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Query: UMLS:C0002871 (anemia)
52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Factors responsible for determining the position of the oxyhemoglobin equilibrium curve during the neonatal period are briefly reviewed and the clinical implications of these changes are examined. Two clinical trials employing exchange transfusions as an adjunct to conventional therapy of the severe respiratory distress syndrome have both demonstrated that this procedure reduces mortality. In neither study was it possible to demonstrate that the improvement was a direct consequence of the reduction in hemoglobin's affinity for oxygen that was produced by the substitution of fetal hemoglobin by adult hemoglobin. Data on the role of the position of the oxyhemoglobin equilibrium curve in the regulation of erythropoiesis during the "anemia of prematurity" demonstrate that the ability to unload oxygen is more important than the absolute hemoglobin level in both the stimulus to erythropoietin production and the clinical manifestations of anemia. The gradual shift of the position of the oxyhemoglobin equilibrium curve which occurs during the early months of life may not be sufficient in all infants to meet the growing preterm infants' metabolic needs without evoking additional cardiac compensation.
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PMID:Clinical implications of the oxyhemoglobin dissociation curve in the neonatal period. 3 60

Using 58Fe, 51Cr and cytological parameters, the authors have examined erythropoiesis in 44 polycythaemia vera patients diagnosed as such on the basis of the usual parameters (exept for determination of the erythropoietin level). In the patients divided into four types the following characteristica were observed. In type I, increased erythropoiesis is evident by accelerated plasma iron clearance, greater PIT and EIT as well as enhanced iron utilization and production indices. In type II, in addition to the former signs of increased erythropoiesis moderately shortened red cell life-span and hyposideraemia characteristic of splenic sequestration and resulting from bleeding and blood letting seem to be accompanied by microcytosis. There is a metaplastic erythropoiesis in type III, bone marrow activity decreases, but the increased erythropoiesis is indicated by several parameters already observed earlier. At the time the iron utilization indicative of effective erythropoiesis is decreased, thus ineffective erythropoiesis and considerably shortened red cell life-span are responsible for the enhanced iron turnover. This is also shown by the regression calculations. In type IV effective erythropoiesis was considerably decreased in the patients with severe anaemia. Sings which are indicative of metaplastic erythropoiesis are absent. In one of the patients the morphological changes characteristic of dyserythropoiesis were found. Although all our patients were given treatment. We believe that these alterations in the character of erythropoiesis are not likely to be the consequences of therapy.
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PMID:Changes in erythropoiesis during the course of polycythaemia vera. 6 14

On the basis of general haematological, clinicochemical, cytomorphological, cytochemical and nuclearmedical investigations the anaemia of chronic haemodialysis can be considered as a renal anaemia modified by a permanent dialysis. It is less characterized by lack of erythropoietin, but more by a strong lack of iron, moderate haemolysis and slight deficiency of folic acid. After gradual diagnostics the substitution treatment with iron is absolutely necessary, medication of folic acid should be attempted. A permanent therapy with 80-120 mg of iron weekly administered parenterally can be successfully performed and 10-15 mg of folic acid daily, which will markedly lower the rate of transfusion.
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PMID:[Anemia in chronic hemodialysis]. 6 88

The injection of erythropoietin or the induction of anaemia with phenylhydrazine leads to changes in murine pluripotent and granulocyte-macrophage stem cells indicating migration from marrow to spleen. In order to evaluate the interrelationship between erythroid differentiation and stem cell migration we have selectively suppressed erythroid differentiation with actinomycin D. Anaemia or EP injection resulted in stem cell changes consistent with migration; actinomycin blocked these changes in anaemic but not EP injected mice while blocking erythropoiesis in both groups. The erythropoietin contained from 0.01 to 1000 microgram/ml of endotoxin as defined by the limulus test; it decreased marrow erythropoiesis and stimulated marrow granulopoiesis. Adsorption of the erythropoietin preparation with limulus lysate removed endotoxin without decreasing erythropoietin activity. Adsorbed erythropoietin stimulated erythropoiesis and not granulopoiesis, and stem cell changes induced by its administration were largely blocked by actinomycin, suggesting that endotoxin in the non-adsorbed erythropoietin caused the actinomycin resistant stem cell changes. The observation that actinomycin blocks both erythroid differentiation and stem cell migration suggests that these two physiologic events are closely linked. The effects of injected erythropoietin on murine haemopoietic stem cells may, to a significant extent, be secondary to the presence of endotoxin in the erythropoietin preparations.
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PMID:Stem cell migration induced by erythropoietin or haemolytic anaemia: the effects of actinomycin and endotoxin contamination of erythropoietin preparations. 8 57

The in vitro effect of parathyroid hormone (PTH) on RNA and heme synthesis by embryonic mouse liver erythroid precursors was examined. PTH produced a dose-dependent effect on RNA synthesis. A maximal increase of 60 +/- 16% (p less than 0.02) was observed with 1.0 U PTH/ml, whereas with higher concentrations a significant decline was found. Furthermore, PTH stimulated heme synthesis after 24 h of incubation. The maximal enhancement of 32 +/- 7% (p less than 0.01) was observed with 0.5 U PTH/ml, a lower effect was obtained with 1.0 U PTH/ml, while 2.0 U PTH/ml caused a pronounced decrease of heme synthesis. These data indicate that PTH affects directly the erythroid precursors by a mechanism similar to that of erythropoietin. The inhibitory effect on the RNA synthesis observed with large doses of PTH may explain at least one of the causes of the anemia reported in patients with primary hyperparathyroidism.
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PMID:Increased RNA and heme synthesis in mouse erythroid precursors by parathyroid hormone. 10 88

