Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Copper deficiency was found in an adult patient who had received excessive daily oral zinc for 10 mo. The deficiency was characterized by hypochromic-microcytic anemia, leukopenia, and neutropenia. Although initially thought to be caused by iron deficiency, the anemia did not respond to oral or intravenous iron. Cessation of zinc tablets and ingestion of an oral copper preparation daily for 2 mo failed to correct the anemia or leukopenia. It was not until shortly after intravenous administration of a cupric chloride solution during a 5-day period, at a total dose of 10 mg, that serum copper and ceruloplasmin levels increased and the anemia, leukopenia, and neutropenia resolved. These data suggest that the elimination of excess zinc is slow and that, until such elimination occurs, the intestinal absorption of copper is blocked.
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PMID:Zinc-induced copper deficiency. 333 23

The effects of elevated dietary ascorbic acid and iron on copper utilization were examined. Male Sprague-Dawley rats were fed one of two levels of Cu (deficient, 0.42 microgram Cu/g, or adequate, 5.74 micrograms Cu/g), Fe (moderate, 38 micrograms Fe/g or high, 191 micrograms Fe/g), and ascorbic acid (low, 0% or high, 1% of the diet) for 20 d. High Fe decreased (p less than 0.05) Cu absorption only in Cu-deficient rats. High ascorbic acid significantly decreased tissue Cu levels in Cu-adequate rats. High Fe with ascorbic acid caused severe anemia in Cu-deficient rats and decreased plasma ceruloplasmin by 44% in Cu-adequate rats. Cu,Zn-superoxide dismutase activity in erythrocytes was decreased (p less than 0.05) by 14% during Cu deficiency but was not affected by Fe or ascorbic acid. These results may be important to individuals with high intakes of Fe and ascorbic acid.
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PMID:Adverse effects of high dietary iron and ascorbic acid on copper status in copper-deficient and copper-adequate rats. 333 44

Anemia and neutropenia developed in a man who took pharmacologic doses of supplemental zinc. Laboratory investigation showed high zinc level, hypocupremia, low ceruloplasmin level, and ringed sideroblasts. All resolved after withdrawal of zinc. Self-administered zinc appears to have caused severe copper deficiency, with secondary anemia and neutropenia. Physicians should be aware of this deleterious and completely reversible effect of megadose mineral therapy. Zinc ingestion or exposure should be considered in the differential diagnosis of unexplained anemia, leukopenia, or sideroblastic anemia.
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PMID:Copper deficiency and sideroblastic anemia associated with zinc ingestion. 340 36

Protein and lipid analyses were conducted on isolated erythrocyte and lymphocyte plasma membranes from 7-wk-old male C57BL copper-deficient and copper-supplemented mice to investigate mechanisms for the altered immunity that accompanies dietary copper deficiency. Beginning at parturition, dams were fed a diet low in copper (0.5 mg/kg) and the offspring were weaned to this diet. Half the dams and their respective offspring received supplemental copper (20 mg/L) in the drinking water (+Cu) and served as controls. Unsupplemented offspring (-Cu) had lower activity of cuproenzymes serum ceruloplasmin, spleen and thymus cytochrome-c oxidase and copper, zinc-superoxide dismutase. The -Cu mice exhibited anemia, splenomegaly and thymic atrophy. Based on the marker enzyme alkaline phosphodiesterase I (APDE-I), lymphocyte plasma membranes were enriched 7- to 10-fold for spleen and thymus, respectively, after discontinuous sucrose density centrifugation. The activity of APDE-I was higher in spleen and thymus samples from -Cu mice than from those of +Cu mice for both crude homogenates and purified plasma membranes. Proteins were fractionated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis followed by silver staining. A yellow-appearing band, Mr 74,000, present in all splenic membrane samples from +Cu mice was not evident in the samples from -Cu mice. Fatty acid methyl esters (FAME) were quantified by gas chromatography. Compared to splenic membranes from +Cu mice, the samples from -Cu mice demonstrated significant changes in all FAME (lower 16:0, 18:0 and 20:3n-6 and higher 18:1n-9, 18:2n-6 and 20:4n-6), including a higher unsaturation index. FAME composition of erythrocyte ghosts from -Cu mice demonstrated similar changes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dietary copper deficiency alters protein and lipid composition of murine lymphocyte plasma membranes. 359 18

Reference serum copper, ceruloplasmin and zinc values were established for 100 healthy white nulliparous students aged 18-23 years resident in Cape Town who had been taking low-dosage triphasic contraceptives for a minimum period of 3 months, and in 100 female students not taking contraceptives. The mean serum copper values were 26.5 +/- 4.2 mumol/l and 16.9 +/- 2.7 mumol/l for those taking and not taking oral contraceptives respectively; corresponding values for ceruloplasmin were 181 +/- 43.9 IU/ml and 110 +/- 22.7 IU/ml respectively. Both differences were statistically significant. Serum zinc values for those on contraceptives were 14.1 +/- 2.1 mumol/l and for the others 14.7 +/- 2.0 mumol/l. There were no differences in the haematological parameters except for a significantly higher mean corpuscular volume in females taking oral contraceptives. Of possible clinical significance in this student population are prevalence rates of 2.2% for anaemia (haemoglobin value less than 11.5 g/dl), 7% for iron deficiency (serum ferritin less than 12 micrograms/l) and 6.6% for iron depletion (serum ferritin 12-20 micrograms/l).
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PMID:Reference values for serum copper, ceruloplasmin and zinc and haematological indices for healthy nulliparous females. 366 Jan 57

