Fig. 3.
Fig. 3. Prussian blue stain showing (top figures) hepatic iron in hepatocytes and portal macrophages, before (left) and after (right) 9 months of chelating therapy with the orally active chelating agent deferiprone in a patient with homozygous β thalassemia. Hepatic iron concentration in the sample on left was approximately 16 mg/g dry weight liver tissue; in that on the right hepatic iron concentration was less than 2 mg/g dry weight tissue. Coronal MRI (lower figures) of hepatic iron before (left) and after (right) therapy with the orally active iron chelating agent deferiprone in the same patient. Complete absence of liver signal in the MRI on the left is compatible with significant iron deposition, while improvement in signal intensity after 9 months of therapy (right) indicates that the liver iron content is reduced compared with that of the previous study. (Reprinted with permission.192 )

Prussian blue stain showing (top figures) hepatic iron in hepatocytes and portal macrophages, before (left) and after (right) 9 months of chelating therapy with the orally active chelating agent deferiprone in a patient with homozygous β thalassemia. Hepatic iron concentration in the sample on left was approximately 16 mg/g dry weight liver tissue; in that on the right hepatic iron concentration was less than 2 mg/g dry weight tissue. Coronal MRI (lower figures) of hepatic iron before (left) and after (right) therapy with the orally active iron chelating agent deferiprone in the same patient. Complete absence of liver signal in the MRI on the left is compatible with significant iron deposition, while improvement in signal intensity after 9 months of therapy (right) indicates that the liver iron content is reduced compared with that of the previous study. (Reprinted with permission.192 )

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