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)

Nickel toxicity was studied in young chicks fed a semi-purified diet. Dietary nickel concentrations of 300 mg/kg and higher resulted in significant reduction in growth rate. Mortality and anemia were observed in chicks receiving 1100 mg/kg nickel. Dietary nickel content of 300 mg/kg resulted in a significant increase in kidney nickel content while higher dietary levels were required to affect the nickel content of other body tissues. Supplementation of nickel toxic diets (500 mg/kg) with 100 mg/kg of cobalt, iron, copper, and zinc did not alleviate the symptoms of nickel toxicity or consistently affect tissue nickel accumulation. The addition of cobalt resulted in a further depression in growth rate when added to the nickel toxic diet. However, subsequent studies showed that this was due to the toxicity of cobalt and no evidence was found for an interaction between these two elements. The lack of interaction of nickel with copper, iron, and zinc is in contrast to the results observed by other investigators at low dietary concentrations of nickel.
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PMID:Studies on nickel metabolism: interaction with other mineral elements. 51 46

The effect of oral cobalt chloride on the anaemia of patients undergoing long-term haemodialysis therapy was investigated in 14 patients taking 25 mg then 50 mg daily. After eight weeks of treatment the mean haematocrit increase in 11 patients completing the trial was 23% of the original level and the 51Cr-red cell volume had increased by 20%. The 51Cr red half-life lengthened after treatment in six patients and the 59Fe plasma half-time shortened in ten patients. After treatment, evidence of increased erythropoietic activity was seen in the bone marrow of five patients. No evidence was found of thyroid of liver dysfunction but three patients developed transient loss of hearing demonstrated by audiometry. Cobalt chloride appears to be helpful in the management of some uraemic patients with refractory anaemia.
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PMID:Cobalt chloride in the treatment of refractory anaemia in patients undergoing long-term haemodialysis. 81 Jan 27

Hyperlipaemia persisted for more than 12 months in rats treated with cobalt chloride, 9 of 20 treated rats and 1 control rat died within the first year, and 8 of the surviving animals developed fibrosarcomas--in 4 of these the tumour was far removed from the injection sites. The results are discussed with reference to the use of cobalt chloride treatment for anaemia in patients with chronic renal failure.
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PMID:Fibrosarcomas induced by cobalt chloride (CoCl2) in rats. 83 22

Tick borne fever is considered to have played a major role in a complex disease syndrome involving mucosal disease and cobalt deficiency in a group of young calves reared on an upland farm in South West Scotland. Anaemia, illthrift, coat colour changes and scour were the main clinical signs.
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PMID:Tick borne fever in association with mucosal disease and cobalt deficiency in calves. 88 11

Twelve anephric patients on maintenance haemodialysis received treatment with oral enteric coated cobalt chloride 25 to 50 mg daily. The change in haemoglobin concentration, and packed cell volume, are recorded and discussed with special reference to possible toxicity and mechanism of action of cobalt. Six of eight patients who completed the first course with cobalt chloride 50 mg daily for 12 weeks showed a significant rise in haemoglobin concentration of 26 to 70 per cent and a fall to near pre-therapeutic levels when cobalt was withdrawn. Evidence of a response was present within two months of starting treatment. Four patients showed a diminution in their blood transfusion requirements and three patients experienced a definite sense of increased well-being during treatment. One patient suffered from side effects of the drug and failed to complete the study because of gastrointestinal disturbance. The improvment in haemoglobin concentration was reproducible in four patients who were given second, and in one case third courses courses with varying doses of cobalt over differing periods of time. Serum cobalt levels tended to stabilize after two months continuous treatment to the therapeutic range of 40-100 mumg per 100 ml. A rapid fall in serum cobalt was seen on cessation of treatment. It is suggested that therapy with enteric coated cobalt chloride at a dose of between 25 and 50 mg per day has a definite place in the treatment of the refractory anaemia of chronic renal failure.
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PMID:The treatment of refractory anaemia of chronic renal failure with cobalt chloride. 94 Sep 22

Cobalt deficiency was produced in goats by feeding them rhode grass hay. The deficient animals excreted increased amounts of methyl malonic acid in their urine, indicating a lack of vitamin B12. Erythrocyte reduced glutathione levels increased with the onset of anemia. There was a concomitant increase in the levels of erythrocyte glutathione reductase (GSSG NADPH Reductase) and glutathione peroxidase (GSH:H2O2 peroxidase)during deficiency. These results are compared with similar observations reported for vitamin B12 deficiency in humans.
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PMID:Erythrocyte glutathione metabolism in cobalt-deficient goats. 103 28

