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At least 91 records · Page 5Linked to original sources
PubMed2001

Exploring the "iron shuttle" hypothesis in chelation therapy: effects of combined deferoxamine and deferiprone treatment in hypertransfused rats with labeled iron stores and in iron-loaded rat heart cells in culture.

Although iron chelation therapy results in a significant improvement in well-being and life expectancy of thalassemic patients with transfusional iron overload, failure to achieve these goals in a substantial proportion of patients underlines the need for improved methods of treatment. In the present studies we used selective radioactive iron probes of hepatocellular and reticuloendothelial (RE) iron stores in hypertransfused rats and iron-loaded heart cells to compare the source of iron chelated in vivo by deferoxamine (DFO) or by deferiprone (L1) and its mode of excretion, to examine the ability of DFO and L1 to remove iron directly from iron-loaded myocardial cells, and to examine the mechanism of their combined interaction through a possible additive or synergistic effect. Our results indicate that L1 given orally is 1.6 to 1.9 times more effective in rats, on a weight-per-weight basis, than parenteral DFO in promoting the excretion of storage iron from parenchymal iron stores but shows no advantage over DFO in promoting RE iron excretion. Simultaneous administration of DFO and L1 results in an increase in chelating effect that is additive but not synergistic. The magnitude of this additive effect is identical to an increase in the equivalent (weight or molar) dose of DFO alone rather than the sum of the separate effects of L1 and DFO. This finding is most probably the result of a transfer of chelated iron from L1 to DFO. These observations may have practical implications for current efforts to design better therapeutic strategies for the management of transfusional iron overload.

Animals↗
PubMed2005

Iron status of the Taiwanese elderly: the prevalence of iron deficiency and elevated iron stores.

Iron status, prevalence of iron deficiency and elevated iron stores, and the effect of gastrointestinal ulceration on iron status in free-living Taiwanese elderly persons were all assessed in a nationally representative, cross-sectional nutrition survey--the Elderly NAHSIT. The survey included blood measurements of iron indices. Data were collected from 1202 elderly men and 1152 elderly women aged 65 years and older. Multiple iron measures, including serum ferritin (SF), transferrin saturation (Tsat), and hemoglobin were used to evaluate the prevalence of iron deficient erythropoiesis (ID) and iron deficiency anemia (IDA). Despite no routine practice of iron fortification in Taiwan, elderly subjects had a low prevalence of ID and IDA. The prevalence of ID was 2.3% in men and 1.4% in women. The prevalence of IDA was 2.5% in men and 2.0% in women. In contrast, 15.7% of men and 9.8% of women had elevated iron stores as diagnosed by SF>300 microg/L. Subjects with a history of gastrointestinal ulceration had significantly lower serum ferritin than those without ulcers, but the prevalence of anemia, ID and IDA was unaffected. In conclusion, elderly people in Taiwan are an iron-replete population with a high prevalence of elevated iron stores and a low prevalence of iron deficiency.

Aged↗
PubMed1999

Performance characteristics of three serum iron and total iron-binding capacity methods in acute iron overdose.

Accurate serum iron and total iron binding capacity (TIBC) measurements may be useful in acute iron overdoses. Two alumina column TIBC methods were found to measure increased TIBC when free iron was present. A homogeneous TIBC method gave consistent results until iron concentrations exceeded 500 micrograms/dL (90 mumol/L), when it began to underestimate the TIBC. Serious iron overdoses require chelation therapy with deferoxamine. Iron recovery was reduced by up to 50% for all 3 methods with clinically achievable concentrations of deferoxamine 8,400 micrograms/dL (150 mumol/L). TIBC measurements by both alumina column methods were reduced by deferoxamine in the presence of free iron and unaffected when the iron concentration was less than the TIBC. The homogeneous TIBC method yielded falsely elevated results in the presence of free deferoxamine. Procedures that measure TIBC by addition of excess ferric iron followed by alumina adsorption are not suitable for monitoring TIBC in acute iron overdose. The homogeneous TIBC assay can be used in acute iron overdose but underestimates TIBC when iron concentrations exceed 500 micrograms/dL (90 mumol/L). None of the methods examined are useful for measuring iron or TIBC in the presence of deferoxamine.

