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

Studies were conducted in suckling mice to investigate copper-dependent anemia. Brindled (Mobr/y) mice, which have a genetic defect that affects copper metabolism, were compared to their normal brothers (Mo+/y) as well as to anemic suckling mice that were copper-deficient (-Cu) because their dams were consuming a diet low in copper and to a fourth group of control suckling mice (+Cu) from copper-supplemented dams. Mice were given a subcutaneous injection of NaCl, FeCl2 or CuCl2 providing 50 micrograms of Na, Fe or Cu, respectively, when 7 days old and were killed 5 days later. Injection of FeCl2 into -Cu mice elevated liver iron 2.7-fold and raised hemoglobin levels to those observed in the +Cu and Mo+/y mice. Ceruloplasmin activity remained low at 5% of control levels. Injection of CuCl2 into -Cu mice resulted in significant increases in body and brain weight, elevations in serum copper and ceruloplasmin activities and hemoglobin levels. Liver copper rose and iron fell, both to levels observed in +Cu and Mo+/y mice. Brain copper and norepinephrine concentrations rose to control levels. Injection of CuCl2 into Mobr/y mice, although resulting in darker pigmentation and normal serum copper and ceruloplasmin levels, failed to stimulate growth or change brain weight. Furthermore, liver and brain copper levels did not rise to normal levels despite significant improvements. Similarly, brain norepinephrine levels rose, but were still below normal. Brindled mice do not respond to copper therapy to the same degree as do -Cu mice. Iron therapy was successful in reversing the anemia of -Cu mice but was without effect on growth or brain development.
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PMID:Repletion of copper-deficient mice and brindled mice with copper or iron. 669 1

Copper deficiency has been described in premature infants on hyperalimentation. The bony abnormalities are generalized and are usually associated with anemia and neutropenia. These changes present with normal serum levels of iron, ascorbic acid, calcium, phosphorus, and magnesium, as well as with depressed levels of copper and ceruloplasmin. They appear at about three to nine months of age in infants with a low birth weight who are receiving total parenteral nutrition, but can be prevented by greater than normal maintenance levels of copper supplements. Established bone changes improve rapidly after the administration of therapeutic supplements.
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PMID:Skeletal changes associated with copper deficiency. 680 88

To test the hypothesis that ferroxidase I (ceruloplasmin) activity is essential for iron mobilization, adult rats were fed a copper sufficient diet with or without the chelating drugs D-penicillamine and triethylenetetramine for 120 days. By day 6 of treatment and for the remainder of the experiment the drug-fed rats showed low plasma copper concentration and low ferroxidase I activity. Plasma ferroxidase II activity in the DPA and TETA groups tended to be slightly lower than that of controls. No animals became anemic. Therefore, persistent low plasma ferroxidase I does not necessarily cause anemia in the adult rat.
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PMID:The effect of copper chelating drugs on liver iron mobilization in the adult rat. 686 Mar 30

To characterize the erythroid homeostatic defect in canine inflammatory states, a single dose of Freund's complete adjuvant was injected subcutaneously to simulate naturally occurring infection and inflammation. After a latent period of 5 to 8 days, a generalized noninfectious inflammatory process was observed, followed by abscessation and drainage. This was accompanied by a modest anemia which decreased from base-line values by as much as 30%. In addition, a disordered iron metabolism was evidenced by depressed serum iron concentrations, total iron binding capacity (transferrin), percentage saturation of transferrin, and decreased numbers of bone marrow sideroblasts. Free RBC protoporphyrin concentrations were increased, as were serum copper, zinc, and ceruloplasmin. Bone marrow reticuloendothelial iron and hepatic nonheme iron were increased. Bone marrow myeloid-erythroid ratios were depressed. Throughout the course of the inflammatory period, the anemia remained normocytic and normochromic. A significant reticulocyte response was not observed.
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PMID:Anemia of inflammatory disease in the dog: clinical characterization. 727 Oct 24

A 6-month-old full-term infant had severe anemia and neutropenia. The patient was being fed cow's milk and a diet of corn flour. Thorough investigation revealed low serum iron concentration, severe hypocupremia, low ceruloplasmin, retardation of bone age, and metaphysial irregularities and spurring. Bone marrow aspirate revealed cytoplasmic vacuolization in precursors of the erythroid and myeloid series and ringed sideroblasts. Therapy with oral iron, folic acid, and vitamin C was futile. Administration of copper sulfate resulted in brisk increase in neutrophils and reticulocytes. The child maintained normal levels of hemoglobin, neutrophils, serum copper and ceruloplasmin, and serum iron one year after copper therapy was discontinued. The probable role of unrecognized copper deficiency in causing anemia in infants more than 6 months of age is discussed, and the importance of serum copper examination in refractory iron deficiency anemia and neutropenia is stressed. To the best of our knowledge, no such case has previously been described in the literature.
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PMID:Copper deficiency with cow's milk diet. 727 67

Ceruloplasmin plasma levels and erythrocyte superoxide dismutase activity were studied in appropriate for gestational age preterm infants (birth weights less than or equal to 1500 g) during the first 10 weeks of life. Preterm infants had significantly lower ceruloplasmin concentrations in cord blood than term infants, the mean level in the preterm infants being 0.07 g/l. At 1 week of age ceruloplasmin levels had risen significantly, whereupon a fall occurred at 2 weeks of age. Ceruloplasmin concentrations increased slowly and progressively from 4 weeks of age. The low ceruloplasmin concentration during the early anemia of prematurity seems not to interfere with iron mobilization. The superoxide dismutase activity per gram hemoglobin in cord blood erythrocytes from normal term infants was significantly lower than that of red blood cells from adults. When the activity was expressed per erythrocyte no difference was found. The normochromic macrocytic red blood cells of the neonate most likely explain this discrepancy. The erythrocyte superoxide dismutase activity of the preterm infants did not change from birth until 10 weeks of age, and the levels seemed adequate judged from the levels found in red blood cells from adults and cord blood from term infants. Neither ceruloplasmin nor erythrocyte superoxide dismutase activity seem to play a role in the etiology of the early anemia of prematurity.
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PMID:Ceruloplasmin levels and erythrocyte superoxide dismutase activity in small preterm infants during the early anemia of prematurity. 732 38

