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)

Serum erythropoietin (EPO) levels were determined in 30 children with iron deficiency anemia. The mean age of the children, hemoglobin (Hb) levels, serum EPO levels and log EPO values were 4.7 +/- 5 years, 6.7 +/- 1.7 g/dl, 2284 +/- 3177 mU/ml and 2.81 +/- 0.82, respectively. In 83 percent of the patients poor diet was the determined cause of iron deficiency and in the remaining 17 percent, chronic blood loss. A significant negative correlation was found between the log EPO values and Hb values (r = 0.62, p < 0.01). There was no significant correlation between log EPO values and the other parameters [sex, age, mean corpuscular volume (MCV) red blood cell (RBC) red cell distribution width (RDW), serum iron, iron binding capacity]. There was a significant difference in the age of the patients with an Hb value < 5.5 g/dl and those with a value > or = 5.5 Significant differences were also observed in log EPO levels among these patients (p < 0.004). The mean Hb value of patients with log EPO values > or = 3 was lower than that in patients with log EPO values < 3 (p < 0.003). In 20 percent of the patients, serum EPO levels were much lower than the values expected from their Hb level. Serum EPO levels were high in all five patients with a history of chronic blood loss.
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PMID:Serum erythropoietin in children with iron deficiency anemia. 943 47

Immunoreactive serum erythropoietin (EPO) was measured in anemic and non-anemic patients with acquired non-severe aplastic anemia (AA; n = 22) and myelodysplastic syndromes (MDS; n = 31) receiving or not androgens to examine the effect of androgen therapy and anemia on EPO levels in these disorders. Soluble transferrin receptor (TfR) and absolute reticulocyte count (ARC) were also assayed in order to evaluate erythropoietic activity. AA and MDS patients were stratified for anemia and androgen treatment as follows: 12 untreated anemic patients; 17 anemic patients during androgen therapy; 14 non-anemic patients without any treatment (> 1 year); and 10 non-anemic patients on androgen therapy. Although EPO levels in non-anemic patients were significantly higher than in healthy controls (n = 29) no statistically significant differences in Hb and EPO values were found between non-anemic patients receiving or not androgen therapy. In the linear regression analysis between Hb and log EPO concentration, no statistically significant differences in the slopes between untreated and androgen-treated anemic groups nor between both groups and patients with iron deficiency anemia (n = 23) were observed. However, the y intercept (log EPO) of regression line was significantly higher in androgen-treated anemic patients than in the androgen therapy-free anemic group. Serum TfR levels were higher in treated than in untreated anemic patients, whereas ARC was not different between both groups. These data seemingly indicate that (1) androgens at pharmacological doses do not increase serum EPO levels in non-anemic AA and MDS patients, and (2) in patients with AA and MDS, androgen-driven EPO stimulation is appreciably enhanced by anemia.
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PMID:Effect of androgen therapy and anemia on serum erythropoietin levels in patients with aplastic anemia and myelodysplastic syndromes. 946 42

Serum erythropoietin (sEpo) concentration is primarily related to the rate of renal production and, under the stimulus of hypoxia, increases exponentially as hemoglobin (Hb) decreases. Additional factors, however, appear to influence sEpo, and in this work, we performed studies to evaluate the role of the red blood cell precursor mass. We first compared the relationship of sEpo with Hb in patients with low versus high erythroid activity. The first group included 27 patients with erythroid aplasia or hypoplasia having serum transferrin receptor (sTfR) levels < 3 mg/L (erythroid activity < 0.6 times normal), while the second one included 28 patients with beta-thalassemia intermedia having sTfR levels > 10 mg/L (erythroid activity > 2 times normal). There was no difference between the two groups with respect to Hb (8.3 +/- 1.6 v 8.0 +/- 1.3 g/dL, P > .05), but sEpo levels were notably higher in patients with low erythroid activity (1,601 +/- 1,542 v 235 +/- 143 mU/mL, P < . 001). In fact, multivariate analysis of variance (ANOVA) showed that, at any given Hb level, sEpo was higher in patients with low erythroid activity (P < .0001). Twenty patients undergoing allogeneic or autologous bone marrow transplantation (BMT) were then investigated. A marked increase in sEpo was seen in all cases at the time of marrow aplasia, disproportionately high when compared with the small decrease in Hb level. Sequential studies were also performed in five patients with iron deficiency anemia undergoing intravenous (IV) iron therapy. Within 24 to 72 hours after starting iron treatment, marked decreases in sEpo (up to one log magnitude) were found before any change in Hb level. Similar observations were made in patients with megaloblastic anemia and in a case of pure red blood cell aplasia. These findings point to an inverse relationship between red blood cell precursor mass and sEpo: at any given Hb level, the higher the number of red blood cell precursors, the lower the sEpo concentration. The most likely explanation for this is that sEpo levels are regulated not only by the rate of renal production, but also by the rate of utilization by erythroid cells.
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PMID:Red blood cell precursor mass as an independent determinant of serum erythropoietin level. 949 Jul 1

