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PubMed1976

Intravenous iron-dextran therapy in the treatment of anemia occurring in surgical, gynecologic and obstetric patients.

An infusion of iron-dextran diluted in 1,000 milliliters of physiologic saline solution was given to 51 patients. The average hemoglobin response was 1.9 grams per deciliter per week. Mean corpuscular volume, mean corpuscular hemoglobin concentration and mean corpuscular hemoglobin deficits also were corrected. There were no allergic reactions. This is an extremely reliable and safe method of replenishing depleted iron in patients.

Adolescent↗
PubMed1998

A protocol for administering intravenous iron dextran in peritoneal dialysis patients.

Intravenous (i.v.) iron has been underutilized in the peritoneal dialysis (PD) population due to poor peripheral access and logistical barriers. In PD patients who are intolerant or nonadherent to oral iron, a convenient method of i.v. iron administration is total dose infusion (TDI). This method of administration involves administering the total therapeutic dose of i.v. iron over one to two administrations. This article will review the literature on the use of parenteral iron in PD patients, and will outline West Coast Dialysis Center's successful protocol for TDI of iron dextran in its PD population.

Adult↗
PubMedDate not supplied

Safety and efficacy of total dose iron dextran administration in patients on home renal replacement therapies.

OBJECTIVE: To determine the safety and efficacy of intravenous total dose iron (TDI) replacement in patients treated with home renal replacement therapy. DESIGN: Prospective open-label study on end points in the population studied. SETTING: Institutional outpatient home dialysis program. PATIENTS: The study included 20 end-stage renal disease (ESRD) patients, performing chronic peritoneal or home hemodialysis, with iron deficiency defined as ferritin < 100 ng/mL and/or an iron saturation < 20%. INTERVENTION: The total dose of iron dextran was calculated and infused at a rate not exceeding 6 mg/min. Hemoglobin, hematocrit, iron studies, and liver function tests (LFTs) were obtained before and 3 to 4 weeks after TDI infusion. Hematocrit of patients failing to achieve an increase in Hct over this period was re-examined 2 to 4 weeks later looking for a delayed response. MAIN OUTCOME MEASURES: Primary end points for efficacy were changes in Hct, ferritin, and iron saturation. Toxicity was measured as reported immediate and delayed symptoms and elevated transaminases and/or alkaline phosphatase levels. RESULTS: A median iron dose of 1000 mg (range, 325-1500 mg) was administered. The infusions were generally well tolerated. Clinical adverse effects were seen in 2 patients weighing less than 50 kg. No increase in LFT results was seen. Hematocrit increased 2.2% (95% CI, 0.5%-3.9%) from 29.0% to 31.2% (p = 0.01) within 4 weeks of infusion. Significant increases also occurred in iron saturation (from 13% to 22%, p = 0.001) and ferritin (from 234 to 305 ng/mL, p = 0.008). Among the 9 patients who did not respond with a significant increase in Hct, 2 had a delayed response, increasing the overall response from 63% at 4 weeks to 71%, 8 weeks after TDI. Inadequate erythropoietin dosing and low-grade infectious/inflammatory disorders may have contributed to a poor response in several patients. CONCLUSION: Total dose iron is a safe and effective means of restoring iron and erythropoietic response in ESRD patients weighing more than 50 kg who receive their renal replacement therapy at home.

Anemia, Iron-Deficiency↗
PubMed1999

HBED: the continuing development of a potential alternative to deferoxamine for iron-chelating therapy.

