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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Terminal renal dysfunction (TRD) was induced in 2 groups of dogs by partial surgical ablation of the kidney. Dogs of a control group and of 1 of the TRD groups were maintained on a diet containing normal phosphorus concentration, whereas dogs of the other TRD group were maintained on a low-phosphorus diet. Mild anemia developed in dogs of both TRD groups and could not be attributed to iron deficiency, increased erythrocyte concentration of 2,3-diphosphoglycerate, or absolute deficiency of erythropoietin (EP). Subsequently, all dogs were acutely depleted of approximately 25% of their blood volume. Erythropoietin concentration in dogs of the TRD groups was lower than that of controls, however, erythroid regenerative capacity was comparable with that of control dogs when plasma parathyroid hormone (PTH) concentration was lowered by reduced dietary intake of phosphorus. The PCV in dogs of the chronic TRD groups had a slight positive correlation with serum EP concentration, and a significant (P less than 0.05) negative correlation with plasma PTH and serum phosphorus and creatinine concentrations, using a correlation matrix. There was no longer a significant correlation between plasma PTH concentration and PCV after controlling for serum creatinine concentration by use of a multiple linear regression analysis. A significant (P less than 0.05) negative correlation also was observed between plasma PTH and serum EP concentrations, but not between serum EP and phosphorus or creatinine concentrations. Significance of the EP and PTH association was reduced when analyzed, using a multiple linear regression analysis that included serum creatinine values.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of parathyroid hormone in the anemia of chronic terminal renal dysfunction in dogs. 261 21

The anemia of Belgrade b/b rats has been shown to be due to intracellular iron deficiency. The aim of this study of erythropoiesis at the progenitor cell level in these rats was to determine if a defect is present in the early phase of red cell production. Both erythroid colony-forming unit (CFU-E)- and erythroid burst-forming unit (BFU-E)-derived colonies were found to be few in untreated b/b rats and made up of a small number of poorly hemoglobinized erythroblasts of different size and irregular cell shape. Following treatment with iron, the anemia of the rats improved, and the number of CFU-E-derived colonies and the number of cells per colony increased, but the peculiar erythroblast morphology persisted. The high serum level of biologically active erythropoietin (Ep) in b/b rats rules out inadequate Ep production as a cause of their anemia. The results presented indicate, in addition to the earlier described defective transmembrane iron transport, a defect in erythroid progenitor cells. The effect of iron treatment in these rats detected in vitro on erythroid progenitors confirms the importance of iron for cellular proliferation.
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PMID:Erythroid progenitors in anemic Belgrade laboratory (b/b) rats. 275 90

The authors studied 35 marrow biopsies from 32 patients with rheumatoid arthritis, systemic lupus erythematosus, mixed connective tissue disease, polymyositis, and psoriatic arthritis. Reasons for biopsy included cytopenia, fever of unknown origin, and malignancy. Cellularity was abnormal in 71%. Plasma cells were increased in 60% and associated with lymphoid aggregates. Immunoperoxidase stains showed polyclonal perivascular plasma cells and increased T-cells forming lymphoid aggregates. Two patients had granulomas without documented infection. Anemic patients had findings consistent with anemia of chronic disease, erythroid aplasia, hemolysis, and iron deficiency. Iron stores were variable. Platelet and granulocyte precursors were variably altered and did not predictably correlate with the presence, absence, or cause of thrombocytopenia and neutropenia. Myelodysplastic syndromes were present in two patients with rheumatoid arthritis. Osteomalacia and osteoporosis were seen, resulting from renal failure and steroids. Marrow findings are unpredictable and reflect the diverse causes of cytopenias in patients with connective tissue disorders.
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PMID:Bone marrow findings in connective tissue disease. 281 17

