The quantitative and/or qualitative distribution of liver iron was assessed in 81 transfusion-dependent thalassemia major patients with chronic liver disease (36 with chronic active hepatitis, 23 with chronic persistent hepatitis, 22 with siderosis). Viral marker studies showed only 3 cases with both HBsAg and anti-HBc posiüvity in the serum, while the others had anti-HBc and anti-HBs or only anti-HBs or no B viral markers. A significantly higher iron overload was found in chronic hepatitis, particularly chronic active hepatitis, than in siderosis. This increased iron overload may be due to less intensive chelation treatment, higher intestinal absorption secondary to lower mean Hb levels, and/or to liver inflammation-depedent iron deposition. The liver iron overload in turn may facilitate the development or persistence of chronic progressive liver disease.

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