Acute Disease↗
PubMed1992

Regulation of iron absorption in iron loaded subjects with end stage renal disease: effects of treatment with recombinant human erythropoietin and reduction of iron stores.

The effects on iron absorption of variation in erythroid activity, haemoglobin and iron stores were studied in six anaemic dialysis-dependent subjects in whom iron stores were increased from previous red cell transfusions. Gastrointestinal mucosal uptake and whole body retention of oral iron were measured at the beginning of the study, after starting treatment with recombinant erythropoietin (but before significant increase in haemoglobin), after partial correction of anaemia, after further reduction of iron stores by repeated phlebotomy, and when erythropoiesis decreased from the discontinuation of treatment with erythropoietin. Between successive measurements, valid comparisons were made in five subjects. Correction of anaemia decreased whole body retention of iron through decreased mucosal uptake (P = 0.032). Further reduction in iron stores through repeated phlebotomy whilst the increase in haemoglobin was maintained by treatment with erythropoietin, tended to increase whole body retention of iron through an increase in mucosal transfer (P = 0.010). With initial enhancement of erythropoiesis in anaemic iron-loaded subjects there was no change in any measured component of iron absorption. However, after correction of anaemia and reduction of iron stores, a decrease in erythropoiesis was associated with decreased whole body iron retention in all subjects through decreased mucosal transfer (P = 0.028). The data suggest that anaemia upregulates mucosal iron uptake, and that erythroid activity upregulates mucosal transfer but that this latter effect may be counter-balanced by iron overload which downregulates mucosal transfer.

Adult↗
PubMed2000

Intravenous iron dextran therapy in patients with iron deficiency and normal renal function who failed to respond to or did not tolerate oral iron supplementation.

PURPOSE: To evaluate the safety and effectiveness of using 500-mg doses of iron as intravenous iron dextran after premedication with diphenhydramine, cimetidine, and dexamethasone. SUBJECTS AND METHODS: We treated 135 iron-deficient adults (26 men, 109 women) with normal renal function (serum creatinine level </=1.5 mg/dL or blood urea nitrogen level </=26 mg/dL) who could not be treated adequately with oral iron supplements due to gastrointestinal symptoms (59%), inadequate hematologic response (39%), severe anemia (19%), or noncompliance (4%). Some patients had more than one reason for treatment. Resolution of iron deficiency was defined as the restoration of transferrin saturation, serum ferritin level, anemia, and abnormal erythrocyte indexes to normal or baseline values. RESULTS: Before treatment with iron dextran, patients had a mean (+/- SD) transferrin saturation of 8% +/- 5%, a median serum ferritin level of 11 ng/mL, and a mean hemoglobin level of 10 +/- 2 g/dL. Ninety-two percent were anemic; 60% had unrecognized or untreated causes of anemia other than iron deficiency. We administered 285 iron dextran infusions (median 2, mean 2 infusions per patient; range 1 to 7). Eighty-seven percent of patients had no adverse reaction; 13% had mild reactions, especially arthralgias and myalgias. No patient had an anaphylaxis-like reaction. Fifty-four (40%) patients had resolution of iron deficiency, 34 (25%) continue to receive therapy, 36 (27%) returned to the care of their primary physician, and 11 (8%) died before iron repletion could be achieved. CONCLUSIONS: Iron-deficient adults with normal renal function who cannot be treated adequately with oral iron supplements can be treated effectively and safely with this intravenous iron dextran regimen.

Adolescent↗
PubMed2003

Influence of parenteral iron preparations on non-transferrin bound iron uptake, the iron regulatory protein and the expression of ferritin and the divalent metal transporter DMT-1 in HepG2 human hepatoma cells.