Iron metabolism in the Belgrade rat was examined in the intact animal and in the reticulocyte suspensions. The plasma iron turnover was increased. However, when allowance was made for the effect of the elevated plasma iron concentration, erythroid marrow capacity for iron uptake was at basal levels. Numbers of erythroid cells in marrow and spleen measured by the radioiron dilution technique were increased. Thus iron uptake was not proportionate to the erythroid hyperplasia in the b/b rat, despite a more than adequate plasma iron supply. This relative deficiency in iron uptake was reflected in a severe microcytosis and elevated red cell protoporphyrin. Reticulocyte incubation studies demonstrated an unimpaired uptake of the transferrin-iron-receptor complex but a marked reduction in iron accumulation. The diferric transferrin molecule, when it did give up iron within the cell, released both of its iron atoms so that only apotransferrin was returned to the media. In contrast to the nearly complete release of iron within the normal reticulocyte, the major portion of iron taken up by the Belgrade reticulocyte was returned to the plasma. The release mechanism that can be impaired in iron-deficient reticulocytes by EDTA or cadmium was shown to be affected by lower concentrations of these substances in the Belgrade reticulocyte. It is concluded that the Belgrade rat has an abnormality of iron release within the absorptive vacuole that is responsible for a state of intracellular iron deficiency, involving the erythron and other body tissues.
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PMID:Iron metabolism in the Belgrade rat. 308 Oct 63

Effects of cadmium (Cd) on in vitro and in vivo erythropoiesis in rats were studied by methylcellulose colony assay. Cd suppressed the in vitro growth of late erythroid progenitors (CFU-E) in a dose-dependent fashion and did not lose its inhibitory potency with increasing doses of erythropoietin (EPO). In addition, in marrow suspension cultures, Cd did not significantly influence 59Fe incorporation into both the cells and heme, and the Cd dose-responsive inhibition curve of the number of living cells was similar to that of CFU-E. These results suggest that the suppression of CFU-E colony formation by Cd is not due to the blocking of either EPO action to stimulate the growth of CFU-E or the iron incorporation into the cells ahd heme, but due to its direct cytotoxic effect. The colony suppression by Cd could be prevented by adding metallothionein to the cultures. On the other hand, oral administration of Cd to animals (100 mg/liter in drinking water) induced an iron deficiency anemia characterized by microcytic hypochromic red cells, decreased plasma iron, and increased total iron binding capacity. Marrow CFU-E density steadily increased as plasma iron decreased due to Cd administration and reached a plateau after 50 days. Plasma EPO titers were also found to be elevated in such a Cd-induced anemia. Parenteral iron administration during the Cd drinking period could completely prevent the development of iron deficiency anemia and the increase of both CFU-E and plasma EPO. There was a hyperbolic correlation between CFU-E and plasma iron or transferrin saturation. These results demonstrate that oral CD administration produces bone marrow hyperplasia at the CFU-E level due to iron deficiency.
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PMID:Effects of cadmium on in vitro and in vivo erythropoiesis: erythroid progenitor cells (CFU-E), iron, and erythropoietin in cadmium-induced iron deficiency anemia. 339 Dec 51

Quantitative measurements of transferrin receptors, tissue transferrin, tissue iron uptake, and erythroid cellularity have been carried out in rats with altered erythropoiesis and altered iron balance. Erythroid receptors increased with erythroid hyperplasia, with the increase in proportion to the increased number of red cell precursors in phenylhydrazine-treated rats. Receptors increased disproportionately in iron deficiency due to both erythroid hyperplasia and an increase in receptors in the individual cell. There was a ratio of 1:1 between cell-related transferrin and receptors in circulating reticulocytes but a disproportionate amount of cell-related transferrin in fixed erythroid tissues (marrow and spleen), suggesting that there was some other reason for the concentration of transferrin in these tissues. Erythron iron uptake was increased in proportion to the increased receptor number in phenylhydrazine-treated animals but was reduced in iron deficiency because of the limited amount of iron-bearing transferrin. These studies demonstrate the dominant role of erythron cellularity and iron status in vivo in determining total receptor number and the importance of receptor number and iron supply in tissue iron uptake.
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PMID:In vivo transferrin-iron receptor relationships in erythron of rats. 340 5

Analysis of radioactive iron kinetics was performed using a multi-compartment model on a series of 300 patients having either a quantitative (aplasia, haemolysis, iron deficiency) or qualitative (dyserythropoiesis, agnogenic myeloid metaplasia) anomaly of iron metabolism. Calculations were performed using a mammillary model of iron metabolism. The study demonstrated that the flux of iron from the plasma to the exchangeable compartment was a constant fraction of the global iron flux, equal to 15%, in those cases without dyserythropoiesis. This suggested that a constant correction for calculations of iron flux from the slope of the initial portion of the radioactive iron elimination curve may be applied to calculations of haemoglobin production and to the movements of iron to its exchangeable pools. Contrary to previously published information, the exchange of iron between the plasma and the exchangeable pools was not related to circulating iron levels when the other parameters were held constant. In the patients with aplastic anaemia the iron flux was diminished, but never eliminated, demonstrating that the exchangeable compartment was not solely erythroblastic, but included non-erythroid transferrin receptors. In dyserythropoietic states and myelofibrosis, the iron flux from the plasma was elevated, indicating that an important fraction of radio-iron leaves the plasma and then returns, without participating in effective erythropoiesis as determined by the appearance in the circulation of labelled viable red blood cells. The determination of this movement permitted the measurement of ineffective erythropoiesis.
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PMID:Radio-iron kinetic studies in anaemia and the measurement of dyserythropoiesis. 341 96