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

In haemodialysis (HD) patients, functional iron deficiency frequently appears due to recombinant human erythropoietin (r-HuEPO) treatment. However, the diagnosis of iron deficiency is not always easy in such patients. Recent studies have shown that the serum transferrin receptor (s-TfR) level is a sensitive, quantitative measure of tissue iron deficiency. In this study, we examined the changes in s-TfR levels in patients with iron deficiency anaemia due to r-HuEPO treatment. We compared s-TfR levels of 24 patients with i.v. administered r-HuEPO (50-70 U/kg/dose) at the end of each dialysis session (three times a week) and diagnosed as having iron deficiency anaemia by routine laboratory methods (ferritin <50 microg/l and transferrin saturation <16%) with s-TfR levels of 32 patients not receiving r-HuEPO and without iron deficiency anaemia. Also, 40 healthy volunteer subjects were included in the study as a control group. Serum ferritin and transferrin receptor levels were measured with ELISAs using monoclonal reagents. There were no differences between the two groups with and without iron deficiency anaemia with respect to mean age, body weight, haemodialysis duration, haemoglobin and serum creatinine levels (p>0.05). For s-TfR levels, while no difference was present between the control and the non-iron deficiency groups (p>0.05), the iron deficiency group had higher s-TfR values than those of both the control and non-iron deficiency groups (p<0.001). Besides, there was an inverse correlation between haemoglobin and s-TfR levels in patients with iron deficiency anaemia (r = -0.85, p<0.0001). We conclude that the measurement of s-TfR levels may be useful in the diagnosis of functional iron deficiency in haemodialysis patients receiving r-HuEPO.
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PMID:The importance of serum transferrin receptor level in the diagnosis of functional iron deficiency due to recombinant human erythropoietin treatment in haemodialysis patients. 993 12

Pregnancy and postpartum anaemia occurs worldwide, particularly in developing countries where it accounts for substantial maternal and infant morbidity and mortality. The main cause is iron deficiency, primarily of dietary origin: 20% of the world population are estimated to have some degree of trace element deficiency. Even in industrialized countries iron deficiency anaemia is common in pregnancy due to the negative iron balance created by the high fetal demand for iron. It is compounded by blood loss during and after delivery, particularly in the absence of adequate prevention and treatment. The main effects of pregnancy and postpartum anaemia (defined by the WHO as hemoglobin values < 110 g/l and < 100 g/l, respectively) present for the mother an increased susceptibility to infection and premature delivery and for the baby intrauterine growth retardation and the consequences of prematurity. Diagnosis and differential diagnosis are thus a major obstetric concern. Iron deficiency can be particularly difficult to diagnose in postpartum anaemia because ferrritin is often falsely elevated due to concurrent infection. Prevention with oral iron + folic acid supplementation has proven effective, as has intravenous iron in more severe cases, while the addition of recombinant erythropoietin augments the effect of iron alone.
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PMID:[Anemia in pregnancy]. 1006 72

Of the uncommon anemias, "common" types include the anemia of renal disease, thalassemia, myelodysplastic syndrome and the anemia of chronic disease. These conditions may be suggested by the clinical presentation, laboratory test values and peripheral blood smear, or by failure of the anemia to respond to iron supplements or nutrient replacement. The principal cause of the anemia of renal disease is a decreased production of red blood cells related to a relative deficiency of erythropoietin. When treatment is required, erythropoietin is administered, often with iron supplementation. In the anemia of chronic disease, impaired iron transport decreases red blood cell production. Treatment is predominantly directed at the underlying condition. Since iron stores are usually normal, iron administration is not beneficial. Thalassemia minor results from a congenital abnormality of hemoglobin synthesis. The disorder may masquerade as mild iron deficiency anemia, but iron therapy and transfusions are often not indicated. In the myelodysplastic syndrome, blood cell components fail to mature, and the condition may progress to acute nonlymphocytic leukemia. The rate of progression depends on the subtype of myelodysplasia, but the leukemia is usually resistant to therapy.
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PMID:'Common' uncommon anemias. 1006 9

