Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0162316 (iron deficiency anemia)
 3,806 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Delayed erythroid recovery is common after bone marrow transplantation (BMT), with some patients continuing to require red blood cell (RBC) transfusion support for as long as 1 year. While the etiology is multifactorial, inadequate stimulation of erythroid progenitors by the erythroid growth factor, erythropoietin, may play a role. In this study, the erythropoietin response to anemia of 70 consecutive patients undergoing BMT at the Johns Hopkins Oncology Center was compared with the erythropoietin response in uncomplicated iron deficiency anemia. Erythropoietin levels were elevated for the degree of anemia early after BMT; however, at the time of marrow recovery, erythropoietin levels were significantly suppressed in both allogeneic and autologous BMT patients compared with the iron-deficient patients. Patients with acute graft-versus-host disease (GVHD) had a more marked suppression of the erythropoietin response to anemia. In the patients who remained anemic for extended periods of time (up to 12 months after BMT), an inadequate erythropoietin response to anemia persisted. Delayed erythroid recovery after BMT is associated with inadequate erythropoietin levels. Therefore, recombinant human erythropoietin may be useful in the treatment of the anemia associated with both autologous and allogeneic BMT.
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PMID:Impaired erythropoietin response to anemia after bone marrow transplantation. 142 81

Erythropoietin (Epo) titers in various hematological states were determined by a radioimmunoassay. Epo titers in patients with uremic anemia and iron deficiency anemia were inversely correlated with their respective hemoglobin concentrations. Epo titers in patients with uremic anemia were significantly lower than those in patients with iron deficiency anemia with comparable hemoglobin concentrations.
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PMID:Serum erythropoietin titers in the anemia of chronic renal failure and other hematological states. 359 44

We have found serum erythropoietin (EPO) concentration significantly (p < 0.01) increased during normal pregnancy. Erythropoietin concentration was significantly (p < 0.05) higher before the 24th gestational week than after it. In pregnant women with iron deficiency anaemia serum EPO concentration was significantly (p < 0.001) higher than in healthy pregnant women. In anaemic women significant (p < 0.001) linear correlation between haemoglobin (hgb) and log serum EPO concentrations was observed. In pregnant women including both healthy and anaemic women log serum EPO concentrations correlated inversely with hgb concentrations (p < 0.01). We conclude that erythropoietin secretion is raised in normal pregnancy and is at highest in the first and second trimesters, when hgb mass begins to grow. In pregnancy with concomitant anaemia a more extensive demand for erythropoietin secretion is obvious.
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PMID:Serum concentrations of erythropoietin in healthy and anaemic pregnant women. 770 68

Erythropoietin (EPO) is a prime stimulating factor for red cell production. EPO is a glycoprotein which has a molecular weight of 34,000, and is mainly produced by the kidney. EPO stimulates the differentiation and proliferation of erythroid progenitor cells in the bone marrow. The rate of production of EPO is regulated primarily by renal oxygen availability. Because anemia reduces renal oxygen availability, anemic stress accelerates EPO production in the kidney. Recently, EPO has mainly been determined by radioimmunoassay. Serum EPO titer is usually inversely correlated with hemoglobin concentration, as typically shown in iron deficiency anemia. Serum EPO titers in aplastic anemia are much higher than those in iron deficiency anemia relative to the hemoglobin concentration. Serum EPO titers in anemia caused by malignancies sometimes differ considerably among patients. Serum EPO in renal anemia usually show low titers irrespective of the degree of anemia. Serum EPO titers in untreated polycythemia vera are lower than those in treated polycythemia vera or secondary polycythemia. Determination of serum EPO is useful in differential diagnosis of polycythemia vera. Recombinant human EPO has been used to treat various anemias including renal anemia, refractory anemia, anemia in malignancies and secondary anemia. Determination of serum EPO titers is also valuable in many other situations of clinical medicine.
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PMID:[Erythropoietin determination in clinical medicine]. 835 Apr 98

Our objective was to discuss the role of erythropoietin in fetal erythropoiesis and to review its clinical uses in perinatal medicine. All relevant articles compiled through a MEDLINE search (years 1986-1997) were reviewed. Erythropoietin is essential for fetal erythropoiesis and is produced in response to hypoxia and anemia. Cord blood erythropoietin is purely fetal and reflects tissue oxygenation. It has been found to be increased in many complicated pregnancies with underlying fetal hypoxia. Erythropoietin could be used as a marker of fetal hypoxia because its concentration rises rapidly by increased production in response to hypoxia. Its measurement might enable more accurate timing of hypoxic injury. In addition, erythropoietin levels have been well correlated with perinatal brain damage and may facilitate treatment of high risk neonates. Erythropoietin has also been used successfully in anemia of prematurity, decreasing the transfusion requirement. However, studies are still needed to determine the optimal doses of erythropoietin and iron supplementations required for maximizing the red blood cell response. Erythropoietin has been examined as potential maternal therapy in various disorders during pregnancy. These include end-stage renal disease, severe antepartum iron deficiency anemia, and postpartum anemia. Erythropoietin has been found to be effective and well tolerated in these conditions. An additional promising use lies in the optimization of maternal red blood cell mass to allow autologous blood donation. This may be critical in cases where a large amount of bleeding might be anticipated, as with placenta previa. This would also minimize the donor transfusion-related hazards. Erythropoietin with its wide clinical applications could improve maternal and neonatal outcome.
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PMID:Erythropoietin in obstetrics. 970 90

