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

The profound anemia of Diamond-Blackfan syndrome (DBS) is due to marrow red cell failure, but the pathogenesis is not understood. Studies by others indicated cell-mediated erythropoietic suppression in this condition. To explore this mechanism further, Ficoll-Hypaque--separated peripheral blood lymphocytes (PBL) from four anemic untreated patients with DBS, or from normals were cocultured with control marrow in vitro and the growth of erythropoietin-responsive stem cell colonies (CFU-E) was dermined. CFU-E numbers obtained from cultures with added normal PBL were not significantly different from the number without PBL. Similarly, CFU-E from cultures with added DBS PBL were not significantly different from the number without PBL (215 versus 220, 229 versus 220 and 84 versus 60, 74 versus 94/10(5) cells, respectively). Mixing marrows from a control and one DBS patient in ratios of 2:1, 1:1, or 1:2 prior to culture failed to disclose a decrease of colony growth. We could not show cellular inhibition of erythropoiesis in these patients with DBS. The mechanism of anemia in this disorder remains an open question.
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PMID:Diamond-Blackfan syndrome: evidence against cell-mediated erythropoietic suppression. 64 16

The renal anaemia is characterized by a decreased new formation of erythrocytes (deficiency of erythropoetin), by haemolysis (uraemic-toxic influences) and by iron deficiency (decreased resorption of iron, blood losses, infectious-toxic component). In long-term haemolysis the iron deficiency increases, in most cases the haemolysis a little decreases, and a deficiency of erythropoietin is not to be established. However, a slight deficiency of folic acid is frequently observed. Apart from the reduction of the retention of substances normally contained in the urine the therapy consists in iron doses and slight doses of folic acid. Only occasionally blood transfusions are necessary.
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PMID:[Renal anemia and its modification by chronic hemodialysis]. 67 11

The oxygen metabolism (pO2, the constant of the oxygen rate consumption, the coefficient of the oxygen distribution), the activity of oxid-reduced and hydrolytic enzymes, the blood supply of the kidney cortex and medulla, were recorded. These data were compared with the erythropoietin activity of plasma in the rats with phenylhydrazine anemia and posttransfusion polycytemia. An obvious reverse interrelationship existed between plasma erythropoietin activity and value of pO2 and blood supply of the cortex. The activity of the above enzymes was practically unchanged. The data obtained suggest that erythropoietin is formed in the cortex of the kidney and its production is controlled by the degree of oxygen supply of the kidney tissue.
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PMID:[Effect of oxygen metabolism in kidney tissue on the development of plasma erythropoietic properties]. 68 1

Amphotericin B was given to six patients with systemic fungal infections. A dose averaging 1.78 g, administered from 42 to 144 days, was associated with a fall in hematocrit to a mean value of 25.8%. Despite this degree of anemia, no elevation of erythropoietin concentrations in urine or serum could be detected. Thus, amphotericin appears to cause anemia by inhibiting erythropoietin production rather than by suppressing bone marrow activity directly.
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PMID:Erythropoietin concentration in amphotericin B-induced anemia. 69 52

The question of a latent erythropoietin (ESF)-deficiency was studied in incipient renal anemia using a double stimulation technique for ESF. After a 4-week stimulation of ESF production with oral administration of fluoxymesterone (flu) intermittent hypoxic ESF stimulation was performed corresponding to a maximum altitude of 4000 m in 7 patients with chronic renal disease without or with incipient renal anemia (mean hematocrit 40%) and in 11 normal subjects (mean hematocrit 46%). Double stimulation in patients was compared with hypoxic stimulation alone and both were compared with controls. After flu alone only ESF excretion was increased in patients and in normal subjects. After flu plus 10 h of hypoxia serum ESF--titers were higher in healthy subjects than in the patients. The mean ESF titer after double stimulation was 81 mU/ml in patients and 115 mU/ml in normal persons. Forty-eight hour ESF excretion was 11 U and 43 U respectively. Compared to hypoxic stimulation alone double stimulation increased serum ESF titers in patients by 5% versus 80% in controls. Correspondingly, ESF excretion was enhanced by 19% and 49%, respectively. Finally, renal ESF clearance was increased by 42% versus 200%. After hypoxia alone non-anemic patients had higher serum ESF titers than healthy controls excluding a latent ESF deficiency in incipient renal anemia. It is concluded that decreased ESF production after double stimulation in patients was due to a nephrotoxic effect of flu followed by a decreased excretory and ESF-producing function of the damaged kidneys.
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PMID:[Erythropoietin in serum and urine in healthy persons and patients with chronic renal disease upon hypoxic stimulation and hypoxic stimulation after pretreatment with fluoxymesterone (author's transl)]. 72 83