To further examine the potential clinical usefulness of the hexadentate phenolic aminocarboxylate iron chelator N, N'-bis(2-hydroxybenzyl)ethylenediamine-N,N'-diacetic acid (HBED) for the chronic treatment of transfusional iron overload, we performed a subchronic toxicity study of the HBED monosodium salt in rodents and have evaluated the iron excretion in primates induced by HBED. The HBED-induced iron excretion was determined for the monohydrochloride dihydrate that was first dissolved in a 0.1-mmol/L sodium phosphate buffer at pH 7.6 and administered to the primates either orally (PO) at a dose of 324 micromol/kg (149.3 mg/kg, n = 5), subcutaneously (sc) at a dose of 81 micromol/kg (37.3 mg/kg, n = 5), sc at 324 micromol/kg (n = 5), and sc at 162 micromol/kg (74.7 mg/kg) for 2 consecutive days for a total dose of 324 micromol/kg (n = 3). In addition, the monosodium salt of HBED in saline was administered to the monkeys sc at a single dose of 150 micromol/kg (64.9 mg/kg, n = 5) or at a dose of 75 micromol/kg every other day for three doses, for a total dose of 225 micromol/kg (n = 4). For comparative purposes, we have also administered deferoxamine (DFO) PO and sc in aqueous solution at a dose of 300 micromol/kg (200 mg/kg). In the iron-loaded Cebus apella monkey, whereas the PO administration of DFO or HBED even at a dose of 300 to 324 micromol/kg was ineffective, the sc injection of HBED in buffer or its monosodium salt, 75 to 324 micromol/kg, produced a net iron excretion that was nearly three times that observed after similar doses of sc DFO. In patients with transfusional iron overload, sc injections of HBED may provide a much needed alternative to the use of prolonged parenteral infusions of DFO. Note: After the publication of our previous paper (Blood, 91:1446, 1998) and the completion of the studies described here, it was discovered that the HBED obtained from Strem Chemical Co (Newburyport, MA) that was labeled and sold as a dihydrochloride dihydrate was in fact the monohydrochloride dihydrate. Therefore, the actual administered doses were 81, 162, or 324 micromol/kg; not 75, 150, or 300 micromol/kg as was previously reported. The new data have been recalculated accordingly, and the data from our earlier study, corrected where applicable, are shown in parentheses.

Administration, Oral↗
PubMed1998

A protocol for coadministration of i.v. iron dextran and heparin in chronic hemodialysis patients.

The coadministration of intravenous iron dextran and heparin as a continuous infusion during hemodialysis (HD) is a safe and effective method used in maintaining and/or increasing iron stores and hematocrit levels in patients with end stage renal disease (ESRD). The technique of mixing iron dextran in low doses with heparin and infusing this mixture via the heparin syringe pump on the dialysis machine has shown to be cost effective, as well as instrumental in reducing the risk of adverse reactions due to rapid infusion or large dose infusion of iron dextran. At the Cleveland Clinic Foundation, we developed a protocol based on this methodology. A total of more than 1,000 doses of intravenous iron dextran and heparin have been administered to our HD patients using this technique, and no adverse reactions have been reported or observed.

Algorithms↗
PubMed1994

Immunologic studies of anaphylaxis to iron dextran in patients on renal dialysis.

Systemic reactions resembling anaphylaxis have occurred after intravenous (IV) iron-dextran administration, a treatment modality that has acquired increased acceptance following the use of erythropoietin for the anemia of patients with chronic renal diseases. Three such patients sustained anaphylactoid reactions immediately after receiving IV test doses of iron-dextran which were their only known exposures. In an effort to determine the mechanism of their reactions, we applied tests for (1) basophil degranulation by iron-dextran, basophil histamine release; (2) a type I anaphylactic reaction, specific IgE antibodies; and (3) an immune complex activation, specific IgG antibodies against iron-dextran. Six other patients with renal diseases served as controls, three of whom had tolerated IV iron-dextran, and three without known exposure. One patient only had any test abnormalities. Her initial positive basophil histamine release and specific IgG antibodies reversed and declined respectively at a 4-month follow-up study. She had developed anaphylaxis, and her studies had been performed at a time after anaphylaxis earlier than the other two. The mechanisms of iron-dextran anaphylaxis may be multiple and not be detectable several months after the incident. Prospective studies will probably be required for a predictive test to be developed.

Adult↗
PubMed1990

Thalamic afferents from the brain stem. An experimental study using retrograde single and double labelling with HRP and iron-dextran in the rat. II. Nucleus laterodorsalis and subnucleus compactus nuclei pedunculo-pontini.

The reticulo-thalamic projection arising from the ncl. latero-dorsalis and from the subncl. compactus nuclei pedunculo-pontini was studied in single and double experiments using 51 injections of HRP and/or iron-dextran. The ncl. latero-dorsalis projects to the midline nuclei, to the ncl. mediodorsalis and to the ncl. ventralis lateralis, and, together with the subncl. compactus, also to the anterior, intralaminar nuclei, to the ncl. ventralis basalis and ncll. posteriores. Part of the substantia grisea centralis pontis adjoining the oral pole of the ncl. latero-dorsalis sends out fibres throughout the region of the above listed nuclei while projecting only scantily to the anterior nuclei and to the ventrobasal complex. The projection from the ncl. laterodorsalis has a major contralateral component (about one third of the labelled cells) whereas the contralateral component arising from the subncl. compactus is very scanty. We found no topographic arrangement in the projection (though there were signs of a crude mediolateral organization). The projection, mainly from the ncl. latero-dorsalis, shows relatively dense collateralization (double-labelled cells): ipsi- as well as contralaterally to the intralaminar nuclei, or collaterals to the ipsilateral intralaminary nuclei and, at the same time, to the contralateral ncl. mediodorsalis. A similar, albeit smaller collateralization, was also seen in the ncl. pedunculo-pontinus, its subncl. compactus: ipsilateral collateralization between the anterior and intralaminar nuclei or between the anterior and posterior intralaminar nuclei of the ipsilateral side.

