Spleen R2 and R2* in iron‐overloaded patients with sickle cell disease and thalassemia major

Brewer, Cheryl A.; Coates, Thomas D.; Wood, John C.

doi:10.1002/jmri.21666

Cited by 61 publications

(67 citation statements)

References 45 publications

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“…With regard to splenic iron quantification, there was a common assumption in human studies that SIC quantification could be derived from the LIC quantification formula (18,19). In contrast, our study showed significant differences between the estimation formulas of LIC and SIC, whatever the chosen MRI parameter.…”

Section: Discussioncontrasting

confidence: 68%

MRI quantification of splenic iron concentration in mouse

Hitti

Éliat

Abgueguen

et al. 2010

Magnetic Resonance Imaging

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Purpose: To quantify hepatic and splenic iron load, which is a critical issue for iron overload disease diagnosis. MRI is useful to noninvasively determine liver iron concentration, but not proven to be adequate for robust evaluation of splenic iron load. We evaluated the usefulness of MRI-derived parameters to determine splenic iron concentration in mice. Materials and Methods:A mouse model of experimental iron load was used. Multi-echo spin-echo images of liver and spleen were acquired at 4.7 Tesla. The parameters were tested at all echoes with and without an external reference. Splenic and hepatic iron concentrations were determined using biochemical assay as the gold standard.Results: Our results show that (i) use of an internal or external reference is essential; (ii) optimal echo times were TE ¼ 19.5 ms and TE ¼ 32.5 ms for the liver and spleen, respectively; (iii) in the liver, the relationship between biochemical and MRI iron concentration determinations is logarithmic; (iv) in the spleen, the best relationship is an inverse function. Conclusion:A single spin-echo sequence allows robust estimation of hepatic and splenic iron content. Parameters classically used for hepatic iron concentration cannot be applied to splenic iron determination, which requires both the specific sequence and the adapted fitting function.

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Section: Discussioncontrasting

confidence: 68%

MRI quantification of splenic iron concentration in mouse

Hitti

Éliat

Abgueguen

et al. 2010

Magnetic Resonance Imaging

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“…Further, the significantly longer duration of exposure to transfusion and chelation in splenectomized patients would also be explained by the older age of these patients rather than their contribution to cardiac iron content as the duration of transfusion and chelation did not differ significantly in patients with cardiac iron loading compared with noncardiac iron loading patients. In line with the observation of Brewer et al, 12 it could be speculated that removing the iron-buffering capacity of the spleen by splenectomy may contribute to myocardial iron loading.…”

Section: Discussionmentioning

confidence: 67%

Myocardial Iron Loading in Patients With Thalassemia Major in Turkey and the Potential Role of Splenectomy in Myocardial Siderosis

Aydınok¹,

Bayraktaroğlu²,

Yıldız³

et al. 2011

Journal of Pediatric Hematology/Oncology

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Iron-induced cardiac disease is the leading cause of death in thalassemia major (TM). Splenectomy is performed in TM to reduce transfusion requirements and iron intake. Prevalence of myocardial siderosis and its relationship with splenectomy in 146 patients with TM were investigated. The patients with myocardial siderosis (T2*<20 ms) accounted for 42% of the cohort. Splenectomized patients had a higher incidence of myocardial siderosis (48%) compared with those having intact spleen (28%) and significantly higher myocardial iron content. Higher myocardial iron content in splenectomized patients may deserve special attention for the role of spleen in iron regulation.

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“…A relationship between pancreatic and cardiac R2* was predictable given that both organs take up NTBI. 8 The relatively high linear correlation in TM patients suggests a graded response in both tissues and has been reported by us 14 and by others. 4 In the present study, the relationship was maintained across multiple time points (an average of 2 studies per patient).…”

Section: Discussionmentioning

confidence: 84%

Pancreatic iron loading predicts cardiac iron loading in thalassemia major

Noetzli¹,

Papudesi²,

Coates

et al. 2009

Blood

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Diabetes mellitus and cardiomyopathy are common in chronically transfused thalassemia major patients, occurring in the second and third decades of life. We postulated that pancreatic iron deposition would precede cardiac iron loading, representing an environment favorable for extrahepatic iron deposition. To test this hypothesis, we examined pancreatic and cardiac iron in 131 thalassemia major patients over a 4-year period. Cardiac iron (R2* > 50 Hz) was detected in 37.7% of patients and pancreatic iron (R2* > 28 Hz) in 80.4% of patients. Pancreatic and cardiac R2* were correlated (r 2 ‫؍‬ 0.52), with significant pancreatic iron occurring nearly a decade earlier than cardiac iron. A pancreatic R2* less than 100 Hz was a powerful negative predictor of cardiac iron, and pancreatic R2* more than 100 Hz had a positive predictive value of more than 60%. In serial analysis, changes in cardiac iron were correlated with changes in pancreatic iron (r 2 ‫؍‬ 0.33, IntroductionIron overload is common in chronically transfused thalassemia major (TM) patients. Liver iron is a surrogate for total body iron burden 1 and has been used for years to monitor chelation therapy in thalassemia patients. 2 Liver iron quantification by magnetic resonance imaging (MRI) is well validated and becoming increasingly routine at major thalassemia centers. 3 It is also now possible to directly image preclinical iron deposition in heart tissue and endocrine glands. 4,5 Extrahepatic tissues have different kinetics of iron uptake and clearance than the liver 6,7 because they selectively, or near selectively, load circulating non-transferrin-bound iron (NTBI). 8 As a result, cardiac iron accumulation exhibits threshold behavior with respect to liver iron concentration 9 and is quite sensitive to the duration of iron chelation therapy. 10 In contrast, the liver is the dominant storage depot for transferrin-mediated iron uptake and fluctuates proportionally to global iron balance. 11 As a result, cross-sectional correlations between heart and liver iron loading are poor 5,12 and longitudinal relationships exhibit complicated, highly nonlinear behaviors. 7 More importantly, dangerous heart iron accumulation and cardiac dysfunction can occur despite apparently superb control of liver iron during prospective longitudinal evaluation. 7,13 These observations demonstrate that iron chelation therapy sufficient for neutral or negative liver iron balance may be inadequate to protect the heart in some patients.Because the heart and pancreas predominantly load NTBI, iron burdens in these organs should be more closely correlated to one another than between the heart and the liver. 8 Recent work by Au et al 4 and by our laboratory 14 supports this hypothesis. Because glucose intolerance/diabetes are common comorbidities with cardiac dysfunction, 11,15 we postulated that pancreatic iron uptake might predict cardiac iron deposition in a clinically useful manner. To test this hypothesis, we compared pancreatic, hepatic, and cardiac iron loading in 131 patients with...

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Spleen R2 and R2* in iron‐overloaded patients with sickle cell disease and thalassemia major

Cited by 61 publications

References 45 publications

MRI quantification of splenic iron concentration in mouse

MRI quantification of splenic iron concentration in mouse

Myocardial Iron Loading in Patients With Thalassemia Major in Turkey and the Potential Role of Splenectomy in Myocardial Siderosis

Pancreatic iron loading predicts cardiac iron loading in thalassemia major

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