BIOMAT Database Logo BIOMAT Database Logo

Oxidative stress and inflammation in iron-overloaded patients with beta-thalassaemia or sickle cell disease. 2006

Patrick B Walter, and Ellen B Fung, and David W Killilea, and Qing Jiang, and Mark Hudes, and Jacqueline Madden, and John Porter, and Patricia Evans, and Elliott Vichinsky, and Paul Harmatz
Children's Hospital Oakland Research Institute, Oakland, CA 94609, USA.

Blood transfusion therapy is life-saving for patients with beta-thalassaemia and sickle cell disease (SCD), but often results in severe iron overload. This pilot study examined whether the biomarkers of tissue injury or inflammation differ in these two diseases. Plasma malondialdehyde (MDA) was significantly increased 1.8-fold in thalassaemia relative to control patients. In contrast, MDA in SCD was not significantly different from controls. In multivariate analysis, the strongest predictors of elevated MDA were liver iron concentration (P < 0.001) and specific diagnosis (P = 0.019). A significant 2-fold elevation of non-transferrin bound iron (NTBI) was observed in thalassaemia relative to SCD. NTBI was not a significant predictor of high MDA in multivariate analysis. SCD patients showed a significant 2.2-fold elevation of the inflammatory marker interleukin (IL)-6 relative to controls, and a 3.6- and 1.7-fold increase in IL-5 and IL-10 relative to thalassaemia. Although alpha-tocopherol was significantly decreased by at least 32% in both thalassaemia and SCD, indicating ongoing oxidant stress and antioxidant consumption, gamma-tocopherol, a nitric oxide-selective antioxidant, was increased 36% in SCD relative to thalassaemia. These results demonstrate that thalassaemia patients have increased MDA and circulating NTBI relative to SCD patients and lower levels of some cytokines and gamma-tocopherol. This supports the hypothesis that the biology of SCD may show increased inflammation and increased levels of protective antioxidants compared with thalassaemia.

UI MeSH Term Description Entries
D007249 Inflammation A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function. Innate Inflammatory Response,Inflammations,Inflammatory Response, Innate,Innate Inflammatory Responses
D007378 Interleukins Soluble factors which stimulate growth-related activities of leukocytes as well as other cell types. They enhance cell proliferation and differentiation, DNA synthesis, secretion of other biologically active molecules and responses to immune and inflammatory stimuli. Interleukin
D007501 Iron A metallic element with atomic symbol Fe, atomic number 26, and atomic weight 55.85. It is an essential constituent of HEMOGLOBINS; CYTOCHROMES; and IRON-BINDING PROTEINS. It plays a role in cellular redox reactions and in the transport of OXYGEN. Iron-56,Iron 56
D008099 Liver A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances. Livers
D008297 Male Males
D008315 Malondialdehyde The dialdehyde of malonic acid. Malonaldehyde,Propanedial,Malonylaldehyde,Malonyldialdehyde,Sodium Malondialdehyde,Malondialdehyde, Sodium
D002097 C-Reactive Protein A plasma protein that circulates in increased amounts during inflammation and after tissue damage. C-Reactive Protein measured by more sensitive methods often for coronary heart disease risk assessment is referred to as High Sensitivity C-Reactive Protein (hs-CRP). High Sensitivity C-Reactive Protein,hs-CRP,hsCRP,C Reactive Protein,High Sensitivity C Reactive Protein
D002648 Child A person 6 to 12 years of age. An individual 2 to 5 years old is CHILD, PRESCHOOL. Children
D005260 Female Females
D005293 Ferritins Iron-containing proteins that are widely distributed in animals, plants, and microorganisms. Their major function is to store IRON in a nontoxic bioavailable form. Each ferritin molecule consists of ferric iron in a hollow protein shell (APOFERRITINS) made of 24 subunits of various sequences depending on the species and tissue types. Basic Isoferritin,Ferritin,Isoferritin,Isoferritin, Basic