Anemia is a very common clinical problem in patients with chronic kidney disease (CKD) and is associated with increased morbidity and mortality in these patients. Erythropoietin is a hormone synthesized that is deficient in the majority of patients with advanced kidney disease, thereby predisposing these patients to anemia. The other cause of anemia is deficiency of iron. Iron deficiency anemia is common in people with CKD and its importance in supporting erythropoiesis is unquestioned, especially in those patients treated with erythropoietin. Intravenous iron is frequently used to treat anemia in CKD patients and is very efficacious in increasing hemoglobin but at the same time there are some safety issues associated with it. The objective of this review is to assess the frequency of adverse drug events associated with four different iron formulations: two iron dextran products known as high and low molecular weight iron dextran, iron sucrose, and sodium ferric gluconate complex. Several electronic databases were searched. In general, with the exception of high molecular weight iron dextran, serious or life-threatening adverse events appeared rare. Iron sucrose has the least reported adverse events and high molecular weight iron dextran has the highest number of reported adverse events. Low molecular weight iron dextran and ferric gluconate fall in between these two for number of adverse drug events.
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PMID:Safety issues with intravenous iron products in the management of anemia in chronic kidney disease. 1932 71

Repeated blood donors manifest clinical, subclinical, and biochemical signs of iron deficiency anemia, have significantly higher erythropoietin and vascular endothelial growth factor (VEGF) concentrations, and decreased tissue oxygen saturation, oxygenated tissue hemoglobin, and regional cerebral oxygen saturation. Erythropoietin and VEGF are potent retinal angiogenic factors which may initiate and promote the retinal angiogenesis process independently or simultaneously. Increases in circulating levels of erythropoietin and VEGF are proportionate to the levels of hematocrit, hypoxemia, and tissue hypoxia. It is suggested that higher erythropoietin production following iron deficiency anemia-induced chronic hypoxemia/ hypoxia may, hypothetically, enhance the risk of retinal angiogenesis and/or neovascularization, possibly by inducing hypoxia inducible factor-1 alpha, which consequently upregulates genes stimulating angiogenesis, resulting in formation of a new vasculature, possibly by modulation of signal transducer and activator of transcription 3 signaling in the retina. Implications of this hypothesis cover erythropoietin doping, chronic hypoxia, and hypoxemic situations, such as angiogenesis-related cardiac and pulmonary diseases.
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PMID:Possibility of enhanced risk of retinal neovascularization in repeated blood donors: blood donation and retinal alteration. 2194 50

Tmprss6-mutated mask mice display iron deficiency anemia and high expression of hepcidin. The aim of the study was to determine the effect of erythropoietin administration on proteins participating in the control of iron homeostasis in the liver and spleen in C57BL/6 and mask mice. Administration of erythropoietin for four days at 50 IU/mouse/day increased hemoglobin and hematocrit in C57BL/6 mice, no such increase was seen in mask mice. Erythropoietin administration decreased hepcidin expression in C57BL/6 mice, but not in mask mice. Erythropoietin treatment significantly increased the spleen size in both C57BL/6 and mask mice. Furthermore, erythropoietin administration increased splenic Fam132b, Fam132a and Tfr2 mRNA content. At the protein level, erythropoietin increased the amount of splenic erythroferrone and transferrin receptor 2 both in C57BL/6 and mask mice. Splenic ferroportin content was decreased in erythropoietin-treated mask mice in comparison with erythropoietin-treated C57BL/6 mice. In mask mice, the amount of liver hemojuvelin was decreased in comparison with C57BL/6 mice. The pattern of hemojuvelin cleavage was different between C57BL/6 and mask mice: In both groups, a main hemojuvelin band was detected at approximately 52 kDa; in C57BL/6 mice, a minor cleaved band was seen at 47 kDa. In mask mice, the 47 kDa band was absent, but additional minor bands were detected at approximately 45 kDa and 48 kDa. The results provide support for the interaction between TMPRSS6 and hemojuvelin in vivo; they also suggest that hemojuvelin could be cleaved by another as yet unknown protease in the absence of functional TMPRSS6. The lack of effect of erythropoietin on hepcidin expression in mask mice can not be explained by changes in erythroferrone synthesis, as splenic erythroferrone content increased after erythropoietin administration in both C57BL/6 and mask mice.
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PMID:Effect of erythropoietin administration on proteins participating in iron homeostasis in Tmprss6-mutated mask mice. 2907 89