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

Administration of oral ferrous salts is the preferred method of treatment for anemia due to iron deficiency. However, in certain clinical situations, the response to oral therapy may be suboptimal. Parenteral iron therapy is effective in these instances and may produce a faster response than the oral route.Of 30 patients treated by total dose intravenous infusion of iron-dextran, a prompt reticulocytosis occurred in all patients except one case associated with systemic lupus erythematosus. Hematologic improvement in this case followed remission of the systemic lupus erythematosus. Hematologic response was complete in 18 patients in five to nine weeks, but could not be evaluated in 11 cases because of recurrent bleeding. There were two adverse reactions: generalized pruritus after injection in one patient, and superficial thrombophlebitis at the injection site of another.The response to therapy in iron deficient anemia is dependent on bone marrow capacity, the severity of the anemia, and the availability of iron. Response was fastest in those who had been severely anemic for prolonged periods of time. Total dose infusion with iron-dextran is a safe and effective treatment for iron deficient anemia in selected cases. Initial response appears to be faster than that on oral therapy with the exception of those with a mild degree of anemia.
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PMID:Intravenous iron-dextran in the treatment of iron deficient anemia. 52 11

Iron deficiency is the most frequent cause of anemia. The correct diagnosis is based on history, peripheral blood findings and investigations of the iron status. Anemia occurs only when iron stores are empty. Iron deficiency anemia is a microcytic, hypochromic anemia. Red blood cells show poikilo- and anisocytosis with predominance of small erythrocytes. In one third of the patients the anemia is accompanied by slight leukopenia. The platelet counts may be normal, increased or decreased. Iron deficiency is documented by decreased serum iron, increased transferrin and decreased iron saturation. Ferritin below 15 ng/ml confirms the depletion of iron. Once the diagnosis of iron deficiency is established, its cause must be investigated. Pregnancy and bleeding are the most frequent conditions leading to iron deficiency. Therapy of iron deficiency involves treatment of the underlying condition as well as reestablishment of iron stores. Oral therapy is the most safe and economical method of correcting iron deficiency. Parenteral therapy should be confined to exceptional situations.
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PMID:[Iron-deficiency anemia: diagnosis and therapy]. 156 14

Iron deficiency frequently complicates both acute and chronic phases of recombinant human erythropoietin (r-HuEPO; EPOGEN [epoetin alfa], AMGEN Inc, Thousand Oaks, CA) therapy for dialysis-associated anemia. During acute correction of anemia, iron needed for new hemoglobin production may outstrip available body iron stores. During maintenance r-HuEPO therapy, blood lost both through the dialysis process and the uremic predisposition to gastrointestinal bleeding promotes ongoing negative iron balance. Failure to recognize and treat iron deficiency may lead to impaired efficacy of r-HuEPO in the anemic patient by converting the anemia associated with chronic renal failure to the anemia associated with iron deficiency. The risk of iron deficiency is assessed by weighing available iron stores, as reflected by the level of serum ferritin, against anticipated iron needs for new hemoglobin synthesis, as measured by the difference between the current and target hemoglobin. Using this approach, body iron reserves can be determined, iron deficits predicted, and appropriate iron replacement therapy planned. Once patients are identified as being at risk for iron deficiency, they are treated prophylactically with oral iron supplements. Parenteral iron therapy is reserved for those at greatest risk for iron deficiency during acute r-HuEPO treatment and those intolerant or unresponsive to oral iron supplements during chronic r-HuEPO treatment. Although no dose-response relationship has been observed in the restoration of iron balance with oral iron supplements, those taking supplements show distinctly higher projected iron stores and daily iron balance than those not given supplements.
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PMID:Iron deficiency in patients with dialysis-associated anemia during erythropoietin replacement therapy: strategies for assessment and management. 266 82

Parenteral iron, in the form of intramuscular injection or intravenous infusion of iron dextran, is commonly used to treat iron deficiency. Constitutional symptoms, anaphylaxis, and rarely death are risks associated with the use of iron dextran for this purpose. However, iron supplementation of TPN solutions to meet daily requirements can be accomplished safely. We propose that iron dextran added to TPN is well tolerated by patients because the amounts employed are small and the infusion times are long. To illustrate, we present a case where rapid administration of parenteral iron was associated with allergic type symptoms. Inclusion of daily requirements of iron in the TPN solution prior to and subsequent to this reaction did not elicit symptoms.
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PMID:Safety of iron dextran in total parenteral nutrition: a case report. 312 81