Animals↗
PubMed2003

Deferoxamine promotes survival and prevents electrocardiographic abnormalities in the gerbil model of iron-overload cardiomyopathy.

We investigated the time course of electrocardiographic (ECG) changes in the Mongolian gerbil model of iron overload and the effects of the iron chelator deferoxamine (DFO) on these changes. Iron overload was produced with weekly subcutaneous injections of low doses (200 mg/kg/wk) or high doses (800 mg/kg/wk) of iron-dextran. DFO was administered subcutaneously at a dose of 200 mg/kg/day to high-dose animals. Our results show that (1) survival of iron-overloaded gerbils is dose-dependent, with median survival times of 68 and 14 weeks for low- and high-dose animals, respectively; (2) both low and high doses produce prolongation of the PR interval and bradycardia in early stages and prolongation of the QT interval, premature ventricular contractions, variable degrees of atrioventricular block, changes in the ST segment, and T-wave inversion at later stages coinciding with the development of heart failure; (3) DFO prevented death during 20 weeks of high-dose iron-dextran; (4) DFO prevented ECG changes, although delayed prolongation of PR intervals and QRS complexes occurred; and (5) despite marked prolongation of survival and prevention of ECG changes, DFO had modest effects on total cardiac iron content. We speculate that DFO chelates a small iron pool located within the cytoplasm of iron-overloaded cardiomyocytes.

Animals↗
PubMed1959

The cellular transformation of injected colloidal iron complexes into ferritin and hemosiderin in experimental animals; a study with the aid of electron microscopy.

As revealed by electron microscopy and electron diffraction, the physical state of ferric hydroxide micelles contained in iron-dextran, saccharated iron oxide, and hydrous ferric oxide ("ferric hydroxide") differs notably from the state of the ferric hydroxide in ferritin or hemosiderin. By virtue of this difference one can trace the intracellular transformation of colloidal iron, administered parenterally, into ferritin and hemosiderin. One hour after intraperitoneal injection of iron-dextran or saccharated iron oxide into mice, characteristic deposits were present in splenic macrophages, in sinusoidal endothelial cells of spleen and liver, and in vascular endothelial cells of various renal capillaries. Four hours after injection, small numbers of ferritin molecules were identifiable about intracellular aggregates of injected iron compounds; and by the 6th day, ferritin was abundant in close proximity to deposits of injected iron compounds. The latter were frequently situated in cytoplasmic vesicles delimited by single membranes. These vesicles were most frequently found in tissue obtained during the first 6 days after injection; and in certain of the vesicles ferritin molecules surrounded closely packed aggregates of injected material. Much unchanged ferric hydroxide was still present in macrophages and vascular endothelial cells 3 to 4 weeks after injection. While electron microscopy left no doubt about the identity of injected ferric hydroxide on the one hand, and of ferritin or hemosiderin on the other, histochemical tests for iron failed in this respect. Precipitation of ferric hydroxide (hydrous ferric oxide) from stabilized colloidal dispersions of iron-dextran was brought about in vitro by incubation with minced mouse tissue (e.g. liver), but not by incubation with mouse serum or blood. Subcutaneous injections of hydrous gel of ferric oxide into mice initially produced localized extracellular precipitates. Most of the material was still extracellular 16 days after injection, though part of it was phagocytized by macrophages near the site of injection; but apparently none reached the spleen in unaltered form. Five days after injection and thereafter, much ferritin was present in macrophages about the site of injection and in the spleen. The findings show that iron preparations widely used in therapy can be identified within cells, and that their intracellular disposition and fate can be followed at the molecular level. Considered in the light of previous work, they indicate that the characteristic structure of the ferric hydroxide micelles in molecules of ferritin is specific, and develops during the union of apoferritin with ferric hydroxide. Apparently this union does not depend upon specific cell components.

Animals↗
PubMed1960

The determination of serum iron after the intravenous injection of iron-dextran.

A rapid technique for the determination of iron in serum, after the intravenous injection of iron-dextran, is presented. Dithionite is used for the reduction of ferric to ferrous iron. The use of a detergent solution enables protein precipitation to be omitted. The iron reagent, 4: 7-diphenyl-1: 10-phenanthroline, and its ferrous complex are both soluble in the dilute detergent solution. Lipaemic serum can be used without affecting the results. The recovery of added ferric iron, as iron-dextran, is quantitative.

