Myocyte Damage and Loss of Myofibers is the Potential Mechanism of Iron Overload Toxicity in Congestive Cardiac Failure in Thalassemia. Complete Reversal of the Cardiomyopathy and Normalization of Iron Load by Deferiprone-Reference-Cited by-同舟云学术

Myocyte Damage and Loss of Myofibers is the Potential Mechanism of Iron Overload Toxicity in Congestive Cardiac Failure in Thalassemia. Complete Reversal of the Cardiomyopathy and Normalization of Iron Load by Deferiprone

Published:2008-01 Issue:1-2 Volume:32 Page:17-28
ISSN:0363-0269
Container-title:Hemoglobin
language:en
Short-container-title:Hemoglobin

Author:

Kolnagou Annita,Michaelides Yiannis,Kontos Christos,Kyriacou Kyriacos,Kontoghiorghes George J.

Publisher

Informa UK Limited

Subject

Biochemistry (medical),Clinical Biochemistry,Genetics (clinical),Hematology

Link

http://www.tandfonline.com/doi/pdf/10.1080/03630260701726491

Reference25 articles.

1. Survival in β-thalassaemia major in the UK: data from the UK Thalassaemia Register

2. Advances in Iron Overload Therapies. Prospects for Effective Use of Deferiprone (L1), Deferoxamine, the New Experimental Chelators ICL670, GT56-252, L1NAll and their Combinations

3. T2 relaxation time study of iron overload in b-thalassemia

4. Low Serum Ferritin Levels are Misleading for Detecting Cardiac Iron Overload and Increase the Risk of Cardiomyopathy in Thalassemia Patients. The Importance of Cardiac Iron Overload Monitoring Using Magnetic Resonance Imaging T2 and T2*

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