Non-transferrin-bound iron in long-term transfusion in children with congenital anemias

Wang, Winfred C.; Ahmed, Nahed K.; Hanna, Marwan

doi:10.1016/s0022-3476(86)80832-0

Cited by 49 publications

(18 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In transfusional iron overload, free iron accumulates in macrophages after iron storage proteins are saturated. This free iron is subsequently transferred to and deposited primarily in parenchymal cells of the liver, heart, pancreas, and endocrine tissues (transfusional hemosiderosis) [36], which have a more limited capacity than macrophages to store iron safely [37]. In the liver, transfusional iron overload often leads to iron deposition as free iron in Kupffer cells as well as hepatocytes [38].…”

Section: Iron Overload and Toxicity From Multiple Transfusionsmentioning

confidence: 99%

Iron overload and toxicity: the hidden risk of multiple blood transfusions

Shander¹,

Cappellini²,

Goodnough³

2009

Vox Sanguinis

180

130

View full text Add to dashboard Cite

show abstract

Section: Iron Overload and Toxicity From Multiple Transfusionsmentioning

confidence: 99%

Iron overload and toxicity: the hidden risk of multiple blood transfusions

Shander¹,

Cappellini²,

Goodnough³

2009

Vox Sanguinis

180

130

View full text Add to dashboard Cite

show abstract

“…Long-term transfusion therapy of, for instance, 20-units RBCs/year is associated with significant iron overload (20 units × 220 mL per unit × 1 mg per mL = 4400 mgm exogenous iron/year) [32]. With repeated transfusions, serum transferrin becomes saturated and the excess circulating iron is transported as NTBI [33]. NTBI enters cells in a dysregulated fashion; a subset of NTBI, called Labile Plasma Iron (LPI), may cause end organ damage secondary to its high redox potential [34].…”

Section: Mechanism Of Transfusion Mediated Iron Overloadmentioning

confidence: 99%

Iron Overload in Sickle Cell Disease

Raghupathy

Manwani

Little

2010

Advances in Hematology

View full text Add to dashboard Cite

In sickle cell disease transfusions improve blood flow by reducing the proportion of red cells capable of forming sickle hemoglobin polymer. This limits hemolysis and the endothelial damage that result from high proportions of sickle polymer-containing red cells. Additionally, transfusions are used to increase blood oxygen carrying capacity in sickle cell patients with severe chronic anemia or with severe anemic episodes. Transfusion is well-defined as prophylaxis (stroke) and as therapy (acute chest syndrome and stroke) for major complications of sickle cell disease and has been instituted, based on less conclusive data, for a range of additional complications, such as priapism, vaso-occlusive crises, leg ulcers, pulmonary hypertension, and during complicated pregnancies. The major and unavoidable complication of transfusions in sickle cell disease is iron overload. This paper provides an overview of normal iron metabolism, iron overload in transfused patients with sickle cell disease, patterns of end organ damage, diagnosis, treatment, and prevention of iron overload.

show abstract

“…Blood transfusion itself usually leads to a transient augmentation of lipid peroxidation products, 42 suggestive for oxidative stress, and prolonged transfusion therapy in infants and adults is associated with elevated NPBI levels in the plasma, 40 which may enhance further peroxidation. However, neither the NPBI levels nor the MDA concentrations increased with subsequent transfusion number in the RHD fetus, whereas the TRAP values increased.…”

Section: Discussionmentioning

confidence: 99%

Non‐protein‐bound iron and free radical damage in fetuses with rhesus haemolytic disease: influence of intrauterine transfusions

Luykx

Berger

Geerdink

et al. 2004

BJOG

View full text Add to dashboard Cite

Objective To determine iron-induced free radical damage in fetal rhesus haemolytic disease (RHD) before and after repeated intrauterine red blood cell transfusions and its relation to hydrops fetalis. Design Prospective, observational study.Setting Department of Obstetrics, Leiden University Medical Centre, the Netherlands.Population Fifty anaemic fetuses, including 13 hydropic ones, 9 preterm and 12 term neonates and 8 female non-pregnant adults. Methods Venous blood plasma samples were collected from 50 fetuses suffering from RHD preliminary to the first, and if appropriate, subsequent intrauterine red blood cell transfusions for determination of iron status including non-protein-bound iron (NPBI) and iron-binding primary antioxidant proteins, total plasma antioxidant capacity and its contributing secondary antioxidants (e.g. vitamin C, uric acid, sulphydryl groups and peroxidation products). Results were compared with values of healthy preterm and term neonates directly at birth and adult controls. Within the fetal haemolytic group, 13 hydropic fetuses were analysed as a separate group. Main outcome measures Non-protein-bound iron, antioxidants, total antioxidant capacity and peroxidation products. Sub analysis of the outcome measures of the hydropic fetuses. Results RHD fetuses had at initial cordocentesis a significantly higher NPBI level and a significantly lower total plasma antioxidant capacity than control babies and adults. Their vitamin C tended to be more oxidised but lipid peroxidation had not increased, when compared with preterm babies. The repeated intrauterine red blood cell transfusions had a positive effect on the total antioxidant capacity of plasma and did not increase the concentration of NPBI. The hydropic fetuses, who had higher NPBI concentrations and lower plasma protein concentrations and total antioxidant capacity, did not show more peroxidation products in plasma than the non-hydropic fetuses. Fetuses without reversal of hydrops despite intrauterine transfusions showed decreasing levels of proteins with subsequent transfusions but peroxidation products remained constant. Conclusion Repeated intrauterine red blood cell transfusions do not lead to free radical damage in the fetus in utero. Iron-induced free radical activity does not appear to play a causative role in the proceeding of hydrops fetalis in RHD.

show abstract

Non-transferrin-bound iron in long-term transfusion in children with congenital anemias

Cited by 49 publications

References 15 publications

Iron overload and toxicity: the hidden risk of multiple blood transfusions

Iron overload and toxicity: the hidden risk of multiple blood transfusions

Iron Overload in Sickle Cell Disease

Non‐protein‐bound iron and free radical damage in fetuses with rhesus haemolytic disease: influence of intrauterine transfusions

Contact Info

Product

Resources

About