Dextrans↗
PubMed1993

[Iron deficiency anemia is not always simple].

BACKGROUND: Malabsorption of oraliron is rare, and more frequently suspected than proved. It could be due to prolonged iron deficiency. CASE REPORTS: Case no. 1: A boy was admitted at the age of 5 months for recurrent bronchitis. His hemoglobin was 8.2 g/dl, mean corpuscular volume (MCV) 60 micron3, mean corpuscular hemoglobin (MCH) 15 ng and mean corpuscular hemoglobin concentration (MCHC) 25 gHb/dl. The serum iron was 1 microgram/dl, iron binding capacity (IBC) was 284 micrograms/dl and ferritin was 14.9 ng/ml. Dietary iron was inadequate. The patient was given ferrous sulfate but iron deficiency persisted at the ages of 11 months and 3 years, probably due to poor compliance. Similar hematologic data (Hb: 6.4 g/dl, MCV 55 micrograms/m3, MCH 13.9 ng, MCHC 24 gHb/dl) were found at the age of 9 years. The patient was then given ferrous sulfate orally as test but the serum iron levels were unchanged during the 4 hours following ingestion. A parenteral iron preparation (iron-dextran, 500 mg) improved the hematologic data. 6 months later, a new oral test with ferrous sulfate improved the serum iron level. Case no. 2: A boy with complex congenital cardiopathy was operated on in the neonatal period and given oral iron at the age of 9 months because of anemia with microcytosis and hypochromia. This anemia was still present at 17 months and was associated with normal or high serum ferritin. Electrophoresis of hemoglobin was normal. At the age of 4 yr 5 mo, Hb was 9.7 g/dl, MCV 62.8 micrograms/m3, MCH 18.4 ng, iron 16 micrograms/dl and ferritin 94.1 ng/ml. An oral test with ferrous sulfate failed to increase the serum iron. The patient was then given parenteral iron-dextran without benefit, and a second oral test remained ineffective. After a second course of parenteral iron-dextran, Hb was 11.5 g/dl, MCV 74.1 micrograms/m3, MCH 23.7 ng while the serum iron remained low (23 micrograms/dl) and ferritin increased to 587 ng/ml. A third oral test with ferrous sulfate was still ineffective, as was a test using 4 mg/kg iron. CONCLUSION: The first patient suffered from iron malabsorption, presumably due to iron deficiency. The second patient could have abnormal metabolism and/or abnormal ferritin.

Anemia, Hypochromic↗
PubMed2002

Immunomagnetic separation reagents as markers in electron microscopy.

Antibodies coupled to magnetic particles have been employed for immunomagnetic cell isolation, but their consequent use for electron microscopy (EM) has not been evaluated. We used commercial antibodies coupled to iron-dextran to isolate T cells and monocytes/macrophages by immunomagnetic adsorption from normal human peripheral blood mononuclear cells. Subsequently, we studied the association of electron-dense immunomagnetic reagents with cell membranes. CD14-positive monocytes/macrophages isolated from fixed peripheral blood mononuclear cells retained electron-dense beads on the plasma membrane, while live cells internalized them. Flow cytometry and electron microscopy measurements of the percentage of cells that bound a CD4-specific immunomagnetic reagent in pan-T cell isolates (containing numerous T cell subtypes) were indistinguishable. The immunomagnetic reagent associated with cells could be secondarily labeled by secondary antibody coupled to colloidal gold. This study shows that these reagents used for cell isolation or just labeling, remain associated with their targets at the cell membrane. Immunomagnetic reagents allow "capturing" of rare cells from complex mixtures, purifying and concentrating them in a single step for subsequent electron microscopy. The large number of commercially available immunomagnetic reagents specific for different human, mouse and rat antigens provides additional resources for visualization of cellular ultrastructure.

Animals↗
PubMed1991

The effect of ligands on the uptake of iron by cells in culture.

