Assessment of iron distribution between liver, spleen, pancreas, bone marrow, and myocardium by means of R2 relaxometry with MRI in patients with β-thalassemia major
✍ Scribed by Olympia Papakonstantinou; Efthymia Alexopoulou; Nikos Economopoulos; Odysseas Benekos; Antonis Kattamis; Stavroula Kostaridou; Vasilis Ladis; Efstathios Efstathopoulos; Athanassios Gouliamos; Nikolaos L. Kelekis
- Publisher
- John Wiley and Sons
- Year
- 2009
- Tongue
- English
- Weight
- 550 KB
- Volume
- 29
- Category
- Article
- ISSN
- 1053-1807
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✦ Synopsis
Abstract
Purpose
To investigate the correlation between the degree of hepatic, splenic, pancreatic, vertebral bone marrow (VBM), and myocardial siderosis, as expressed by relaxation rate (R2 = 1/T2) values, in patients with thalassemia.
Materials and Methods
R2 relaxation rate values of liver, spleen, VBM, pancreas, and myocardium were estimated in 68 consecutive transfusion‐dependent patients with β‐thalassemia major and 10 healthy controls using a respiratory triggered 16‐echo Carr‐Purcell‐Meiboom‐Gill (CPMG) spin echo sequence.
Results
Hepatic R2 values were significantly increased in all 68 patients; VBM, pancreatic, and myocardial R2 values were increased in 67/68, 35/47, and 47/61 patients, whereas five patients showed decreased pancreatic R2 attributed to fatty degeneration. Of the 39 nonsplenectomized patients, splenic R2 values were decreased in 30 and normal in nine patients. Hepatic R2 values correlated with splenic (r = 0.63, P < 0.001), VBM (r = 0.52, P < 0.001), but not with myocardial and pancreatic R2 values.
Conclusion
Despite positive correlations between the degree of hepatic, splenic, and VBM siderosis, as expressed by respective R2 values, there was variability of iron distribution patterns in thalassemic patients. Unpredictable patterns of iron distribution may be seen, such as normal signal of the spleen in the presence of siderotic liver, resembling primary hemochromatosis. Fatty degeneration of the pancreas was not uncommon. J. Magn. Reson. Imaging 2009;29:853–859. © 2009 Wiley‐Liss, Inc.