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

The erythropoietic activity in the sera of 18 patients with sideropenic anemia was investigated. The ex-hypoxic mouse bioassay was used and the 48 hour incorporation of radioiron into the peripheral blood was measured. The level of erythropoietin found was compared to the hemoglobin concentration and the PCV values in those patients. The statistically significant correlation was found between erythropoietin in the patients sera and the degree of anemia. Higher erythropoietin values were found in men as compared to women with the same severity of anemia. It was concluded that the results obtained in this study can be used as control values when erythropoietic activity in the sera of patients with different hematological disorders is measured.
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PMID:[Erythropoietin in sideropenic anemias]. 75 83

1. The plasma clot method of McLeod, et al8 was used to study the inhibitors of erythroid colony forming cells (CFU-E and BFU-E) in sera of patients with anemia of uremia. 2. Compared to sera from hematologically normal human subjects, sera from undialyzed patients with anemia of uremia produced a significant inhibition of CFU-E and BFU-E. 3. A marked reduction in the inhibitor(s) of CFU-E was seen in sera of 3 out of 4 patients following 16 wks of intermittent hemodialysis. 4. Creatinine, guanidine, guanidinosuccinic acid and guanidinobutyric acid had no effect on the erythroid colony forming cells. 5. Together with the relative erythropoietin deficiency, inhibitor(s) of the erythroid progenitor cell compartment may play a major role in the mechanism of the anemia of renal insufficiency.
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PMID:Inhibitors of erythroid colony forming cells in sera of azotemic patients with anemia of renal disease. 75 44

Erythropoiesis in spleens of lethally irradiated Lewis rats grafted with 4-35 X 10(6) syngeneic marrow cells was inhibited or delayed during the test period of 5 days; this was in marked contrast to observation in irradiated mice. The mechanism of this inhibition was the subject of this study. Pretreatment of recipients 9 days prior to irradiation with the cytotoxic drugs cyclophosphamide (CY), busulfan (BUS), or dimethylmyleran (DMM), or the induction of iron deficiency with anemia in recipients reversed this delayed erythropoiesis. However, neither iron-deficiency anemia nor pretreatment with BUS or DMM affected the ability of irradiated recipients to reject 20 to 50 X 10(6) allogeneic marrow cells. The administration of commercial preparations of erythropoietin to hosts stimulated erythropoiesis moderately. However, proliferation of syngeneic marrow cells was not enhanced when infused into lethally irradiated Spontaneous Hypertensive (SH) inbred-strain rats which have high levels of endogenous erythropoietin. Finally, plasma from irradiated rats treated with phenylhydrazine to produce severe anemia was rich in erythropoietin but failed to stimulate erythropoiesis in the cell transfer system. Two hypotheses are considered: (1) Irradiation inhibits the secretion of a factor (not erythropoietin) responsible for initiating early stages in differentiation of transplanted stem cells; iron-deficiency anemia and cytotoxic drugs stimulate the secretion of this factor. (2) Normal rats secrete a factor which suppresses erythropoiesis; iron-deficiency anemia and cytotoxic drugs inhibit the production or function of this factor. Cellular rather than humoral factors may by involved.
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PMID:Delayed erythropoiesis in irradiated rats grafted with syngeneic marrow: effects of cytotoxic drugs and iron-deficiency anemia. 78 11

Thymectomized, irradiated and syngeneic bone marrow-repopulated (TIR) mice, after hemopoietic recovery, were more effective in producing erythropoietin than normal controls in response to hypobaric hypoxia. Mice which were only thmectomized responded to hypoxia with more erythropoietin production than controls but less than TIR animals. It is suggested that lymphoid elements of thymic origin may produce inhibitors of the erythropoietic system. This may play a role in the anemia of lymphomas and certain other clinical syndromes.
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PMID:Effect of the thymus on erythropoietin production in response to hypobaric hypoxia in mice. 78 62

The anemia of dialyzed uremic patients is due to several factors: loss of blood and proteins; increased destruction of erythrocytes, and alteration of erythropoietin feedback. In an anemic dialyzed patient the number of reticulocytes is normal while a sudden worsening of the anemia is followed by severe reticulocytosis.
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PMID:Pathogenetic aspects of anemia in long-term hemodialyzed patients. 82 Dec 89