It is widely assumed that standard parenteral iron preparations are degraded in the reticuloendothelial cells and that the iron is subsequently incorporated into transferrin. Hepatocytes or other epithelial cells have been considered as not affected. We show that this picture should be carefully reconsidered. By using the human hepatoma cell line HepG2 we showed that the parenteral iron preparations ferric saccharate and ferric gluconate donated iron to the cells as efficiently as low molecular weight iron and stimulated non-transferrin bound iron uptake. This led to inactivation of the iron regulatory protein 1 and to an increase in the expression of ferritin and of the divalent metal transporter (DMT-1). Ferric dextran was only a weak stimulator of ferritin and DMT-1 expression. The observed changes in iron metabolism occurred at concentrations of parenteral iron that can also be found in the plasma of patients after i.v. infusion. We conclude that parenteral iron also influences the iron metabolism of non-reticuloendothelial cells like HepG2 cells. Further the increase in the expression of the transporter DMT-1 in HepG2 cells after iron treatment is in contrast to the regulation in the duodenum and may be involved in the upregulated uptake of potentially toxic non-transferrin bound iron from the circulation to store it in the non-toxic form of ferritin.

Biological Transport↗
PubMed2001

Expression of the duodenal iron transporters divalent-metal transporter 1 and ferroportin 1 in iron deficiency and iron overload.

BACKGROUND & AIMS: Imbalances of iron homeostasis are accompanied by alterations of intestinal iron absorption. The identification of divalent-metal transporter 1 (DMT1) and ferroportin 1 (FP1) has improved our understanding of transmembrane iron trafficking. To gain insight into the regulatory properties of these transporters in the duodenum, we studied their expression in patients with hereditary hemochromatosis (HFE-associated and non-HFE-associated), secondary iron overload, and iron deficiency. METHODS: DMT1, FP1 messenger RNA (mRNA), and protein expression were analyzed in duodenal biopsy specimens from patients by means of TaqMan real-time polymerase chain reaction, Western blotting technique, and immunohistochemistry. RESULTS: DMT1 and FP1 mRNA levels are positively correlated with each other in all patient groups (P < 0.001). Moreover, DMT1 and FP1 mRNA levels were significantly increased in patients with iron deficiency, HFE and non-HFE hemochromatosis, whereas they were unchanged in patients with secondary iron overload. Alterations in DMT1 and FP1 mRNA levels were paralleled by comparable changes in the duodenal expression of these proteins. In patients with normal iron status or iron deficiency, significant negative correlations between DMT1, FP1 mRNA, and serum iron parameters were found, which were absent in subjects with primary hemochromatosis. CONCLUSIONS: DMT1 and FP1 are centrally involved in iron uptake/transfer in the duodenum and in the adaptive changes of iron homeostasis to iron deficiency and overload.

Adult↗
PubMed2002

Role of hypolipidemic drug clofibrate in altering iron regulatory proteins IRP1 and IRP2 activities and hepatic iron metabolism in rats fed a low-iron diet.

In addition to reducing the expression of transferrin and ceruloplasmin genes, hypolipidemic peroxisome proliferators may alter iron homeostasis in the liver. Therefore, this study investigates the effects of clofibrate on proteins related to liver iron metabolism in a rat model using a 2 x 2 experimental design: two dose levels of clofibrate in diet (0 and 0.5%) and two dietary iron levels (35 ppm as normal level and 15 ppm as low-iron diet). Twenty-four Wistar rats were assigned to the four diets and fed for 6 weeks. Subsequent measurements of iron parameters in the blood and the liver indicated that, in addition to mild anemia and the reduction in serum iron and total iron-binding capacity, clofibrate treatment altered IRP1 and IRP2 activities differentially and increased mitochondrial aconitase both at activity and protein levels. At both normal and low-iron intakes, clofibrate caused a 50% reduction in serum iron and TIBC with a corresponding reduction in transferrin mRNA. The RNA-binding activities of IRP1 were selectively activated by clofibrate treatment even though liver iron concentration was not depleted. The RNA-binding activity of IRP2 was selectively activated by the low iron intake and correlated with an increase of transferrin receptor mRNA, while clofibrate treatment offset the effects of the low iron intake.