Anaemia is common in renal insufficiency and has various causes: 1) depressed marrow production of red cells, probably due to reduced production of erythropoietin, though the possibility of direct marrow inhibition on the part of uraemic toxins cannot be ruled out, together with iron deficiency, as occurs in prolonged dialysis management; 2) greater red cell destruction attributable to extraglobular factors and other mechanisms (microangiopathy, drugs, etc.); 3) greater blood loss following thrombocytopenia, reduced platelet adhesivity and agglutinability, dialysis. The main premisses on which the treatment of anaemia of uraemic patients is based are discussed.
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PMID:[Anemia in chronic renal insufficiency]. 73 54

In 13 bilateral nephrectomized patients serum erythropoietin (SEp) activity could be measured quantitatively by use of the highly sensitive fetal mouse liver cell assay. SEp concentration in the majority of the cases was below the mean of normal controls. There was a significant positive correlation between SEp levels and hematocrits, suggesting erythropoietin (Ep) deficiency to be a causative factor in the anemia of the anephric state. Androgen therapy stimulated extrarenal Ep production in all of 5 anephric patients studied.
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PMID:Serum erythropoietin concentration in anephric patients. 74 98

In a longitudinal study the individual values of serum erythropoietin (SEp) in end-stage renal failure were investigated in 15 patients. SEp was determined by use of the foetal mouse liver cell assay on three occasions: (A) 2--6 months before the onset of RDT, (B) on day of first dialysis, and (C) 2--6 months following the onset of RDT. In every patient SEp increased from (A) to (B), and decreased again from (B) to (C). Changes of haematocrit were exactly opposite to changes of SEp. The results demonstrate that even in the terminal stage of chronic renal failure erythropoietin production is stimulated or suppressed in response to variations in the degree of anaemia.
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PMID:Sustained negative feedback between haematocrit and serum erythropoietin concentration in end-stage renal failure. 74 Jun 77

A teenage boy with mixed-cellularity Hodgkin disease presented with severe anemia secondary to pure red cell aplasia of marrow without evidence of lymphomatous infiltration or hemolysis. In vitro studies of the patient's serum demonstrated an inhibitor of erythropoietin activity which appeared to be an IgG but which did not directly bind erythropoietin. The patient's anemia resolved and the inhibitor disappeared following chemotherapy for Hodgkin disease. Presumably, the inhibitor was directed at a very early stage of red blood cell production. This phenomenon may be related to other autoimmune manifestations occasionally seen in patients with lymphomas. The case is presented to bring attention to the unusual occurrence of red cell aplasia in Hodgkin disease. Several hypotheses concerning significance and etiology of the anemia are detailed.
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PMID:Hodgkin disease and red cell aplasia. 74 84

Anemia is a constant complication of uremia. As it has been suggested that uremic toxins (middle molecules) play an important role in the mechanism of anemia, we studied the activities of three heme-synthesizing enzymes: delta-aminolevulinic acid dehydratase, porphobilinogen deaminase and ferrochelatase. In 26 patients on regular dialysis therapy, all three enzymes had significantly lower values than in normal control subjects. From our results, it can be assumed that the decreased heme biosynthesis in chronic uremic patients might be caused by a lack of erythropoietin or by uremic toxins inhibiting erythropoietin and/or heme-synthesizing enzymes.
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PMID:Heme synthesis in anemia of the uremic state. 75 May 46


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