The relationship between serum erythropoietin (EP) and hemoglobin (Hb) concentrations was investigated in patients of iron deficiency anemia (IDA) in the course of iron replacement therapy to elucidate how the therapy induced changes in that relationship. At first Hb-dependent EP levels were determined in 123 IDA patients prior to the treatment by the third-degree logarithmic regression of EP on the Hb deficit (d-Hb). Following the start of iron supply, the deviation of observed EP values from the predicted level (EPc), i.e., delta-EP, was most obvious at the next phase of the onset of reticulocyte crisis; however, this deviation reduced with the alleviation of IDA. The value in maximum phase (delta-EPmx), as individually defined for each of 95 patients, correlated significantly with the severity of the pretreatment ID state (r = 0.502, p < 0.01). Partial correlation analysis revealed that about 80% of this gap was attributable to the ID state. Also, it was assumed that EP upregulation was twice that attributable to the Hb-deficit factor alone. The phase sequence of the delta-EP versus d-Hb relationship in 21 relapsed patients demonstrated a different rout from that observed in their improvement phase. The ID state-induced upregulation of EP, i.e., EPc, was followed by a therapy-induced overshooting drop that was attributable to acute uptake of EP by shifted erythroid precursors. From the viewpoint of erythropoietic regulation, the subsequent down-regulation of EP in the mid to late phases was considered appropriate for the prevention of Hb over production.
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PMID:[Decrease serum erythropoietin level induced by iron replacement therapy in patients with iron deficiency anemia]. 1035 37

The cause of anemia in chronic renal failure is multifactorial. Decreased erythropoietin (EPO) production is the main pathogenetic factor, but iron deficiency is the primary cause of unresponsiveness to EPO therapy. The diagnosis of iron deficiency in patients with chronic renal failure is difficult. We assessed the sensitivity and specificity of serum ferritin, total iron-binding capacity, transferrin saturation index, erythrocyte ferritin, and serum transferrin receptor in 63 patients with chronic renal failure undergoing dialysis (47 men, 16 women) with iron deficiency anemia. They were selected on the basis of clinical stability and absence of factors that may interfere with iron metabolism. None of the patients had received intravenous iron therapy or recombinant human erythropoietin (rHuEPO). Bone marrow biopsy with iron staining was the reference standard for iron stores. The receiver operating characteristic (ROC) curve and the area under the curve were calculated to assess the sensitivity and specificity of iron metabolism parameters. The parameter with the largest area under the ROC curve was serum ferritin (0.83). A cut point of 121 microgram/L showed a sensitivity and a specificity of 75%. The areas under the ROC curves of serum transferrin receptor and erythrocyte ferritin were 0.69 and 0.68, respectively. The remaining parameters showed areas under the ROC curve less than 0.65. Although serum transferrin receptor and erythrocyte ferritin may be acceptable markers for iron deficiency in stable chronic renal failure patients, serum ferritin level continues to be the most reliable diagnostic parameter. Transferrin saturation index is not a reliable parameter for the diagnosis of iron deficiency in stable patients not treated with rHuEPO.
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PMID:Diagnosis of iron deficiency in chronic renal failure. 1046 62

While the crucial role of haemoglobin in aerobic exercise has been well accepted, there is still a great deal of controversy about the optimal haematological parameters in the athletic population. The initial part of this review will examine the question of anaemia in athletes. The most common finding in athletes is a dilutional pseudoanaemia that is caused by a plasma volume expansion, rather than an actual blood loss. It is not a pathological state and normalises with training cessation in 3 to 5 days. This entity should be distinguished from conditions associated with lowered blood counts, such as intravascular haemolysis or iron deficiency anaemia. The evaluation of true anaemia states in the athlete must take into account not only blood losses secondary to exercise, such as foot strike haemolysis or iron losses through sweat, but non-athletic causes as well. Depending on the age and sex of the athlete, consideration must be given to evaluation of the gastrointestinal or genitourinary systems for blood loss. Finally, a comprehensive nutritional history must be taken, as athletes, especially women, are frequently not consuming adequate dietary iron. The second section of the paper will deal with the very contentious issue of sickle cell trait. While there have been studies demonstrating an increased risk of sudden death in people with sickle cell trait, it is still quite rare and should not be used as a restriction to activity. Further, studies have demonstrated that patients with sickle cell trait have an exercise capacity that is probably normal or near normal. However, in the cases of sudden death, it has been secondary to rhabdomyolysis occurring among sickle cell trait athletes performing at intense exertion under hot conditions, soon after arriving at altitude. The recommendations are that athletes with sickle cell trait adhere to compliance with the general guidelines for fluid replacement and acclimatisation to hot conditions and altitude. The final section of the paper examines the issue of haematological manipulation for the purposes of ergogenic improvement. Although experiments with blood doping revealed improvements in running time to exhaustion and maximal oxygen uptake, the introduction of recombinant erythropoietin has rendered blood doping little more than a historical footnote. However, the improvements in performance are not without risk, and the use of exogenous erythropoietin has the potential for increased viscosity of the blood and thrombosis with potentially fatal results. Until a definitive test is developed for detection of exogenous erythropoietin, it will continue to be a part of elite athletics.
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PMID:Sports haematology. 1068 81


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