Aconitate Hydratase↗
PubMed2003

Iron intake and regulation: implications for iron deficiency and iron overload.

Although iron deficiency anemia is the most common nutritional deficiency worldwide and in the United States, the health effects of iron overload merit increased attention. In the United States, public health interventions such as fortification and enrichment of foods with iron were undertaken to reduce the prevalence of iron deficiency anemia and improve health. These measures, along with iron supplementation, remain controversial, because additional exposure to dietary iron places some segments of the population at increased risk of iron excess. The health consequences of unmistakable iron excess are exemplified by hemochromatosis, an iron storage disease associated with liver damage further exacerbated by alcohol consumption. Progressive liver damage associated with this condition is generally attributed to increased oxidative stress. In otherwise healthy individuals, more modest levels of iron storage may occur if iron is provided by supplements or otherwise added to the food supply. Increased iron intake and storage have been linked to a variety of chronic diseases. The associations are not firmly established but are of considerable public health importance.

Absorption↗
PubMed2007

Assessment of chelatable mitochondrial iron by using mitochondrion-selective fluorescent iron indicators with different iron-binding affinities.

Chelatable cellular iron, and chelatable mitochondrial iron in particular, has yet to be well characterized, so the overall strength with which these "loosely bound" iron ions (presumably mainly Fe(II)) are intracellularly/intramitochondrially bound is unclear. We have previously reported the first selective mitochondrial iron indicator: rhodamine B 4-[(1,10-phenanthrolin-5-yl)aminocarbonyl]benzyl ester (RPA). With this compound as a model, we have now developed two additional mitochondrial iron indicators with very different iron-binding affinities and have applied these to the study of the chelatable iron pool in the mitochondria of isolated rat liver cells. With the new indicator rhodamine B 4-[(2,2'-bipyridin-4-yl)aminocarbonyl]benzyl ester (RDA), with 2,2'-bipyridine as chelating unit (log beta(3)=17.5), essentially the same iron concentration (16.0+/-1.9 microM) was determined as with RPA (log beta(3)=21.1), despite the four orders of magnitude difference in Fe(II)-binding affinity. This not only demonstrates the reliability of the procedure, but also confirms that iron complexation by these indicators does not induce any significant release of iron from the iron-storage proteins on the timescale of the experiment. In contrast, the indicator rhodamine B 4-[bis(pyridin-2-ylmethyl)aminomethyl]benzyl ester (PIRO), with an N,N-bis(pyridin-2-ylmethyl)amine group as chelating component (log beta(2)=12.2), could not compete against the array of endogenous ligands. The intramitochondrial concentrations of the three indicators were determined to be in the range of 100 microM: that is, about three orders of magnitude lower than the total concentration of endogenous compounds that might chelate iron ions. It is therefore estimated that chelatable mitochondrial iron ions are bound by endogenous ligands with apparent stability constants (log K(app)) of between 9 and 14.

Animals↗
PubMed1982

Proposal for the standardization of the serum unsaturated iron binding capacity assay, and results in groups of subjects with normal iron stores and with prelatent, latent, and manifest iron deficiency.

