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At least 649 records · Page 36Linked to original sources
PubMed2002

The effect of iron deficiency anaemia on the levels of haemoglobin subtypes: possible consequences for clinical diagnosis.

The purpose of the present study was to quantify the effect of iron deficiency anaemia on the levels of HbA2, HbF, and HbA1C. Complete blood counts (CBC) were performed on 730 university students. Serum ferritin, HbA2, HbF, and HbA1C levels were determined for all microcytic/hypochromic subjects. It was found that 81 (11.1%) of the students were microcytic/hypochromic, of which 47 (58.1%) were found to be iron deficient. Twenty-six (32.1%) were beta-thalassemia carriers, 4 (4.9%) were beta-thalassemia carriers with iron deficiency and 4 (4.9%) remained undiagnosed. All the anaemic students were treated with oral iron and followed for 20 weeks. The mean HbA2 level rose significantly (from 1.89% +/- 0.45 to 2.19% +/- 0.53, P < 0.001) after iron treatment. HbF levels were not significantly different after iron treatment (0.94% +/- 0.18 before and 0.95% +/- 0.17 after treatment, P > 0.05). HbA1C fell significantly after iron treatment, from a mean of 6.15% +/- 0.62 to 5.25% +/- 0.45 (P < 0.001). In conclusion, iron deficiency must be corrected before making any diagnostic or therapeutic decisions based on HbA2 and HbA1C levels.

Anemia, Hypochromic↗
PubMed1998

Effective utilization of erythropoietin with intravenous iron therapy.

INTRODUCTION: Iron replacement therapy reduces the demand for erythropoietin (EPO) in some dialysis patients. It has been postulated that iron supply to the bone marrow is a rate-limiting step in the process of erythropoiesis under erythropoietin stimulation. METHODS: We evaluated the economic benefit of intravenous iron therapy for this purpose in a prospective, non-blinded study of 22 haemodialysis patients, 16 male, six female, mean age 62 years (range 24-80 years). All patients had a serum ferritin (SF) of < or = 60 microg/L, despite oral iron therapy. Patients with high aluminium and/or parathyroid hormone (PTH) levels, underlying bleeding/haematological disorders or active inflammatory diseases were excluded. Patients were established on subcutaneous EPO and given intravenous iron over seven consecutive dialysis sessions (total dose 1050 mg) and supplemental monthly doses with regular monitoring for 4 months. RESULTS: The median EPO dose was 4000 units/week (mean 6050 units/week) pre-treatment and 2000 units/week (mean 3700 units) at 6 weeks post intravenous iron therapy (P=0.03). No serious adverse events occurred in the 154 treatment sessions of intravenous iron. Mean haemoglobin (Hb) level remained constant at 6 and 12 weeks (P=0.087). Serum ferritin levels (P< 0.0001) rose significantly, while a reduction in transferrin saturation (TS) became significant at the end of the study (P=0.0047). The use of intravenous iron allowed a substantial monthly cost saving per patient in our unit. CONCLUSION: Intravenous iron therapy is a safe and cost-effective method for maintaining or improving Hb levels with a more effective utilization of EPO in patients with low SF levels despite oral iron therapy.

Adult↗
PubMed2003

IsdG and IsdI, heme-degrading enzymes in the cytoplasm of Staphylococcus aureus.

Staphylococcus aureus requires iron for growth and utilizes heme as a source of iron during infection. Staphylococcal surface proteins capture hemoglobin, release heme from hemoglobin and transport this compound across the cell wall envelope and plasma membrane into the bacterial cytoplasm. Here we show that Staphylococcus aureus isdG and isdI encode cytoplasmic proteins with heme binding properties. IsdG and IsdI cleave the tetrapyrrol ring structure of heme in the presence of NADPH cytochrome P450 reductase, thereby releasing iron. Further, IsdI complements the heme utilization deficiency of a Corynebacterium ulcerans heme oxygenase mutant, demonstrating in vivo activity of this enzyme. Although Staphylococcus epidermidis, Listeria monocytogenes, and Bacillus anthracis encode homologues of IsdG and IsdI, these proteins are not found in other bacteria or mammals. Thus, it appears that bacterial pathogens evolved different strategies to retrieve iron from scavenged heme molecules and that staphylococcal IsdG and IsdI represent examples of bacterial heme-oxygenases.

Base Sequence↗
PubMedDate not supplied

Safety profiles of Fe2+ and Fe3+ oral preparations in the treatment of iron deficiency anemia in children.

