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

Lead, cadmium, and mercury are toxic metals that are not essential for nutrition. However, the toxic effects of these metals may be mediated or enhanced by interactions or deficiencies of nutritionally essential metals. Lead competes with calcium, inhibiting the release of neurotransmitters, and interferes with the regulation of cell metabolism by binding to second-messenger calcium receptors, blocking calcium transport by calcium channels and calcium-sodium ATP pumps, and by competing for calcium-binding protein sites and uptake by mitochondria. Dietary deficiencies of calcium, iron, and zinc enhance the effects of lead on cognitive and behavioral development. Iron deficiency increases the gastrointestinal absorption of cadmium, and cadmium competes with zinc for binding sites on metallothionein, which is important in the storage and transport of zinc during development. Selenium protects from mercury and methyl mercury toxicity by preventing damage from free radicals or by forming inactive selenium mercury complexes.
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PMID:Nutrition and metal toxicity. 787 32

Exposure of rats to high dietary levels of sodium saccharin (NaSac) started in utero produce physiological effects at 30 days post-birth that are similar to those found in pups of iron-deficient dams. These similarities suggest that some of the changes due to NaSac are secondary to iron deficiency. The present experiment investigated whether the effects of 7.5% dietary NaSac in the newborn rat could be prevented by dietary iron and/or folate supplementation. The NaSac-related effects prevented by iron supplementation included anaemia, decreased serum iron and folate, increased serum cholesterol and triglyceride and increased serum vitamin E. Folate supplementation prevented NaSac-induced depression of serum folate and increase in serum vitamin E. Although bladder hyperplasia was increased by dietary iron and/or folate supplementation, the majority of the urinary chemistry changes associated with NaSac treatment were not affected. The results show that some physiological changes associated with NaSac treatment in the newborn rat may occur as a consequence of iron deficiency rather than a direct effect of NaSac treatment. These changes may be independent of the urinary and bladder effects, which are not reversed by iron supplementation.
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PMID:Effects of dietary iron and folate supplementation on the physiological changes produced in weanling rats by sodium saccharin exposure. 822 26

We studied the mechanism of erythropoietin (EPO)-induced hypertension (HTN) in rats with chronic renal failure (CRF). After partial nephrectomy, rats were randomized into four groups. Group A received EPO, 150 U/kg, two times weekly for 6 wk to prevent anemia; group B received placebo injections and became anemic; group C received EPO but was kept anemic by dietary iron deficiency; and group D received placebo and regular transfusions to match hematocrit (Hct) in group A. Blood pressure (BP), Hct, platelet cytosolic calcium ([Ca2+]i) and magnesium concentration, and pressor and vasodilatory responses were determined. By design, Hct in groups A and D were comparable and significantly greater (P < 0.01) than in groups B and C. Despite divergent Hct values, the EPO-treated groups A and C showed a significant rise in BP compared with the placebo-treated groups B and D. HTN occurred whether EPO therapy was begun immediately or 4 wk after nephrectomy. EPO therapy augmented the elevation of basal [Ca2+]i and restored the defective thrombin-mediated rise of platelet [Ca2+]i in CRF animals. EPO therapy did not alter caudal artery contraction in response to either 68 mM K(+)-induced depolarization, angiotensin II or alpha 1-agonist, methoxamine in vitro, or the pressor response to angiotensin II in vivo. However, EPO therapy impaired the hypotensive response to nitric oxide (NO) donors, sodium nitroprusside and S-nitroso-N-acetyl-D,L-penicillamine, and reversed the CRF-induced upregulation of guanosine 3',5'-cyclic monophosphate production by thoracic aorta in vitro. Thus EPO-induced HTN in CRF rats is Hct independent and is associated with and perhaps causally related to increased basal and stimulated [Ca2+]i and impaired vasodilatory response to NO.
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PMID:Role of nitric oxide resistance in erythropoietin-induced hypertension in rats with chronic renal failure. 876 88