Experiments were conducted in copper deficient male and female rats fed diets containing fructose or starch in order to determine whether the same type of interaction between copper status and dietary carbohydrate found in male rats also occurs in the female rat. Mortality occurred only in the male rats fed the fructose diet deficient in copper with 40% of the animals dying during the 8 week study. Only anemia, hypercholesterolemia, increased BUN, heart hypertrophy and reduced body weight were observed in these animals which could be related to their mortality. Despite the increased mortality, plasma ceruloplasmin, erythrocyte SOD and hepatic copper concentrations were reduced to a similar extent in all rats regardless of the sex of the animals or of the type of dietary carbohydrate fed. The results of the present study indicate that although direct measurements of copper status of female rats fed fructose diet deficient in copper are similar to their male counterpart, they are apparently protected from the lethal consequences of the deficiency.
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PMID:Female rats are protected against the fructose induced mortality of copper deficiency. 374 32

Normocytic anemia with granulocytopenia occurred in a 23 year old man with acrodermatitis enteropathica who received high doses of zinc sulphate orally for 12 months. Copper deficiency was suspected to be the cause of this anemia when extreme hypocupremia and hypoceruloplasminemia were found. Oral zinc therapy was stopped and intravenous supplements of copper were followed by reticulocytosis and complete correction of the anemia and granulocytopenia. Plasma copper and ceruloplasmin levels normalized. Up to now copper deficiency has never been reported during zinc treatment in acrodermatitis enteropathica. We conclude that the copper status should be monitored during oral zinc therapy in this condition.
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PMID:Copper responsive anemia, induced by oral zinc therapy in a patient with acrodermatitis enteropathica. 401 88

The way in which iron is handled by the duodenal mucosa, the reticuloendothelial system, the hepatic parenchymal cell, and the normoblast was investigated in copper-deficient swine.Copper-deficient swine failed to absorb dietary iron at the normal rate. Increased amounts of stainable iron were observed in fixed sections of duodenum from such animals. When (59)iron was administered orally, the mucosa of copper-deficient animals extracted iron from the duodenal lumen at the normal rate, but the subsequent transfer to plasma was impaired.When intramuscular iron supplements were given to copper-deficient pigs, increased amounts of iron were found in the reticuloendothelial system, the hepatic parenchymal cells, and in normoblasts (sideroblasts). Hypoferremia was observed in the early stages of copper deficiency, even though iron stores were normal or increased. When red cells that were damaged by prolonged storage were administered, the reticuloendothelial system failed to extract and transfer the erythrocyte iron to the plasma at the normal rate. Administration of copper to copper-deficient animals with normal iron stores resulted in a prompt increase in the plasma iron. The observed abnormalities in iron metabolism are best explained by an impaired ability of the duodenal mucosa, the reticuloendothelial system, and the hepatic parenchymal cell to release iron to the plasma. It is suggested that copper is essential to the normal release of iron from these tissues. This concept is compatible with the suggestion made by others that the transfer of iron from tissues to plasma requires the enzymatic oxidation of ferrous iron, and that the plasma copper protein, ceruloplasmin, is the enzyme (ferroxidase) which catalyzes the reaction. Because excessive amounts of iron were found in normoblasts, it is suggested that an additional defect in iron metabolism affects these cells and plays a major role in the development of anemia. As a result of the proposed defect, iron cannot be incorporated into hemoglobin and, instead, accumulates as nonhemoglobin iron.
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PMID:Iron metabolism in copper-deficient swine. 567 26

Experiments were conducted in suckling mice to investigate copper-dependent anemia. Brindled (Mobr/y) mice, which are not anemic, 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 a fourth group of suckling mice that served as dietary controls (+Cu). Compared to +Cu and Mo+/y mice, -Cu mice were smaller and exhibited cardiac hypertrophy and significant atrophy of lymphoid tissues (spleen and thymus), Mobr/y mice were also small and demonstrated modest atrophy of both liver and spleen. Cu levels were decreased in all -Cu mouse tissues studied, whereas Fe levels tended to be unaltered. Mobr/y mice also exhibited lower tissue Cu levels in soft tissues, except for kidney and small intestine; however, Cu levels in Mobr/y mice were greater than in -Cu mice. Functional copper deficiency was demonstrated in -Cu tissues by decreases in cytochrome c oxidase (CO) and cuprozinc-superoxide dismutase (SOD). The magnitude of the change was tissue specific. Mobr/y tissues, which were low in Cu, also exhibited decreased SOD and CO activity. However, the drop in Mobr/y tissue was less than in -Cu tissue. This was most pronounced in bone marrow, where both CO and SOD were four times higher in Mobr/y than in -Cu mice. Both Mobr/y and -Cu mice had low serum ceruloplasmin activities. The presence of anemia in -Cu mice and the absence of anemia in Mobr/y mice may result from a more severe copper-deficient state in erythropoietic tissues in -Cu mice rather than from differences in ceruloplasmin activity.
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PMID:Changes in tissue growth, concentrations of copper, iron, cytochrome oxidase and superoxide dismutase subsequent to dietary or genetic copper deficiency in mice. 631

We report a child with the presentation of Wilson's disease as acute fulminant hepatic failure and severe hemolysis. Our review of the literature suggests the following criteria for considering this diagnosis in the child with acute liver failure: discordance between mildly elevated serum transaminases and extremely elevated bilirubin levels; anemia associated with hemolysis (increased reticulocytes in the absence of bleeding); elevated hepatic copper; and other copper metabolic abnormalities (elevated serum copper, excessive 24-hour urine copper excretion, and reduced serum ceruloplasmin). Establishing the correct diagnosis enhances the possibility of detecting asymptomatic siblings or other family members in whom early inauguration preventive therapy should be successful.
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PMID:Fatal fulminant hepatitis with hemolysis in Wilson's disease. Criteria for diagnosis. 648 63


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