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Erythropoietin Levels (erythropoietin + level)
Selected AbstractsSerum Erythropoietin and Aging: A Longitudinal AnalysisJOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 8 2005William B. Ershler MD Objectives: To determine the changes in serum erythropoietin with age in patients with and without anemia and to assess the importance of certain comorbidities on changes in erythropoietin level and the development of anemia. Design: Clinical history, hematological parameters, and serum erythropoietin levels were examined at 1- to 2-year intervals for 8 to 30 years. Setting: Baltimore Longitudinal Study on Aging (BLSA), National Institute on Aging. Participants: One hundred forty-three BLSA participants. Measurements: Complete blood count and serum chemistries were performed at the time of each visit, and archived serum samples were used for erythropoietin level. Results: Although all subjects were healthy and without anemia at the time of initial evaluation, some developed chronic illness,most notably hypertension and diabetes mellitus. Erythropoietin levels rose significantly for the group as a whole, and the slope of the rise was found to be greater for those who did not have associated diabetes mellitus or hypertension. During the subsequent years, subjects who developed anemia but did not have hypertension or diabetes mellitus had the greatest slope in erythropoietin rise over time, whereas those with hypertension or diabetes mellitus and anemia had the lowest erythropoietin slope. Conclusion: The increase in serum erythropoietin with aging may be compensation for subclinical blood loss, increased red blood cell turnover, or increased erythropoietin resistance of red cell precursors. It is suspected that, with very advanced age, or in those with compromised renal function (e.g., diabetes mellitus or hypertension), the compensatory mechanism becomes inadequate and anemia results. [source] Loss of the JAK2 intramolecular auto-inhibition mechanism is predicted by structural modelling of a novel exon 12 insertion mutation in a case of idiopathic erythrocytosisBRITISH JOURNAL OF HAEMATOLOGY, Issue 6 2008Elena Albiero Summary We report a novel gain-of-function JAK2 exon 12 insertion mutation in a patient with idiopathic erythrocytosis and low serum erythropoietin level. To date, only rare cases of such mutations have been reported in the JAK2 exon 12. Using computer-based structural modelling we propose that this mutation causes the loss of the JAK2 auto-inhibition step, leading to the constitutive activation of JAK2 tyrosine kinase-dependent activity. Our model-based hypothesis provides a useful approach for the investigation of the phenotype-genotype relationship in myeloproliferative disorders involving JAK2. [source] The soluble transferrin receptor in dysplastic erythropoiesis in myelodysplastic syndromeEUROPEAN JOURNAL OF HAEMATOLOGY, Issue 1 2007Georgia Metzgeroth Abstract Objectives:,In individuals without iron deficiency, the soluble transferrin receptor (sTfR) directly reflects the erythropoietic activity. This study investigated sTfR concentrations in ineffective, dysplastic erythropoiesis in myelodysplastic syndrome (MDS). Methods:,To exclude influences of other myeloid cells on sTfR, only patients with refractory anemia (RA), refractory anemia with ringed sideroblasts (RARS) and 5q, syndrome were included. sTfR was measured nephelometrically (normal range 0.81,1.75 mg/L). Results:,Thirty-four untreated MDS patients (RA = 14, RARS = 10, 5q, syndrome = 10) were enrolled and analysed. The mean sTfR value of all MDS patients (1.30 ± 0.8 mg/L, range 0.2,3.8) did not differ from our control group. In 5q, syndrome, the mean sTfR concentration (0.80 ± 0.5 mg/L) was significantly lower than in RA (1.32 ± 0.4 mg/L, P = 0.02) and RARS (1.75 ± 1.1 mg/L, P = 0.03). Subdividing MDS according to their amount of erythroid mass in bone marrow a significant difference of sTfR between patients with decreased (0.70 ± 0.4 mg/L), normal (1.32 ± 0.4 mg/L) and increased (2.06 ± 0.9 mg/L) erythropoiesis was observed. MDS patients with sTfR values below the reference range of 0.81 mg/L required transfusions in 90% of cases and showed higher erythropoietin levels compared to MDS patients with sTfR levels ,0.81 mg/L (P = 0.01). There was a good agreement between sTfR and the amount of polychromatic erythroblasts observed (r = 0.68, P < 0.001). Conclusion:,In conclusion, the serum concentration of sTfR reflects erythropoietic activity in MDS, but it is in particular determined by the degree of erythroid maturation and the severity of ineffective erythropoiesis. Low sTfR values in MDS are associated with a reduced, poorly differentiated erythropoiesis and requirement of blood transfusions. [source] Erythropoietin for the treatment of anemia associated with hematological malignancyHEMATOLOGICAL ONCOLOGY, Issue 1 2001T. J. Littlewood Abstract Anemia is common in patients with hematological malignancy. Most patients will have their anemia attributed to the anemia of chronic disease. The anemia of chronic disease is caused by cytokine mediated suppression of erythropoiesis and low serum erythropoietin levels are found in the majority of patients with cancer. Many of these anemic patients will be symptomatic with fatigue. Data from many studies indicates that treatment of anemic patients with erythropoietin will increase their hemoglobin concentration, decrease transfusion need and also improve their quality of life. A recent study also suggests that improving the hemoglobin level may improve the patients' prognosis but this finding needs to be confirmed. Copyright © 2001 John Wiley & Sons, Ltd. [source] Serum Erythropoietin and Aging: A Longitudinal AnalysisJOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 8 2005William B. Ershler MD Objectives: To determine the changes in serum erythropoietin with age in patients with and without anemia and to assess the importance of certain comorbidities on changes in erythropoietin