During iron deficiency rat and human erythrocyte membrane enzyme activities (Total ATPase and Ouabainsensitive Na+.K+ ATPase) showed significant (P < 0.001) decrease. The influence of iron deficiency on erythrocyte Na+ and K+ was also studied in rats and humans. The former parameter showed a significant (P < 0.01) increase while the latter showed a downward trend. Plasma Fe and Total Iron Binding capacity (TIBC) in iron deficiency varied significantly (P < 0.05) from normal values. These results suggest a defect in erythrocyte membrane function and a possible potentiating effect of intracellular Na+, plasma Fe and TIBC on ATPase activity in iron deficiency. Values obtained for rats and humans showed differences in the activities of membrane ATPase in iron deficiency anaemia.
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PMID:Abnormalities in adenosine triphosphatase of the erythrocyte membrane in iron deficiency anaemia. 890 64

The effect of physical exercise and vitamin C on iron absorption after oral iron administration was investigated. Eight healthy male subjects without iron deficiency were studied after administration of 100 mg ferric sodium citrate complex, 100 mg ferric sodium citrate complex with 200 mg ascorbic acid, and without iron intake, both under resting conditions and after a 1-h bicycle ergometer test at moderate exercise. Serum concentrations for iron, transferrin, and ferritin were measured before and 30 min, and 1, 2, and 4 h after each administration. Under resting conditions administration of 100 mg ferric sodium citrate led to a significant increase in serum iron concentrations. When ferric sodium citrate was administered with vitamin C, iron values increased significantly further. Ingestion of iron together with physical exercise resulted in a higher serum iron concentration than under resting conditions. The maximum increase, reached after 4 h, was 48.2% with exercise and 8.3% without. In combination with exercise, the addition of 200 mg vitamin C did not further increase serum iron concentration. In conclusion, 1 h of moderate exercise enhanced the rate of iron absorption. Under resting conditions the combination of ferric sodium citrate with vitamin C led to significantly increased postabsorption serum iron concentrations compared with iron administration without vitamin C.
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PMID:Effect of physical exercise and vitamin C on absorption of ferric sodium citrate. 897 Jan 40

Separate or joint ingestions of water solutions of sodium nitrite and/or N-diethylamine by rats fed iron deficiency diet caused sharp increasing of N-nitrosodiethylamine level in stomach, a decreasing of Hb and increasing of MetHb concentrations in blood of animal. These effects were greater on iron deficient diet than on control diet. The nitrite ingestion caused a decline level of cytochrome P-450 and inhibition of lipid peroxidation in rat liver.
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PMID:[Effects of iron deficiency on toxic action of nitrites and endogenous synthesis of N-nitrosamines]. 912 17

Use of recombinant human erythropoietin in patients with end-stage renal disease has highlighted iron deficiency as the major cause of resistant anemia. The current mainstay of intravenous (i.v.) iron replacement therapy, iron dextran, has been shown in prior studies to have a risk of serious life-threatening anaphylaxis of just under 1 per 100 patients exposed. The current study assessed the safety profile of an alternative i.v. iron, sodium ferric gluconate complex in sucrose (Ferrlecit), as compared with iron dextrans. Sodium ferric gluconate complex in sucrose, a unique chemical preparation, has been in use since 1959, principally in Europe, at a rate of approximately 2.7 million i.v. doses per year (1992 to 1996) in Germany and Italy alone. For iron dextran, usage in the United States was comparable--principally renal hemodialysis--and estimated from market sources at 3.0 million doses per year (1995). From 1976 to 1996, there were 74 allergic adverse events reported for sodium ferric gluconate complex in sucrose to the World Health Organization (WHO), German Health Bureau, and the manufacturer (all combined). For the years 1992 to 1996, sodium ferric gluconate complex in sucrose had an allergy event reporting rate of 3.3 allergy episodes per million doses per year compared with a similar rate of 8.7 reported allergy events per million doses per year for iron dextran in the United States in 1995. Case fatalities for sodium ferric gluconate complex in sucrose and iron dextran within these reports were then compared. For sodium ferric gluconate complex in sucrose, there were no reports of deaths over the entire period (1976 to 1996). However, for iron dextrans, there were 31 fatalities among 196 allergy/anaphylaxis cases reported in the United States between 1976 and 1996, yielding a case-fatality rate of 15.8%. These data show that sodium ferric gluconate complex in sucrose, when compared with iron dextrans in comparably sized patient usage populations with similar total rates of reporting of allergic events, has a significantly lower reported mortality rate (P < 0.001). Thus, the data justify usage of sodium ferric gluconate complex in sucrose as the safer iron replacement therapeutic agent.
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PMID:Sodium ferric gluconate complex in sucrose: safer intravenous iron therapy than iron dextrans. 1007 Sep 26

