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Query: UMLS:C0162316 (iron deficiency anemia)
3,806 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Present investigation was undertaken to elucidate the significance of changes in erythrocyte zinc levels in anemia. A preliminary study for the determination of erythrocyte zinc by atomic absorption spectrophotometry was done. The simple dilution method, in which zinc was determined directly from a sample of erythrocyte lysed and diluted with deionized water, appeared satisfactory in view of its rapidity, simplicity and accuracy. Of importance is that the temperature of sample and standard solution had to be matched. By using the above method, the mode of changes in erythrocyte zinc levels was investigated in healthy individuals and it was found that erythrocyte zinc expressed per gram of hemoglobin was inversely correlated to mean corpuscular hemoglobin concentration (MCHC). This relationship was also shown in patients with iron deficiency anemia and phlebotomy-induced anemia in rabbits. However, erythrocyte zinc expressed per milliliter of packed red cells was generally increased in these cases. The difference of erythrocyte zinc levels between 9:00 a.m. and 3:00 p.m. was not statistically significant. In addition, the levels of the B and of the C type erythrocyte carbonic anhydrases were assayed immunochemically. It was ascertained that there was a significant correlation between erythrocyte zinc levels and those of total carbonic anhydrase. This, the clinical importance of changes in erythrocyte zinc levels in anemia was discussed in relation to the role of this zinc - metalloenzyme.
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PMID:[Determination of erythrocyte zinc by atomic absorption spectrophotometry: Its significance in iron deficiency anemia (author's transl)]. 82 Jun 20

Normal red blood cells, preincubated for 75 min with 1.15 mM menadione sodium bisulfite lose potassium and water on subsequent incubation at 37 degrees C for 24 h without menadione. The potassium loss is increased by addition of calcium and prevented by addition of glucose. Since normal red cells treated with menadione behave like untreated hypochromic cells, both from beta-thalassaemia or iron deficiency anaemia in respect to membrane permeability to potassium, it may be supposed that menadione induces in normal red cells an abnormality similar to that naturally occurring in hypochromic cells.
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PMID:Increased potassium permeability induced in vitro by menadione in normal human red cells. 84 Dec 69

Patients with Hb SC disease were found to have microcytic and hyperchromic red cell indices despite mild reticulocytosis. Iron deficiency anemia was ruled out by the finding of normal serum ferritin levels. In order to determine whether the microcytosis was due to coexistent alpha-thalassemia, restriction endonuclease mapping was performed on genomic DNA extracted from peripheral blood leukocytes. Patients with Hb SC disease had microcytic indices despite the presence of a full complement of four alpha-genes (alpha alpha/alpha alpha), suggesting that the microcytosis may be due to cellular dehydration (or xerocytosis), since the mean corpuscular hemoglobin concentration in Hb SC disease patients was significantly higher than in controls. This possibility was investigated further by the determination of RBC cation content. RBC Na levels were similar in SC and normal red cells. Hb SC RBCs, however, had significantly reduced K levels. These findings show that RBC cation content, and thus cell water, is decreased in Hb SC disease. The decreased RBC K level in the presence of normal cellular Na concentration suggests selective K loss that is not due to inhibition of the Na K pump. Ouabain-insensitive K+ efflux was increased to four times normal in SC cells. Cell dehydration was confirmed by the demonstration of increased high-density RBCs on discontinuous Stractan density gradients and by osmotic gradient ektacytometry. Cellular dehydration and its sequelae were worse in CC erythrocytes and milder in AC cells than in Hb SC red cells. Taken together, these data indicate that in Hb SC disease the RBCs are severely dehydrated and typically microcytic and hyperchromic. Hb SC RBCs seem to be dehydrated due to selective K loss. These findings suggest a functional interrelationship between Hb SC, the red cell membrane, and cation regulation.
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PMID:The xerocytosis of Hb SC disease. 294 42