An effort has been made to standardize the indirect iron saturation excess method for the determination of the serum unsaturated iron binding capacity (UIBC) and thus to relinquish the direct adsorption methods for the assay of the serum total iron binding capacity (TIBC) which give falsely high results due to unspecific binding of the saturating iron to serum proteins. In order to eliminate the interfering effects of hydrolytic polymerization of iron(III) on the saturation of apotransferrin in serum and on the colorimetric determination of the unbound iron excess at pH 8.3, conditions have been studied for the preparation of the iron-nitrilotriacetate-complex (Fe(NTA)2) solution at pH 8.3 with respect to its reactivity with the reductant sodium ascorbate and with the chromogen bathophenanthroline-disulfonate in photometric standards and in samples containing iron-saturated serum. The validity of the results for the UIBC thus obtained has been investigated (1) by direct spectrophotometric titration with Fe(NTA)2 of the apotransferrin in serum by measuring the absorbance of transferrin at 470 nm in 50-mm cuvettes, and of the UIBC using the modified indirect iron saturation excess assay, both of which gave the same saturation points, and (2) by the correlation of the TIBC obtained from serum iron determinations and the UIBC, with the transferrin concentration measured by the radial immunodiffusion assay. Results of UIBC determinations are presented along with serum iron concentration, TIBC, and transferrin saturation in groups of subjects with normal iron stores and prelatent, latent, and manifest iron deficiency.

Anemia, Hypochromic↗
PubMed2001

Disposition, accumulation and toxicity of iron fed as iron (II) sulfate or as sodium iron EDTA in rats.

A study was performed to provide data on the disposition, accumulation and toxicity of sodium iron EDTA in comparison with iron (II) sulfate in rats on administration via the diet for 31 and 61 days. Clinical signs, body weights, food consumption, food conversion efficiency, hematology, clinical chemistry and pathology of selected organs were used as criteria for disclosing possible harmful effects. Determination of iron and total iron binding capacity in blood plasma and non-heme iron analysis in liver, spleen and kidneys were used to assess the disposition and accumulation of iron originating from sodium iron EDTA or iron (II) sulfate. It was concluded that, under the conditions of the present study, iron is accumulated from the diet in liver, spleen and kidneys in a dose-dependent manner, and iron derived from FeEDTA is taken up and/or accumulated less efficiently in liver and spleen than iron from FeSO(4). Moreover, feeding iron up to 11.5 and 11.2 mg/kg body weight/day, derived from FeSO(4) and FeEDTA, respectively, did not result in tissue iron excess nor in any other toxicologically significant effects.

Animals↗
PubMed2003

Serum iron concentration as a tool to measure relative iron absorption from elemental iron powders in man.

OBJECTIVE: To present a new method for measuring the relative bioavailability (RBV) of commercial elemental iron powders by investigating induced changes of serum iron concentration (S-Fe) in relation to ferrous sulphate (FeSO4). Earlier studies have shown that in a group of subjects there is good agreement between the increase in S-Fe and the amount of iron absorbed from a simple iron salt as FeSO4. METHODS: The study included two groups of male blood donors (n=2 x 16 subjects) who were served three meals with an interval of approximately nine weeks between each one. In one group the meal was fortified with reduced iron, ferrous sulphate or no iron at all. In the other group the meal was fortified with electrolytic iron, ferrous sulphate or no iron. The S-Fe increase was followed for 6 h. Studying the non-iron meals was necessary so that the basal diurnal variation in the S-Fe during the six hours could be measured and subtracted. RESULTS: The mean S-Fe increase calculated as the area under the curve (AUC) from the reduced iron (RBV=0.43) and the electrolytic iron (RBV=0.73) differed significantly from the AUC following FeSO4 (p=0.002 and p=0.021, respectively). The difference between the reduced and the electrolytic iron was also statistically significant (p=0.036). CONCLUSION: Measuring increases in S-Fe could be a reliable and simple method to determine the RBV in comparative studies of elemental iron powders in relation to FeSO4.

Adult↗
PubMed1995

Determination of iron absorption using erythrocyte iron incorporation of two stable isotopes of iron (57Fe and 58Fe) in very low birthweight premature infants.

