytes]. 981 35


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