Anemia and neutropenia caused by copper deficiency is a well-known consequence of long term total parenteral nutrition in the literature. We present 6 bed-ridden elderly patients who developed anemia and neutropenia after receiving enteral nutrition for a long time (mean: 3.3 years) In all 6 patients, serum copper and ceruloplasmin level were very low, and the mean of their hematological data were as follows: WBC 2,200/microliters, neutrophil 554/microliters, hemoglobin 8.1 g/dl, platelet 260 x 10(3)/microliters, respectively. The bone marrow examination showed cytoplasmic vacuolization of both myeloid and erythroid precursors, and maturation arrest of granulopoiesis. Then, copper sulfate was administrated by enteral tube to 6 patients, and the improvement of anemia and neutropenia was observed within a month. A 82-year-old woman who received enteral nutrition for 3.5 years with sever anemia (Hb 3.7 g/dl) and neutropenia (neutrophil 350/microliters), showed a marked improvement in hematological data (Hb 8.0 g/dl, neutrophil 4, 092/microliters, respectively) after two months by administering the copper supplementation. The exact cause of the anemia and neutropenia in copper deficiency is unclear, but it is suggested that the decreased activity of enzyme containing copper may be related. Hematological abnormalities due to copper deficiency should be cared during long term enteral nutrition with long termed bed-ridden elderly patients.
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PMID:[Anemia and neutropenia in elderly patients caused by copper deficiency for long-term enteral nutrition]. 782 95

The effect of route of erythropoietin (EPO) administration was assessed in sixteen hemodialysis patients who completed a randomised crossover study of thrice weekly subcutaneous (SC) and intravenous (IV) erythropoietin with an EPO-free washout period separating the two phases of treatment. Route of EPO administration had no significant effect on absolute reticulocyte counts, and change in hemoglobin (Hb) during the first six weeks of therapy, at a constant EPO dose (120 iu/kg/week). Similarly, there was no significant difference in EPO dose requirement between the two routes, both during and after correction of anemia, and after maintenance of target Hb (10-12 g/dl) for an eight-week period (end of maintenance period dose; median [range]; SC EPO: 120 [30-367] iu/kg/week, IV EPO: 124.5 [37-377] iu/kg/week). Following EPO withdrawal, Hb fell at a rate of 0.38 (0.14-0.69) g/dl/week. Route of EPO administration did not influence the incidence of thrombotic and hypertensive side effects, or increases in dialysis heparin requirement and albumin, and decreases in ferritin, alpha-1-antitrypsin and ceruloplasmin during the study period. In conclusion, thrice weekly SC and IV EPO are comparable in terms of efficacy and safety.
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PMID:Erythropoietin response and route of administration. 805 Feb 10

Female rats are protected from the lethal effects of a dietary copper (Cu) deficiency, but female mice fed a Cu-deficient diet develop atrial thromboses and die. To further investigate the effect of sex on Cu status in mice (n = 16), male and female adult Swiss-Webster mice were fed Cu-supplemented (8.4 mg Cu/kg) or Cu-deficient (0.3 mg Cu/kg) diets with deionized water for 43-49 days. Six female mice, but only one male mouse, fed the Cu-deficient diet died during the experiment. Both male and female mice fed the Cu-deficient diet exhibited typical features of deficiency. The severity of anemia and the values observed for several indicators of Cu status (plasma ceruloplasmin [EC 1.16.3.1.] and erythrocyte copper-zinc superoxide dismutase [EC 1.15.1.1.] activities, cardiac Cu) were similar in both male and female Cu-deficient mice. However, cardiac enlargement (0.97 vs 0.73 g/100 g body wt, P < 0.05), cardiac edema (79.9% vs 78.2% cardiac water, P < 0.05) and depletion of renal Cu (10.4 vs 12.5 micrograms/g dry weight, P < 0.05) were more severe in female compared with male, Cu-deficient mice. Furthermore, although hepatic Cu was significantly (P < 0.05) lower in female Cu-deficient compared with Cu-supplemented mice, it was not significantly decreased by deficiency in male mice. These data indicate that the female mice experienced a more extreme form of Cu deficiency than the males.
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PMID:Contrasting effects of a dietary copper deficiency in male and female mice. 810 71

Zinc ingestion has become increasingly popular in the lay and food faddist population. Herein described by way of a case report and review of the 13 cases in the literature is the syndrome of severe anemia associated with excessive and prolonged intake of oral zinc. The syndrome is characterized by anemia, granulocytopenia, and bone marrow findings of vacuolated precursors and ringed sideroblasts. Serum analysis reveals increased zinc levels, decreased copper levels, and a decrease in ceruloplasmin. The mechanism appears to be zinc-induced copper deficiency, which is instrumental in producing the profound bone marrow abnormalities, as zinc itself is of low toxicity. Importantly, the syndrome is totally reversible with cessation of zinc intake. Hematologists should be aware of this form of reversible sideroblastic anemia.
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PMID:Zinc-induced sideroblastic anemia: report of a case, review of the literature, and description of the hematologic syndrome. 817 83


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