Following the intravenous injection of 1 mg of BCG into Mice an anemia with erythroblastopenia is observed in spite of a high level of erythropoietin. A preferential differentiation of hematopoietic stem cells to leucocytes is observed with a concomitant of the differentiation to erythrocytes.
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PMID:[Preferential differentiation of hematopoietic stem cells in mice after intravenous injection of BCG]. 82 56

Eight men with chronic renal disease in the stage of compensated retention were given high doses of the androgen fluoxymesterone (40 mg/m2/day) for erythropoietin stimulation for 4 weeks. Seven of them showed a transient significant average rise in the serum creatinine level of 3.8 to 6.1 mg% which partly regressed only 8 to 12 weeks after stopping the medication. The rise in serum creatinine which appears under fluoxymesterone is attributable to a transient increase in the renal excretory function disturbance and/or a raised catabolism. Warning should be given against the further use of this drug in the treatment of renal anemia.
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PMID:[Rise in serum creatinine under the androgen fluoxymesterone in chronic renal disease (author's transl)]. 82 97

The association between anemia and chronic renal failure has been recognized since the early 19th century. With the introduction of regular dialysis treatment, an understanding of all aspects of this uremic complication has become of great importance, including an appreciation of the hazards of multiple blood transfusions. This analysis of hemoglobin levels and transfusion requirements in 84 dialysis patients focuses specific attention on hemolytic mechanisms, blood loss, and the effect of bilateral nephrectomy on erythropoiesis. Because no replacement for renal erythropoietin is available, particular attention must be paid to less important, but partially correctable factors that contribute to anemia. Blood transfusion requirements can then be reduced to a minimum, together with the risks of hypersplenism, hepatitis, and sensitization of the patient to alloantigens.
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PMID:Anemia in hemodialysis patients. 83 15

Various factors are involved in the pathogenesis of anemia in dialysis patients. Reduced erythropoiesis is mainly attributed to erythropoietin deficiency. Stimulation of erythropoiesis may be promoted by androgens. Substitution of iron is recommended in case of iron deficiency. As a rule, supplementation of vitamin B12 is not necessary, but administration of folic acid is recommended. Treatment of anemia in renal failure is rendered more effective by increased technical efficiency in hemodialysis permitting a relatively protein-rich diet. Blood transfusions are not necessary during routine treatment of dialysis. Since bilateral nephrectomy will always provoke severe anemia, it should be reserved to special cases of severe hypertension. Until now, no conservative therapy has been developed which would allow optimal treatment of anemia in dialysis patients. Successful renal transplantation still is, and will be, the best therapeutic intervention.
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PMID:[Anemia in terminal kidney failure. Pathogenesis and therapy]. 83 56

Using a methylcellulose clonal cell culture technique, we examined serial changes in erythropoietic precursors in the femur, spleen, and blood of mice prepared with bleeding, erythropoietin injections, or hypertransfusion with packed red blood cells. Significant changes were observed for all hemopoietic organs in the number of erythropoietic burst-forming units (BFU-E) and erythrocytic colony-forming units (CFU-E). In mice prepared with bleeding or erythropoietin injections, the serial changes of BFU-E and CFU-E were similar to but less striking than those seen in mice with phenylhydrazine-induced anemia. The transient decline in the femoral BFU-E coincided with the temporary increase in the splenic and blood BFU-E. A more pronounced increase in CFU-E was noted in the femur and spleen of these mice. In hypertransfused mice, the direction of the changers in the erythropoietic precursors was opposite. While femoral BFU-E increased mildly, a significant drop was noted in the splenic and blood BFU-E. Both femoral and splenic CFU-E declined and remained low while erythrocytosis presisted. Next, we examined the proliferative state of the erythropoietic precursors in the marrow and spleen using short-term incubation with high specific tritiated thymidine. In the marrow and spleen of normal mice, the BFU-E and CFU-E in the DNA synthetic phase was about 36 and 74%, respectively. Neither induction of anemia with phenylhydrazine hydrochloride nor polycythemia with hypertransfusion caused changes in the proliferative state of the precursors. These results indicate that the serial changes in the number of BFU-E represent migration of BFU-E from marrow to spleen rather than BFU-E proliferation. Marrow CFU-E increased in anemic mice and decreased in polycythemic mice without changes in their proliferative state. It is possible that the target of erythropoietic stimulation in mice may be cells at maturational stages intermediate between BFU-E and CFU-E.
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PMID:Erythropoietic precursors in mice under erythropoietic stimulation and suppression. 84 18


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