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

The major diseases of iron metabolism are iron deficiency anaemia, which could be treated using Fe2+ or Fe3+ salt supplements, and iron overload, which could arise either from an increased gastrointestinal absorption of iron or from recurrent blood transfusions. While the former form of iron overload could be treated by phlebotomy the latter requires the use of a chelator. Desferrioxamine is the only clinically available chelator for the treatment of iron overload but its use worldwide is limited because it is expensive and orally inactive. Several alpha-ketohydroxy heteroaromatic chelators have been synthesised and tested for their iron binding properties at physiological pH. The synthetic route involves the benzylation of the hydroxyl group of maltol using benzyl chloride, the conversion of the benzylated maltol to the 1-alkyl benzylated pyridine derivative by introducing the corresponding alkylamine in alkaline conditions and the cleavage of the benzyl group in acid to form the 1-alkyl-2-methyl-3-hydroxypyrid-4-one. All the chelators are water soluble and stable at a wide range of pH, forming stable, water soluble, coloured iron complexes with a molar ratio of approximately 3 chelator: 1 iron at pH 7.4 and lower molar ratio of chelators to iron complexes at acidic pH. When the 1-methyl, 1-ethyl and 1-propyl, -2-methyl-3-hydroxypyrid-4-ones were mixed at pH 7.4 with transferrin, ferritin and haemosiderin substantial amounts of iron were released.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:New synthetic approach and iron chelating studies of 1-alkyl-2-methyl-3-hydroxypyrid-4-ones. 343 80

A maize-based iron- and protein-deficient diet is commonly cited as the most important cause of porotic hyperostosis among American Indian agriculturalists. An alternative to this maize dependence hypothesis is suggested by the analysis of 432 crania from the nonagricultural, fish-dependent population of the Channel Island area of southern California. Cribra orbitalia, a form of porotic hyperostosis associated with iron deficiency anemia, is just as common among these fisherpeople, whose diet was rich in iron and essential amino acids, as it is among maize-dependent agriculturalists. Northern Channel Island crania have much more cribra orbitalia than those from the California mainland. The highest incidence is on San Miguel, a small geographically isolated island with a shortage of fresh water and terrestrial resources. The Indians who lived on Santa Cruz, the largest of the northern Channel Islands with the greatest diversity of terrestrial plants and animals, have less cribra orbitalia than those who lived on Santa Rosa or San Miguel Island. This geographical distribution appears to be explained by island-mainland and interisland differences in water contamination, exposure to fish-borne parasites, and nutritional adequacy of the diet. The prevalence of porotic hyperostosis in a population with a heavy dietary dependence on marine resources shows that among prehistoric American Indians, this condition is not always associated with an iron- and protein-deficient diet of cultigens. It seems likely that high nutrient losses associated with diarrheal disease are often more significant in the etiology of porotic hyperostosis than a low dietary intake of essential nutrients.
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PMID:Porotic hyperostosis in a marine-dependent California Indian population. 351 81

The results of a zinc-protoporphyrin (ZPP) screening in 1983 among first-grade schoolchildren in Hospitalet de Llobregat (Catalonia, Spain) are presented. Tap water in this industrial city comes from the Llobregat river and is extremely hard, with an excessive level of salts. At this time, Spanish gasoline had high levels of lead. The purpose of the study was to evaluate the effect of environmental pollution on subclinical lead poisoning. These were 428 children in the study, 67% of those eligible. Causes for non participation were being absent from school on the screening day or lack of parental consent for participation in the study. Only in two children levels of ZPP above 40 theta g/100 ml were found; both cases had iron deficiency anemia with low blood lead levels. Mean ZPP levels were somewhat higher in the Collblanc district, which suffers higher air pollution from street traffic, and in children living in houses built before 1940. The relevance and implications of these findings are discussed.
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PMID:[Lead poisoning in the school-aged child: results of a screening program using zinc protoporphyrin]. 366 52