level and the development of anemia. Design: Clinical history, hematological parameters, and serum erythropoietin levels were examined at 1- to 2-year intervals for 8 to 30 years. Setting: Baltimore Longitudinal Study on Aging (BLSA), National Institute on Aging. Participants: One hundred forty-three BLSA participants. Measurements: Complete blood count and serum chemistries were performed at the time of each visit, and archived serum samples were used for erythropoietin level. Results: Although all subjects were healthy and without anemia at the time of initial evaluation, some developed chronic illness,most notably hypertension and diabetes mellitus. Erythropoietin levels rose significantly for the group as a whole, and the slope of the rise was found to be greater for those who did not have associated diabetes mellitus or hypertension. During the subsequent years, subjects who developed anemia but did not have hypertension or diabetes mellitus had the greatest slope in erythropoietin rise over time, whereas those with hypertension or diabetes mellitus and anemia had the lowest erythropoietin slope. Conclusion: The increase in serum erythropoietin with aging may be compensation for subclinical blood loss, increased red blood cell turnover, or increased erythropoietin resistance of red cell precursors. It is suspected that, with very advanced age, or in those with compromised renal function (e.g., diabetes mellitus or hypertension), the compensatory mechanism becomes inadequate and anemia results. [source] Nucleated red blood cell counts and erythropoietin levels in high-risk neonatesPEDIATRICS INTERNATIONAL, Issue 6 2002Ülfet Vatansever Abstract Background: The presence of increased numbers of nucleated red blood cells (NRBC) and increased levels of erythropoietin (EPO) in the circulation of neonates has been associated with states of relative hypoxia. The aim of this study is to assess the pattern of NRBC counts and EPO levels in a group of high-risk neonates under stress conditions and determine the short-term outcome for these babies by using these parameters. Methods: There were 69 high-risk neonates; 14 intrauterine growth retarded (IUGR), 25 preterm infants, 18 term infants with asphyxia and 12 infants of diabetic mothers. Control groups included healthy, term infants delivered either vaginally (n = 18) or with cesarean section (n = 19). Three blood samples were obtained from each infant within 12 h (initial), 3 days and 7 days after birth to measure NRBC counts and EPO levels. Neonatal and short-term outcomes at 3 and 6 months of age were determined. Results: There was no significant difference among the groups with regard to the initial serum EPO concentrations. The initial NRBC counts were significantly lower in the control groups compared with the study groups (P = 0.002). While there was no significant difference between patients with good and poor outcome in terms of EPO concentrations of initial samples, a significant difference existed in terms of NRBC counts (P = 0.038). Conclusions: Both serum EPO level and NRBC count provide limited clinical benefit in the detection of pathological conditions of the neonatal period, but NRBC count determination seems to be especially helpful in predicting short-term neurodevelopmental outcome. [source] Role of hypoxia and cAMP in the transdifferentiation of human fetal cardiac fibroblasts: Implications for progression to scarring in autoimmune-associated congenital heart blockARTHRITIS & RHEUMATISM, Issue 12 2007Robert M. Clancy Objective Identification of isolated congenital heart block (CHB) predicts, with near certainty, the presence of maternal anti-SSA/Ro antibodies; however, the 2% incidence of CHB in first offspring of anti-SSA/Ro+ mothers, 20% recurrence in subsequent pregnancies, and discordance in identical twins suggest that an environmental factor amplifies the effect of the antibody. Accordingly, this study was carried out to explore the hypothesis that hypoxia potentiates a profibrosing phenotype of the fetal cardiac fibroblast. Methods Evidence of an effect of hypoxia was sought by immunohistologic evaluation of CHB-affected fetal heart tissue and by determination of erythropoietin levels in cord blood. The in vitro effect of hypoxia on gene expression and phenotype in fibroblasts derived from fetal hearts and lungs was investigated by Affymetrix arrays, quantitative polymerase chain reaction (PCR), immunofluorescence, and immunoblotting. Results In vivo hypoxic exposure was supported by the prominent intracellular fibroblast expression of hypoxia-inducible factor 1, in conduction tissue from 2 fetuses in whom CHB led to death. The possibility that hypoxia was sustained was suggested by significantly elevated erythropoietin levels in cord blood from CHB-affected, as compared with unaffected, anti-SSA/Ro,exposed neonates. In vitro exposure of cardiac fibroblasts to hypoxia resulted in transdifferentiation to myofibroblasts (a scarring phenotype), as demonstrated on immunoblots and immunofluorescence by increased expression of smooth muscle actin (SMA), an effect not seen in lung fibroblasts. Hypoxia-exposed cardiac fibroblasts expressed adrenomedullin at 4-fold increased levels, as determined by Affymetrix array, quantitative PCR, and immunofluorescence, thus focusing attention on cAMP as a modulator of fibrosis. MDL12,330A, an adenylate cyclase inhibitor that lowers the levels of cAMP, increased expression of fibrosis-related proteins (mammalian target of rapamycin, SMA, plasminogen activator inhibitor type 1, and type I collagen), while the cAMP activator forskolin attenuated transforming growth factor ,,elicited fibrosing end points in the cardiac fibroblasts. Conclusion These findings provide evidence that hypoxia may amplify the injurious effects of anti-SSA/Ro antibodies. Modulation of cAMP may be a key component in the scarring phenotype. Further assessment of the susceptibility of cardiac fibroblasts to cAMP modulation offers a new research direction in CHB. [source] |