Due to limited erythropoiesis, iron needs for the premature infant during the first 2 months of life are low. With the potential for increased use of erythropoietin in the preterm infant, iron requirements may become markedly higher. The ability of the preterm infant to absorb iron, therefore, becomes crucial. Previous studies using single stable isotopes of iron without metabolic balances were unable to quantitatively determine iron absorption since the percentage of absorbed iron appearing in the erythrocyte could not be measured. The objective of the current study was to determine iron absorption using the method of erythrocyte iron incorporation of two stable isotopes of iron given by the enteral and parenteral route to very low birth weight (VLBW) infants. Results obtained were compared to iron absorption values from studies using single isotopes and metabolic balance techniques. Six VLBW premature infants (gestational age 26.8 +/- 1.7 weeks, postnatal age 3.6 +/- 1.9 weeks, birth weight 863 +/- 117 g) were studied. Iron dosages were (i.v.) 0.15 mg/kg (57FeSO4) and (enteral) 1.5 mg/kg (58FeSO4). Erythrocyte isotope ratios, 57Fe/54Fe and 58Fe/54Fe, were determined by inductively coupled plasma mass spectrometry (ICP/MS) from single blood samples (100 microliters) collected before and after concurrent enteral (58Fe) and parenteral (57Fe) administration of isotopes. Only 17.8% of the i.v.-infused iron dose was incorporated into hemoglobin on day 15. Using a correction factor based on the percentage of i.v. iron (57Fe) incorporated into erythrocytes, the corrected incorporation of 58Fe was calculated to be 26.3 +/- 13.0% of the enteral dose of 58FeSO4.

Absorption↗
PubMed1986

Potential role of in vitro iron bioavailability studies in combatting iron deficiency: a study of the effects of phosvitin on iron mobilization from pinto beans.

Iron deficiency and iron overload affect one billion people worldwide. Treatment of iron malnutrition can be enhanced by an understanding of iron bioavailability from the diet. We have focused on the development of in vitro methods for determining iron bioavailability in the hopes of providing both an understanding of the chemical basis leading to the inhibition or enhancement of iron absorption and the provision of methodologies which will allow nutritionists around the world to ascertain iron bioavailability of local foods and food combinations. The study reported here focuses on the effects of phosvitin, a suspected inhibitor of iron absorption found in egg yolks, on the chemistry of iron during the in vitro enzymatic digestion of pinto beans. Three basic types of information were obtained. First, the total soluble iron was determined during in vitro enzymatic digestion under simulated oral, gastric (pH 2) and duodenal (pH 6) conditions. Phosvitin was found to have a strong solubilizing effect at pH 6 and pH 2 when in the presence of ascorbate. Pyrophosphate also leads to high iron mobilization. A second approach is to determine the static Fe2+ and Fe3+ concentrations following in vitro enzymatic digestion of pinto beans at pH 2 and pH 6. Ascorbic acid enhanced the total soluble iron at both pH values, however, only at pH 2 was a large proportion of the iron found in the Fe2+ state and then only in the presence of phosvitin but not pyrophosphate. A third approach is to determine the amount of Fe2+ formed in the digestive supernatant during a 10-min incubation with ferrozine.(ABSTRACT TRUNCATED AT 250 WORDS)

Ascorbic Acid↗
PubMed1996

Iron utilization after iron dextran administration for iron deficiency in patients with dialysis-associated anemia: a prospective analysis and comparison of two agents.

We sought to determine the rate and extent of iron utilization after administration of intravenous iron dextran and to compare the efficacy of iron dextran preparations of differing molecular weight. We randomized patients to receive either a 500-mg dose of iron dextran molecular weight (MW) 267,000 (group A) or iron dextran MW 96,000 (group B) administered in five sequential 100-mg doses, and examined indices of iron status before and at weekly intervals up to 4 weeks later. Although mean iron utilization was greater in the nine group A patients (46.7% +/- 21.3%) than in the 11 group B patients (31.7% +/- 26.6%), the difference was not statistically significant (P = 0.19). Iron utilization in both groups was substantially incomplete. Changes in serum ferritin and hemoglobin did not differ between the treatments (P = 0.49 and P = 0.34, respectively). We conclude that iron utilization after iron dextran administration is substantial within the first week after completing a course of therapy, associated with stable iron indices after the first 2 weeks, and incomplete for at least the first 4 weeks. Degree of iron utilization appears independent of molecular weight within the range we examined.