In the bone-marrow, non-haemoglobin iron can predominantly be found in the reticulum. Slight granules containing iron can also be observed in parts of erythroblasts by means of the Berlin blue reaction. These cells are called sideroblasts. In chemical respect, non-haemoglobin iron consists of ferritin soluble in water and haemosiderin insoluble in water. Erythroblasts will only take their iron from plasma transferrin. For the most part, this iron uptake is being regulated by erythropoietin adapting erythropoiesis to the oxygen requirements of the tissue. The iron contained in erythroblasts is predominantly utilized for haemoglobin synthesis in these cells. A slight part is being taken up by ferritin. The bone-marrow reticulum will phagocytise aged erythrocytes and store liberated iron as ferritin and haemosiderin. Part of the iron is being delivered again to plasma transferrin. With constant serum iron level the liberation of iron from the reticulo-endothelial tissue must correspond to the iron uptake by erythropoiesis. The absence of iron capable of being coloured in the bone-marrow reticulum is considered to be a reliable parameter of iron deficiency. It enables the diagnosis of iron deficiency anaemia to be made even in those patients with serum iron level and a total iron binding capacity lying within the normal range and no hypochromia of erythrocytes being present. It enables iron deficiency anaemia to be separated from sideropenic anaemia with reticulo-endothelial siderosis in differential-diagnostic manner. Even in patients with sideroblastic anaemia, iron colouring of bone-marrow smears is required for ensuring the diagnosis. Recently, a separation has also been made for idiopathic anaemia with abnormal sideroblasts. In these patients there is an increased risk for acute leukemia to develop.
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PMID:[Iron in bone marrow]. 618 56

In a series of pregnant women with iron deficiency anaemia treated by a total dose infusion of iron dextran, the non-haem iron content of the placenta at term was studied histochemically and by chemical analysis. Within a few days of the infusion the Prussian blue reaction on the placenta was very strong, but was negative by ten days after the infusion. Chemical analysis showed that both the water-insoluble fraction (haemosiderin) and the water-soluble fraction (ferritin) of the non-haem iron were increased soon after the infusion, but three weeks after the infusion they were almost the same as in untreated controls. Pinocytosis of iron dextran by the trophoblast and increased transport of transferrin-bound iron to the placenta are considered as possible causes for this large uptake of iron by the placenta.
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PMID:Effect of total dose infusion of iron dextran on the storage iron content of the human placenta. 708 94

Micronutrient malnutrition, particularly vitamin A deficiency (VAD), iron deficiency anaemia (IDA) and iodine deficiency disorders (IDD), poses a serious threat to the health of vulnerable segments of population. Dietary Inadequacy is the primary cause of VAD and IDA, while poor iodine content of soil and water due to environmental iodine deficiency is the main determinant of IDD. Three major intervention strategies are available for the control of micronutrient malnutrition: supplementation of the specific micronutrients; fortification of foods with micronutrients; and horticulture intervention to increase production and nutrition education to ensure regular consumption of micronutrient rich foods. In India currently the national nutrition programmes being implemented for preventing these deficiencies are based on short term supplementation like periodic mega dosing of vitamin A, distribution of iron and folic acid tablets, and salt iodisation. Though these have been in operation for over two decades, there has been no perceptible biological impact on the prevalence of micronutrient malnutrition. Among the constraints, the most important are: lack of coordination, shortage of resources and manpower, inadequate and irregular supplies, lack of proper orientation and training to the functionaries, poor monitoring and supervision and absence of nutrition education. Integrated and multi-sectoral approaches are required to achieve the goals set under the National Nutrition Policy. These should include community-friendly nutrition education to increase awareness and motivation; active people's participation; food fortification; nutrient supplementation; nutrition oriented horticulture programmes; orientation of functionaries, and establishment of integrated micronutrient surveillance. Concerted and focussed efforts are needed to combat micronutrient malnutrition by the 2000 AD.
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PMID:Strategies for control of micronutrient malnutrition. 867 41


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