Low serum iron concentration is not rare in chronic hemodialysis patients. Therefore it is important to differentiate true iron deficiency from reactive low serum iron concentration. We have evaluated the utility of determining serum ferritin concentration to differentiate iron deficiency in chronic hemodialysis patients with persistent low serum iron concentration. Parenteral iron therapy (40 mg/week, group 1, n = 12) for 3 months caused a 3.0% increase in hematocrit level compared to a group 2 (n = 12; p less than 0.05). Serum ferritin concentration in logarithmic scale was significantly correlated with serum iron concentration (r = 0.671; p less than 0.05). The change in hematocrit level was significantly correlated with that in serum iron concentration (r = 0.648; p less than 0.05), but not with the change in serum ferritin concentration. Persistent low serum iron concentration may be an indication for iron supplement even though the serum ferritin concentrations are in the normal range.
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PMID:An evaluation of serum ferritin determination in chronic hemodialysis patients with persistent low serum iron concentration. 317 63

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

Recombinant human erythropoietin (rHuEpo) has been associated with clinical and symptomatic improvements as well as improvements in quality of life in patients with anemia of chronic renal failure. However, resistance to rHuEpo therapy, related to insufficient iron stores, occurs often. Although many patients treated with rHuEpo take oral iron, patients continue to develop iron deficiency. Parenteral iron is a safe and effective alternative in replacing iron stores to sustain erythropoiesis in patients treated with rHuEpo.
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PMID:Current perspectives: iron management during therapy with recombinant human erythropoietin. 826 8

Iron is an essential trace element, and iron deficiency is common. Underlying causes must be carefully investigated (occult bleeding, carcinoma). Mild forms of iron deficiency may be due to rapid growth, an inappropriate diet, menstrual bleeding or pregnancy. As a rule, they can be corrected by dietary means. Pharmacological doses of iron may irritate the intestinal mucosa, limiting the size of the individual dose and impairing compliance. Overdosing can be fatal. The duration of medication depends upon the rapidity with which deficient hemoglobin iron and iron stores can be replenished. Failure of treatment may be due to a wrong diagnosis, persistent bleeding or disturbed absorption. Parenteral administration of iron should be reserved for patients in whom oral iron replacement fails.
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PMID:[Therapy of iron deficiency. Diagnostic prerequisites--therapeutic procedures]. 840 70

Iron deficiency is the most common nutritional problem worldwide, especially in the developing countries. Oral iron supplementation programs have failed because of noncompliance and gastrointestinal toxicity, thereby necessitating parenteral administration of iron. For parenteral administration, only iron-carbohydrate complexes are currently used, because monomeric iron salts release free iron, thereby causing oxidant injury. However, iron-carbohydrate complexes also have significant toxicity, and they are expensive. We have proposed the hypothesis that monomeric iron salts can be safely administered by the parenteral route if iron is tightly complexed to the ligand, thereby causing clinically insignificant release of free iron, and the kinetic properties of the compound allow rapid transfer of iron to plasma transferrin. A detailed analysis of the physicochemical and kinetic properties reveals that ferric iron complexed to pyrophosphate or acetohydroxamate anions may be suitable for parenteral administration. We have demonstrated that infusion of ferric pyrophosphate into the circulation via the dialysate is safe and effective in maintaining iron balance in patients undergoing maintenance hemodialysis. Parenteral administration of monomeric iron compounds is a promising approach to the treatment of iron deficiency in the general population and merits further investigation.
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PMID:Treatment of iron deficiency anemia: are monomeric iron compounds suitable for parenteral administration? 1107 64

Iron-deficiency anemia impairs growth and intellectual development in children, which can be reversed only by early diagnosis and iron supplementation. Oral supplementation can efficiently replace stores, but in many cases parenteral iron is needed. Unfortunately some adverse reactions have limited its use in children. We compared the efficacy and safety of intramuscular and intravenous administration in 33 evaluable children with severe iron deficiency and/or iron-deficiency anemia who failed to respond to oral iron supplementation. Nineteen children received intravenous infusion and 14 intramuscular injections. All children showed recovery from iron-deficiency anemia, with statistically similar improvement in hemoglobin levels. The duration of treatment was longer in those receiving intramuscular injection. Parenteral iron therapy for the treatment of iron-deficiency anemia is a rapid, easy, and definitive solution to a long-troubling situation. We suggest the use of parenteral iron, in particular intravenous iron, in children who do not recover from severe iron-deficiency anemia after oral therapy. We should consider the physical and neuropsychological sequelae of long-lasting iron deficiency in children and the fact that oral supplementation is less likely to replace iron stores.
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PMID:Parenteral iron supplementation for the treatment of iron deficiency anemia in children. 1190 41


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