Two hundred Hausa primigravidae at Zaria were divided into five groups in a randomized double-blind trial of antenatal oral antimalarial prophylaxis, and haematinic supplements. Group 1 received no active treatment. Groups 2 to 5 were given chloroquine 600 mg base once, followed by proguanil 100 mg per day. In addition, group 3 received iron 60 mg daily, group 4 folic acid 1 mg daily, and group 5 iron plus folic acid. Forty-five percent were anaemic (haemoglobin (Hb) less than 11.0 g dl-1) at first attendance before 24 weeks of gestation, and malaria parasitaemia (predominantly Plasmodium falciparum) was seen in 27%, of whom 60% were anaemic. The mean Hb fell during pregnancy in group 1, and seven patients in this group had to be removed from the trial and treated for severe anaemia (packed cell volume (PCV) less than 0.26). Only five patients in the other groups developed severe anaemia (P = 0.006), two of whom had malaria following failure to take treatment. Patients in group 1 had the lowest mean Hb at 28 and 36 weeks of gestation, and patients receiving antimalarials and iron (groups 3 and 5) had the highest Hb at 28 weeks, but differences were not significant, possibly due to removal from the trial of patients with severe anaemia. Anaemia (Hb less than 12.0 g dl-1) at six weeks after delivery was observed in 61% of those not receiving active treatment (group 1), in 39% of those protected against malaria but not receiving iron supplements (groups 2 and 4) and in only 18% of patients receiving both antimalarials and iron (groups 3 and 5). Folic acid had no significant effect on mean Hb. Proguanil was confirmed to be a highly effective causal prophylaxis. Prevention of malaria, without folic acid supplements, reduced the frequency of megaloblastic erythropoiesis from 56% to 25%. Folic acid supplements abolished megaloblastosis, except in three patients who were apparently not taking the treatment prescribed. Red cell folate (RCF) concentrations were higher in subjects with malaria, probably due to intracellular synthesis by plasmodia. Infants of mothers not receiving antimalarials appeared to have an erythroid hyperplasia. Maternal folate supplements raised infants' serum folate and RCF. Fourteen per cent had low birth weight (less than 2500 g), and the perinatal death rate was 11%; the greatest number were in group 1, but not significantly. A regime is proposed for the prevention of malaria, iron deficiency, folate deficiency and anaemia in pregnancy in the guinea savanna of Nigeria.
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PMID:The prevention of anaemia in pregnancy in primigravidae in the guinea savanna of Nigeria. 353 Jan 58

Mild-to-moderate thrombocytopenia has been reported as an occasional finding in patients with iron deficiency. The present case describes a multiparous woman who presented with increased menorrhagia, severe anemia (3.0 g/dl) and thrombocytopenia (9,000 platelets/mm3). Her bone marrow examination showed iron deficiency, megakaryocytopenia, and erythroid hypoplasia but no other evidence of a primary marrow disorder. Her symptoms, the thrombocytopenia and the megakaryocytopenia, resolved with iron replacement. This case demonstrates the profound degree to which thrombopoiesis can be affected in iron deficiency.
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PMID:Severe thrombocytopenia in iron deficiency anemia. 356 74

In both experimental animals and human subjects iron absorption over a wide dosage range was quantitatively equivalent from ferrous salts and a ferric polymaltose complex under basal conditions. The comparable bioavailability was maintained when demand was increased by iron depletion or erythroid stimulation and depressed by expansion of body stores or impaired erythropoiesis. This common pattern for iron retention from both salt and complex supports the interchangeable use of these products in therapy of absolute iron deficiency.
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PMID:Equivalent bioavailability of iron from ferrous salts and a ferric polymaltose complex. Clinical and experimental studies. 356 65


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