Related Publications

Patrick B Walter, and Ellen B Fung, and David W Killilea, and Qing Jiang, and Mark Hudes, and Jacqueline Madden, and John Porter, and Patricia Evans, and Elliott Vichinsky, and Paul Harmatz
Oxidative stress in β-thalassaemia and sickle cell disease.
December 2015, Redox biology,
Patrick B Walter, and Ellen B Fung, and David W Killilea, and Qing Jiang, and Mark Hudes, and Jacqueline Madden, and John Porter, and Patricia Evans, and Elliott Vichinsky, and Paul Harmatz
The thalassaemia syndromes. VI. Two subtypes of sickle cell-beta thalassaemia disease: (a) normocytic type of sickle cell-beta thalassaemia disease (b) microcytic type of sickle cell-beta thalassaemia disease.
January 1967, Acta haematologica,
Patrick B Walter, and Ellen B Fung, and David W Killilea, and Qing Jiang, and Mark Hudes, and Jacqueline Madden, and John Porter, and Patricia Evans, and Elliott Vichinsky, and Paul Harmatz
Magnetic resonance imaging in the evaluation of iron overload in patients with beta thalassaemia and sickle cell disease.
September 2004, British journal of haematology,
Patrick B Walter, and Ellen B Fung, and David W Killilea, and Qing Jiang, and Mark Hudes, and Jacqueline Madden, and John Porter, and Patricia Evans, and Elliott Vichinsky, and Paul Harmatz
Spleen R2 and R2* in iron-overloaded patients with sickle cell disease and thalassemia major.
February 2009, Journal of magnetic resonance imaging : JMRI,
Patrick B Walter, and Ellen B Fung, and David W Killilea, and Qing Jiang, and Mark Hudes, and Jacqueline Madden, and John Porter, and Patricia Evans, and Elliott Vichinsky, and Paul Harmatz
Microarray analysis of liver gene expression in iron overloaded patients with sickle cell anemia and beta-thalassemia.
June 2009, American journal of hematology,
Patrick B Walter, and Ellen B Fung, and David W Killilea, and Qing Jiang, and Mark Hudes, and Jacqueline Madden, and John Porter, and Patricia Evans, and Elliott Vichinsky, and Paul Harmatz
Fracture prevalence and relationship to endocrinopathy in iron overloaded patients with sickle cell disease and thalassemia.
July 2008, Bone,
Patrick B Walter, and Ellen B Fung, and David W Killilea, and Qing Jiang, and Mark Hudes, and Jacqueline Madden, and John Porter, and Patricia Evans, and Elliott Vichinsky, and Paul Harmatz
Sickle cell beta-thalassaemia compared with sickle cell anaemia in Algeria.
April 1984, Scandinavian journal of haematology,
Patrick B Walter, and Ellen B Fung, and David W Killilea, and Qing Jiang, and Mark Hudes, and Jacqueline Madden, and John Porter, and Patricia Evans, and Elliott Vichinsky, and Paul Harmatz
Non-haem iron-mediated oxidative stress in haemoglobin E beta-thalassaemia.
January 2010, Annals of the Academy of Medicine, Singapore,
Patrick B Walter, and Ellen B Fung, and David W Killilea, and Qing Jiang, and Mark Hudes, and Jacqueline Madden, and John Porter, and Patricia Evans, and Elliott Vichinsky, and Paul Harmatz
Sickle-cell haemolglobin C disease and sickle-cell beta thalassaemia in white South Africans.
September 1972, South African medical journal = Suid-Afrikaanse tydskrif vir geneeskunde,
Patrick B Walter, and Ellen B Fung, and David W Killilea, and Qing Jiang, and Mark Hudes, and Jacqueline Madden, and John Porter, and Patricia Evans, and Elliott Vichinsky, and Paul Harmatz
Sickle cell beta thalassaemia in Jamaica.
November 1973, The British journal of radiology,
Copied contents to your clipboard!