A cobalt excretion test was performed in 50 patients with various, mainly hematologic, disorders and was found to be an accurate and easily obtainable index of iron absorption. The test was found to be of very limited value in predicting iron stores. The cobalt excretion test may have some usefulness as a simple, apparently safe, noninvasive test for identification of persons with iron depletion resulting from uncomplicated blood loss. However, in more complex circumstances, it fails to differentiate iron deficiency anemia from anemia due to other causes.
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PMID:Cobalt excretion test as index of iron absorption and diagnostic test for iron deficiency. 111 13

The defect in iron (Fe) absorption in X linked anaemia (sla) remains an enigma; absorption of a tracer dose of Fe is impaired in mice raised on an iron-containing cube diet but not in those raised on an iron-deficient diet. Because cobalt (Co) shares a similar intestinal transport pathway with Fe, a study was made of the effect of iron deficient diet on Co absorption. The duodenum of sla and genetically normal mice was perfused for 30 min with labelled solutions containing Co or Fe. Co uptake and transfer were similar in sla and normals fed cubes whereas Fe uptake and transfer were less in sla than in normals. The iron deficient diet caused an increase in the uptake and transfer of Co and Fe in sla and normals. When Co and Fe were perfused together in sla fed deficient diet, the uptake and transfer of each metal was less than when performed alone. The distribution of Fe and Co in subcellular mucosal fractions was determined by a differential centrifugation technique. Deficient diet resulted in a directionally similar change in the subcellular distribution of Co and Fe in sla and normals. The increase in Co as well as Fe absorption in the sla on an iron deficient diet to the same high level found in genetically normal animals, and the inhibitory effect of each metal on the absorption of the other suggests that the absorption defect in sla is unlikely to be due to a primary defect in the function of the transport carrier.
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PMID:Integrity of the iron transport process in mice with X-linked anaemia. 121 31

The myocardial cobalt concentration in a patient who died 3 months after treatment with cobalt was 25-80 times greater than the concentration in control samples. Blood cobalt concentrations in maintenance hemodialysis patients who had been treated 13-20 months previously with cobaltous chloride were significantly higher than those in maintenance hemodialysis patients who had not received cobalt. Prospective studies of blood cobalt concentrations in maintenance hemodialysis patients and normal subjects after the administration of cobaltous chloride were carried out. It was found that prolonged elevation of blood cobalt concentrations occurred in both normals and maintenance hemodialysis patients, but that the blood cobalt concentrations were much higher in the dialysis patients. The urinary excretion of cobalt following the administration of a single dose of cobaltous chloride was studied in two normal subjects. Cobalt metabolism and toxicity are discussed. In view of the limited therapeutic gains to be expected and because of the lack of information regarding the long term significance of elevated blood cobalt concentrations, it is concluded that cobalt should not be used in the treatment of the anemia of patients with sever renal failure.
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PMID:Possible cobalt toxicity in maintenance hemodialysis patients after treatment with cobaltous chloride: a study of blood and tissue cobalt concentrations in normal subjects and patients with terminal and renal failure. 125 58

Erythropoietin (EPO) is the primary humoral regulator of mammalian erythropoiesis. The single-copy EPO gene is normally expressed in liver and kidney, and increased transcription is induced by anemia or cobalt chloride administration. To identify cis-acting DNA sequences responsible for regulated expression, transgenic mice were generated by microinjection of a 4-kilobase-pair (kb) (tgEPO4) or 10-kb (tgEPO10) cloned DNA fragment containing the human EPO gene, 0.7 kb of 3'-flanking sequence, and either 0.4 or 6 kb of 5'-flanking sequence, respectively. tgEPO4 mice expressed the transgene in liver, where expression was inducible by anemia or cobalt chloride, kidney, where expression was not inducible, and other tissues that do not normally express EPO. Human EPO RNA in tgEPO10 mice was detected only in liver of anemic or cobalt-treated mice. Both tgEPO4 and tgEPO10 mice were polycythemic, demonstrating that the human EPO RNA transcribed in liver is functional. These results suggest that (i) a liver inducibility element maps within 4 kb encompassing the gene, 0.4 kb of 5'-flanking sequence, and 0.7 kb of 3'-flanking sequence; (ii) a negative regulatory element is located between 0.4 and 6 kb 5' to the gene; and (iii) sequences required for inducible kidney expression are located greater than 6 kb 5' or 0.7 kb 3' to the gene. RNase protection analysis revealed that human EPO RNA in anemic transgenic mouse liver and hypoxic human hepatoma cells is initiated from several sites, only a subset of which is utilized in nonanemic transgenic liver and human fetal liver.
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PMID:Human erythropoietin gene expression in transgenic mice: multiple transcription initiation sites and cis-acting regulatory elements. 230 68


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