[Parenteral iron replacement].
Explore the source record for details and available documents.
Administration, Oral↗
SEARCH · Search PubMed
Results for “Iron-Dextran Complex”
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Comparative response to single or divided doses of parenteral iron for functional iron deficiency in hemodialysis patients receiving erythropoietin (EPO).
EPO treatment rapidly corrects anemia in patients with end-stage renal failure treated with hemodialysis, as long as sufficient iron is available. Absolute and relative (to demand) iron deficiency blunts the erythropoietic response and parenteral iron is frequently required during the course of therapy to restore EPO efficacy. Since the optimum time course of iron administration to restore EPO response in the short term is unknown, we compared three protocols of i.v. iron dextran administration in apparent functionally iron-deficient HD patients on oral iron therapy (hemoglobin < 10.0 g/dl plus ferritin < 100 micrograms/l and/or transferrin saturation < 20%). Intravenous iron (Imferon; Fisons Pty Ltd.) was given either as a single 600 mg dose (n = 15, Group I) or in divided doses of 100 mg administered on 6 successive dialyses (n = 14, Group II) or weekly for 6 weeks (n = 14, Group III). Response was monitored for 8 weeks. No adverse effects were observed. Collectively, mean hemoglobin increased (p < 0.01) by 0.4-0.5 g/dl plateauing at 4 weeks (between group comparison, p = 0.92). Mean ferritin concentrations changed with time (p < 0.01), peaking at 2 weeks in Groups I and II and at 4 weeks in Group III. Mean transferrin saturation levels also increased during the study (p < 0.001). The between group comparisons for the trends in iron indices were significant (p < 0.01 and 0.05 respectively). As there were no clinically significant differences in hemoglobin response at 4 weeks, single dose iron infusion would seem to be the most expedient in the short term, however frequent small doses are similarly effective.
Aged↗
The absence of toxicity in intraperitoneal iron dextran administration: a functional and histological analysis.
OBJECTIVE: To determine the influence of iron dextran intraperitoneal administration on the function and histology of the peritoneum in rats undergoing chronic peritoneal dialysis. DESIGN: Prospective, randomized experimental study. MATERIALS: Fifty-four Sprague-Dawley rats were divided into five groups: 3 study groups--high dose group (H), n = 12; intermediate dose (M), n = 12; and low dose group (L), n = 12--a dialysis control group (D), n = 12; and a tissue control (C), n = 7. INTERVENTIONS: The study groups were given Dianeal containing iron dextran in a concentration of 0.5, 0.25, and 0.125 mg/L (groups H, M, and L respectively). Group D was given standard Dianeal. Group C was never dialyzed. MAIN OUTCOME MEASURES: A 2-hour peritoneal equilibrium test (PET) was performed on the eighth day, at 3 months, and at 6 months. After the final PET, the animals were sacrificed and the peritoneal membrane was evaluated by gross inspection and light microscopy (silver, prussian blue, and trichrome staining). RESULTS: Peritoneal transport of small solutes followed the same pattern in all groups, increasing over time. The peritonitis index was similar in the groups. No iron deposits or morphologic differences were seen in the gross inspection of the peritoneal cavity. No peritoneal iron deposition was detected in the histological analysis with prussian blue staining. No differences were noted in the light microscopic analysis of the mesothelial cell layer (silver staining), nor did the morphometric analysis of the submesothelial space show any differences in thickness between the groups. CONCLUSION: These findings suggest the absence of toxic effects of iron dextran on the peritoneal cavity of rats in the concentrations studied. Further studies should be performed to evaluate the effectiveness of these dosages delivered intraperitoneally to maintain iron homeostasis.
Animals↗
Maintaining iron balance with total-dose infusion of intravenous iron dextran.
Recombinant human erythropoietin (rHuEPO) is an important component of anemia management in patients with chronic renal failure, however, it can lead to functional iron deficiency (FID). Patients with FID are less likely to have an optimal response to rHuEPO (Cavill et al., 1997). Intravenous (i.v.) iron dextran is often required to replace iron losses, maintain adequate iron stores, and correct iron deficiency. The following article provides a rationale for the use of IV iron dextran and details one unit's protocol and experience with its use.
Anemia, Iron-Deficiency↗
[Parenteral iron therapy: problems and possible solutions].
To investigate whether there are differences in the frequency of ADRs (adverse drug reactions) to parenteral iron preparations, we compared the results of 4 different data collections which contain observations in particular on i.m. or i.v. iron dextran and i.v. iron hydroxide sucrose complex, primarily in relation to anaphylactic/anaphylactoid reactions and common exanthemas. 1. In 206 patients of the department of general internal medicine in a city/teaching hospital (in association with the Swiss Foundation for Comprehensive Hospital Drug Monitoring--CHDM), 4 probably allergic reactions to i.m. iron dextran were found, one with acute severe dyspnea, cyanosis and flush, 3 with slight generalized, probably allergic reactions. Data from the USA on i.v. iron dextran do not show marked differences in the frequency of ADRs as compared with our data with i.m. administration. 2. A group of 400 otherwise healthy patients of the obstetric department of Zurich University Hospital were treated with i.v. iron sucrose for anemia due to iron loss during pregnancy or following childbirth. Seven generalized skin reactions, 4 in the form of flush and 3 of common exanthema, occurred. 3. In a retrospective study on patients on maintenance hemodialysis with chronic renal insufficiency and anemia, a questionnaire was answered by the medical heads of 17 selected hemodialysis units in Switzerland. Response was 100%. During around 8100 patient-years with approximately 160,000 ampoules of iron sucrose (with 100 mg elementary iron), not a single life threatening reaction was observed; only 5-7 situations of rapidly reversible blood pressure fall occurred, some 10 with flush, and one each with urticaria and vomiting/diarrhea. 4. The relatively good tolerance of i.v. iron sucrose in patients with chronic renal failure may be due either to reduced immune competence in patients with chronic renal insufficiency and/or to the use of the preparation itself, or probably both. 5. In ADRs of allergic appearance to iron sucrose, the 7 generalized skin reactions occurred on the first day of the injections, as did those under iron dextran. Preexisting hypersensitivity must be taken into consideration. 6. If our experience is confirmed, preventive measures with i.v. iron sucrose, mainly in patients with chronic renal insufficiency, could be reduced.
Adult↗
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↗
Chronic administration of iron dextran into the peritoneal cavity of rats.
Explore the source record for details and available documents.
Animals↗
Concerns expressed regarding total dose infusion article--February 1998 issue.
Explore the source record for details and available documents.
Anemia↗
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↗
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↗
Stability of iron dextran (DexFerrum) in peritoneal dialysis bags.
Explore the source record for details and available documents.
Anemia, Iron-Deficiency↗
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↗
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↗
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↗
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↗
[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↗
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↗
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↗