Uremic women on hemodialysis with metabolic bone disease (hyperparathyroidism, osteomalacia resulting from defective vitamin D metabolism) and anemia (erythropoietin deficiency) are known to give birth to infants without bone disease or anemia. Therefore, skeletal development (enchondral and desmal bone formation) and hepatic erythropoiesis were evaluated in fetuses of uremic rats. These fetuses failed to show defective mineralisation or evidence of bone disease. Bolus injection of high doses of exogenous PTH into the maternal or fetal organism did not affect fetal bone histology. In addition, no apparent defect of bone mineralisation or bone formation was found in fetuses of ricketic rats. Normal mineralisation in the offspring of uremic rats may be explained by fetal hyperphosphatemia and/or insensitivity of fetal (woven) bone mineralisation to vitamin D. Absence of fetal anemia (normal hematocrits, normal density of hematopoietic cells in the liver) in the presence of maternal anemia is presumably due to the insensitivity of fetal erythropoiesis to erythropoietin.
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PMID:Fetal development in experimental uremia. 14 12

The role of a plasma inhibitor of erythropoiesis is evaluated in rats with Walker-256 carcinoma (W-256). Plasma from tumor-bearing rats was treated by gel filtration chromatography (Sephadex G-150) and fractions were combined into four pools on the basis of mol. wt. Inhibitory activity was assayed by adding an aliquot of the plasma fractions to normal rat marrow cells which were cultured for 24 hr with and without erythropoietin. 59Fe-heme synthesis, [3H]thymidine DNA synthesis, and 14C-leucine protein synthesis were studied. The results indicated that cultures containing the high mol. wt. pool (greater than 400,000 daltons) had significantly decreased heme, DNA and protein synthesis. This inhibitor also diminished the response to erythropoietin in polycythemic mice. The lower mol. wt. pool stimulated heme synthesis in vitro. To identify the inhibitor further, plasma lipoprotein classes were isolated by density gradient ultracentrifugation. The very low density lipoprotein (VLDL) and chylomicron fractions markedly inhibited DNA, protein and heme synthesis. Low density and high density lipoprotein fractions were inactive. A lipoprotein inhibitor of erythropoiesis was also identified in cancerous ascitic fluid, and to a lesser degree, in normal rat plasma. We suggest that this VLDL inhibitor of marrow erythropoiesis is a contributing factor in the anaemia of cancer.
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PMID:Liproprotein inhibitor of bone marrow cells in tumor-bearing rats. 22 31

Peripheral blood and bone marrow specimens from 6 patients with Ph1-positive CML were evaluated for their content of erythropoietic and granulopoietic colony-forming progenitor cells. Specimens obtained from untreated patients showed marked increases in all compartments the most dramatic of which were for CFU-E and circulating CFU-C. This increased cell flow down the early stages of the red cell pathway in CML suggests that heightened proliferation and differentiation of primitive hemopoietic cells may be a more general phenomenon than previously suspected in this disease. In 5 of 6 patients, abnormal erythroid progenitors capable of proliferation and differentiation into hemoglobinized erythroblasts in cultures containing less than 0.002 units of erythropoietin/ml were regularly detected. In the 6th patient abnormal growth was not seen in cultures of the initial marrow obtained but was detected in cultures set up with peripheral blood taken 7 months later. The unexplained amplification of the erythropoietic compartment and the ability of some of these cells to mature in vitro in the virtual absence of erythropoietin is at variance with the anemia characteristic of untreated patients. This suggests the possibility of a major differentiation block at the level of CFU-E. Further studies of the properties of erythroid progenitors in these patients should help to provide new insights into the pathogenesis of CML and may provide useful markers for monitoring engrafted cell function after autotransplantation of patients in blast crisis.
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PMID:Abnormalities in the erythroid progenitor compartments in patients with chronic myelogenous leukemia (CML). 29 48

The serum levels of granulocyte colony-stimulating factor (CSF) and erythropoietin (Ep) were measured in 16 patients with iron-deficiency anemia and 15 patients with the anemia of chronic disease. Levels of both CSF and Ep in the serum of patients with iron-deficiency anemia had an inverse linear relationship to the level of the packed cell volume (PCV). There was no correlation between PCV and the levels of CSF or Ep in the serum of patients with the anemia of chronic disease. The similarity in the behavior of CSF and Ep in iron-deficiency anemia suggests that they may be influenced by similar control mechanisms or have a common cellular or molecular source.
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PMID:Granulopoietic and erythropoietic activity in patients with anemias of iron deficiency and chronic disease. 30 61

Following extensive bowel resection, a young woman experienced severe malnutrition; subsequent administration of parenteral nutrition precipitated the copper deficiency syndrome. This consisted of hypocupremia, subnormal ceruloplasmin levels, anemia, and severe neutropenia. The bone marrow was megaloblastic, vacuolated, and sideroblastic; granulocytic maturation was not observed beyond the myelocyte stage. Copper sulfate therapy was followed by a marked reticulocytosis, increase in hematocrit, and recovery of neutrophils. Additional studies indicated that both serum and urinary erythropoietin values were low; serum activity increased after copper supplementation. Abnormal granulopoiesis was demonstrated using the in vitro granulocyte colony assay. The patient's granulcoytic stem cells were normal on two occasions; however, mixing studies showed that culture of the patient's copper-deficient marrow with her copper-deficient serum yielded significantly reduced numbers of granulocyte colonies. Thus, copper appears to be a necessary element for normal hematopoiesis; lack of this trace element may result in ineffective erythropoiesis and granulopoiesis.
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PMID:Observations on the anemia and neutropenia of human copper deficiency. 30 69


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