Iron supplementation has become an integral part of the management of patients receiving epoetin therapy, and clinicians have found it necessary to learn how and when to use it to the best advantage. Three routes of administration for iron are available: oral, intramuscular, and intravenous. Oral iron has the advantage of being simple and cheap, but it is limited by side-effects, poor compliance, poor absorption, and low efficacy. Intravenous iron is the best means of guaranteeing delivery of readily available iron to the bone marrow, but it requires greater clinical supervision. The i.v. iron preparations vary widely in their degradation kinetics, bioavailability, side-effect profiles, and maximum dose for single administration. Iron dextran is hampered by a small but significant risk of anaphylaxis, whereas all i.v. iron preparations can induce "free iron" reactions if the circulating plasma transferrin is overloaded. Intravenous iron may be given in advance of epoetin therapy, as concomitant treatment to prevent the development of iron deficiency, as treatment of absolute or functional iron deficiency, or as adjuvant therapy to enhance the response to epoetin in iron-replete patients. Markers of iron status that may indicate a need for i.v. iron include a serum ferritin of less than 100 microg/liter, a transferrin saturation of less than 20%, and a percentage of hypochromic red cells more than 10%. Various regimens are available for giving i.v. iron: low-dose administration of 20 to 60 mg every dialysis session in hemodialysis patients, medium-dose administration of 100 to 400 mg, and high-dose administration of 500 to 1000 mg. Iron sodium gluconate can only be given as a low-dose regimen because of toxicity, whereas the only preparation suitable for high-dose administration is iron dextran. Although concerns have been raised regarding iron overload and long-term toxicity with i.v. iron therapy in terms of increased risk of infections, cardiovascular disease, and malignancy, there is little evidence to substantiate this in patients receiving epoetin. Care should be taken, however, to prevent the serum ferritin rising above 800 to 1000 microg/liter and the transferrin saturation above 50%. Provided this is done, the benefits of i.v. iron almost certainly outweigh the risks in terms of optimizing the response to epoetin therapy.
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PMID:Strategies for iron supplementation: oral versus intravenous. 1008 88

Breast-feeding is to be encouraged during the first six months of life. Iron deficiency is extremely rare in exclusively breast-fed infants during this period. Any cow-milk based formula used should be iron-fortified. During the second half of infancy, the iron content of weaning foods is important in preventing iron deficiency. Indeed, owing to the low iron content of dairy products, it is hard to compose a weaning diet sufficiently rich in iron to meet the demands of rapidly growing infants, if it is to include substantial amounts of cow milk, sour milk or yoghurt. Accordingly, the Paediatric Committee on Nutrition and Health, of the Swedish Paediatric Association and the National Food Administration, recommend delaying the introduction of cow's milk and cow-milk products until the infant is 10-12 months of age. Until then, breast-feeding, and the use of iron-fortified formula or gruel with modified protein and sodium content are encouraged; iron-fortified porridges of softer consistency can be prepared to circumvent the need of extra fluids, or porridge can be served with breast milk or iron-fortified formula; small amounts of milk may be used for cooking purposes.
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PMID:[Recommendations for prevention of iron deficiency. Delay cow's milk intake as a beverage to infants until 10-12 months of age!]. 1037 60

Human milk is the preferred feeding for all infants, including premature and sick newborns, with rare exceptions. However, modern technology has produced alternative, "humanized formulae", which closely mimic the composition of human milk. The ingestion of human milk, "humanized formulae" or whole cow's milk has consequences for human nutrition. Gastroesophageal reflux, iron deficiency, calcium and sodium excesses or deficiencies may be influenced by the type and amount of milk fed to the infant. Likewise, neurological development and the likelihood of developing diabetes or cancer may also be influenced by early dietary practices. Until new information is available, we should continue to pattern formulae for older infants after breast milk, but with sufficient protein, calories, lipid and minerals to support optimal growth.
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PMID:Cow's milk versus formula in older infants: consequences for human nutrition. 1056 25


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