Uptake of iron by a mammalian epithelial cell line (CNCM I-221) was shown to be dependent on the nature of the iron complex. Iron uptake was demonstrated by cytochemical staining and determination of redox-reactive iron in cell lysates. Three classes of ligands were investigated: (i) low molecular weight hydrophilic compounds, represented by ethylenediamine-tetraacetic acid (EDTA) and other charged ligands such as adenosine phosphates (ATP, ADP, AMP) and diethylenetriaminepentaacetic acid (DTPA), (2) low-molecular weight lipophilic ligands such as 8-hydroxyquinoline (8-HQ) and (3) a high molecular mass ligand, dextran. Iron complexed to 8-HQ accumulated intracellularly, the uptake rate of iron being 4.16 fmoles cell-1 h-1 of exposure at 37 degrees C or 3.86 fmoles cell-1 h-1 at 4 degrees C. Iron-dextran was endocytosed and retained in phagosomes. The uptake rate of iron following exposure to iron dextrans was found to be 5.6 fmoles cell-1 h-1 of exposure at 37 degrees C. In contrast to iron/8-HQ, uptake of iron dextran by cells was inhibited at 4 degrees C. Iron complexed to low molecular weight hydrophilic ligands was not taken up by cells. Cytotoxicity was measured by reduction of plating efficiency or tritiated thymidine incorporation. These tests showed that toxic effects of added iron were demonstrable only in cells exposed to the complex with 8-HQ.

Adenosine Diphosphate↗
PubMed1988

Studies on haemosiderin and ferritin from iron-loaded rat liver.

Haemosiderin has been isolated from siderosomes and ferritin from the cytosol of livers of rats iron-loaded by intraperitoneal injections of iron-dextran. Siderosomal haermosiderin, like ferritin, was shown by electron diffraction to contain iron mainly in the form of small particles of ferrihydrite (5Fe2O3.9H2O), with average particle diameter of 5.36 +/- 1.31 nm (SD), less than that of ferritin iron-cores (6.14 +/- 1.18 nm). Mössbauer spectra of both iron-storage complexes are also similar, except that the blocking temperature, TB, for haemosiderin (23 K) is lower than that of ferritin (35 K). These values are consistent with their differences in particle volumes assuming identical magnetic anisotropy constants. Measurements of P/Fe ratios by electron probe microanalysis showed the presence of phosphorus in rat liver haemosiderin, but much of it was lost on extensive dialysis. The presence of peptides reacting with anti-ferritin antisera and the similarities in the structures of their iron components are consistent with the view that rat liver haemosiderin arises by degradation of ferritin polypeptides, but its peptide pattern is different from that found in human beta-thalassaemia haemosiderin. The blocking temperature, 35 K, for rat liver ferritin is near to that reported, 40 K, for human beta-thalassaemia spleen ferritin. However, the haemosiderin isolated from this tissue, in contrast to that from rat liver, had a TB higher than that of ferritin. The iron availability of haemosiderins from rat liver and human beta-thalassaemic spleen to a hydroxypyridinone chelator also differed. That from rat liver was equal to or greater, and that from human spleen was markedly less, than the iron availability from either of the associated ferritins, which were equivalent. The differences in properties of the two types of haemosiderin may reflect their origins from primary or secondary iron overload and differences in the duration of the overload.

Animals↗
PubMed2003

Chronic use of sodium ferric gluconate complex in hemodialysis patients: safety of higher-dose (> or =250 mg) administration.

BACKGROUND: Almost all hemodialysis (HD) patients require intravenous iron therapy to correct their anemia and maintain their iron stores. Sodium ferric gluconate complex (SFGC) is approved by the Food and Drug Administration (FDA) for treatment of iron deficiency anemia in HD patients at individual doses up to 125 mg over 10 minutes (12.5 mg/min) and has been shown to have a superior safety profile compared with iron-dextran. Higher individual doses of SFGC would permit more rapid repletion of iron stores and greater flexibility in maintenance iron therapy as well as simplify treatment of peritoneal dialysis patients and chronic kidney disease patients. METHODS: The authors reviewed the safety and tolerability of higher-dose SFGC infusions (> or =250 mg) in 144 HD patients who were previously tolerant to a single 125-mg dose of SFGC. These 144 patients received a total of 590 doses of > or =250 mg of SFGC; 571 doses were 250 mg SFGC, and most of these were infused over 1 hour, an infusion rate of 4.17 mg/min. The other 19 doses were 312.5 mg (n = 1), 375 mg (n = 14), and 500 mg (n = 4). Infusion rates varied from 1.22 mg/min to 25.0 mg/min. RESULTS: Only one patient was considered intolerant to higher-dosing SFGC after having pruritus after a second 250-mg dose of SFGC. Three patients had nonserious events that did not preclude further dosing of SFGC. CONCLUSION: Administration of 250 mg SFGC over 1 hour is safe and well tolerated. Individual doses of 375 mg and 500 mg SFGC also were well tolerated, but further research and experience are needed to confirm the safety and tolerance of these doses.

Anemia, Iron-Deficiency↗