The major purpose of this study was to compare the oxidant-related toxicities of the different oral iron preparations in children with iron deficiency anemia (IDA); the second aim was to investigate the side effects of iron preparations. Seventy-two children with IDA were randomly included in the Fe(2+) group (n = 39) or the Fe(3+) group (n = 33). Some oxidizable substrates (erythrocytes malondialdehyde (MDA), urine 8-isoprostane, and basal and Cu-stimulated-oxidized LDL and antioxidant enzyme (superoxide dismutase (SOD), catalase and glutathione peroxidase) activities were evaluated at the beginning and at the 1st, 3rd, and 6th months of therapy. Side effects due to medication were recorded. While at the end of the 1st month SOD levels were significantly increased in Fe(3+) group, at the 6th month evaluation, basal-oxidized LDL levels were significantly increased in the Fe(3+) group, as was urine 8-isoprostane in the Fe(2+) group. No other difference was found between two groups. In conclusion, there were minimal differences between children treated with ferric or ferrous iron in antioxidant system activities, the status of oxidizable substrates, and clinical toxicities.

Administration, Oral↗
PubMed1951

Mechanism of proteinuria. III. A comparison of the functional and structural aspects of the effects of certain intraperitoneally administered proteins on hemoglobin excretion in the rat.

Intraperitoneal administration of bovine albumin sharply increases glomerular permeability to hemoglobin in the rat kidney. In addition, bovine albumin "saturates" the tubular absorption mechanism and inhibits the tubular absorption of subsequently administered hemoglobin. Egg white, ovalbumin, and ovomucoid, in contrast, do not produce significant changes in glomerular permeability to hemoglobin or in the tubular absorption of hemoglobin. These effects have been demonstrated both by physiologic measurements and by the morphologic demonstration of the absorbed proteins.

Animals↗
PubMed1951

Mechanism of proteinuria. IV. Effect of renin on hemoglobin excretion.

1. Administration of renin to the rat causes an increase in the glomerular permeability to hemoglobin and a decrease in tubular absorption of this substance as measured by functional methods. 2. Morphologic examination in the rat and in the rabbit reveals an increased concentration of hemoglobin in the tubular lumina, confirmatory evidence of increased permeability. However, there is no significant effect upon the formation of hemoglobin droplets within the renal cells. 3. By analogy with the events observed in neutral red "secretion," it is suggested that hemoglobin is absorbed by both a "direct" and an "indirect" mechanism and that renin administration affects or depresses the "direct" mechanism only.

Animals↗
PubMed2003

Iron supplements inhibit zinc but not copper absorption in vivo in ileostomy subjects.

BACKGROUND: Iron supplements may inhibit intestinal zinc and copper uptake because these elements may compete for binding to a transporter molecule (divalent metal transporter 1) that is located on the apical side of the small intestinal epithelium. OBJECTIVE: We quantified the interaction between different amounts of administered iron and the absorption of zinc and copper in humans. DESIGN: Eleven subjects with an ileostomy [mean (+/- SD) age: 55 +/- 9 y] ingested a stable-isotope-labeled zinc and copper solution containing 12 mg Zn ((66)Zn and (67)Zn) and 3 mg Cu ((65)Cu) in the presence of 0, 100, or 400 mg Fe as ferrous gluconate on 3 respective test days. Subsequently, 1 mg (70)Zn was injected intravenously. Subjects collected ileostomy effluent and urine for 24 h and 7 d, respectively. Zinc status and true zinc absorption were calculated from the urinary excretion of the zinc isotopes. Apparent copper absorption was calculated from ileostomy effluent excretion of the orally administered copper isotopes. RESULTS: Zinc status did not differ significantly between the 3 iron doses. Mean (+/- SEM) zinc absorption was significantly higher in the absence of iron than with the concomitant ingestion of 100 or 400 mg Fe (44 +/- 22% compared with 26 +/- 14% and 23 +/- 6%, respectively; P < 0.05), whereas zinc absorption did not differ significantly between the 100- and 400-mg Fe doses. Apparent copper absorption was 48 +/- 14%, 54 +/- 26%, and 53 +/- 7% in the presence of 0, 100, and 400 mg Fe, respectively, and did not differ significantly between the 3 iron doses. CONCLUSION: Oral iron therapy may impair zinc absorption and thus zinc status in a dose-independent fashion but does not affect copper absorption.

C-Reactive Protein↗