Anemia↗
PubMed1993

Recombinant iron-regulatory factor functions as an iron-responsive-element-binding protein, a translational repressor and an aconitase. A functional assay for translational repression and direct demonstration of the iron switch.

The translation of ferritin and erythroid 5-aminolevulinate synthase mRNAs is regulated via a specific high-affinity interaction between an iron-responsive element in the 5' untranslated region of ferritin and erythroid 5-aminolevulinate synthase mRNAs and a 98-kDa cytoplasmic protein, the iron-regulatory factor. Iron-regulatory factor was expressed in vaccinia-virus-infected HeLa cells (hIRFvac) and in Escherichia coli (hIRFeco). An N-terminal histidine tag allowed a rapid one-step purification of large quantities of soluble recombinant protein. Both hIRFvac and hIRFeco bound specifically to iron-responsive elements and were immunoprecipitated by iron-regulatory-factor antibodies. Using in-vitro-transcribed chloramphenicol-acetyltransferase mRNAs bearing an iron-responsive element in the 5' untranslated region, specific repression of chloramphenicol-acetyltransferase translation by hIRFvac and hIRFeco was demonstrated in wheat-germ extract. In addition, hIRFvac and hIRFeco were shown to display aconitase activity. Treatment of hIRFvac and hIRFeco with FeSO4 resulted in a drastic reduction in iron-responsive-element-binding of iron-regulatory factor, but caused a strong stimulation of its aconitase activity. The results establish that recombinant iron-regulatory factor is a bifunctional protein; after purification, it binds to iron-responsive elements and represses translation in vitro. Following iron treatment, iron-responsive-element binding is lost and aconitase activity is gained. No eukaryotic co-factor seems to be required for the conversion of the iron-responsive-element binding to the aconitase form of the protein.

Aconitate Hydratase↗
PubMed2005

Intravenous iron sucrose versus oral iron supplementation for the treatment of iron deficiency anemia in patients with inflammatory bowel disease--a randomized, controlled, open-label, multicenter study.

OBJECTIVES: Anemia is a frequent complication in patients with inflammatory bowel disease (IBD). The optimal route for iron supplementation to replenish iron stores has not been determined so far. We therefore evaluated the efficacy and safety of intravenous iron sucrose as compared with oral iron sulfate for the treatment of iron deficiency anemia (IDA) in patients with IBD. METHODS: A randomized, prospective, open-label, multicenter study was performed in 46 patients with anemia and transferrin saturation <or=20% and/or serum ferritin concentrations <or=20 microg/L. The intravenous group received a single dose of iron sucrose of 7 mg iron/kg body weight, followed by five 200 mg infusions for the following 5 wks. The oral group received iron sulfate 100-200 mg per day for 6 wks. RESULTS: While a comparable increase in hemoglobin was observed for both administration routes (median increase 0.25 g/L in the intravenous group vs 0.21 g/L in the oral group), only iron sucrose led to a rise in serum ferritin concentrations. Intractable gastrointestinal adverse events caused permanent study drug discontinuation in five patients (20.8%) receiving iron sulfate, whereas only one patient (4.5%) had to be withdrawn because of side effects due to iron sucrose. CONCLUSIONS: Although being equal in short-term efficacy and overall tolerability our results suggest a better gastrointestinal tolerability for iron sucrose. Larger trials are mandatory to prove a possible advantage of iron sucrose in short- and long-term efficacy as well as in tolerability over iron sulfate in the management of IDA in IBD.

Abdominal Pain↗