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Persons in this latter group develop more severe iron overload, and many become transfusion dependent in adulthood.Efficiency of erythropoiesis and effect of transfusion in β-thalassemia.

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Patients with TI may maintain Hb concentrations between 6 and 9 g/d L and may be asymptomatic or have manifestations of a hyperhemolytic phenotype with marked EMH, resulting in hepatosplenomegaly and skeletal abnormalities.In either clinical syndrome, relative excess of α-globin synthesis leads to formation of hemichromes and increased erythroid precursor apoptosis (Figure 1A), causing IE, extramedullary expansion, and splenomegaly.contribute to iron overload that, if left untreated, accounts for most of the morbidity and mortality in this disease.In contrast, decreased iron intake limits hemichrome and ROS formation, ameliorating IE by reducing apoptosis, and improving erythrocyte survival in circulation. Patients with TI are usually transfusion independent with a clinical course intermediate in severity between TM and asymptomatic heterozygotes (Figure 2A).Coinherited genetic traits that influence the balance of α/β globin synthesis (eg, persistent production of Hb F and coinheritance of α-thalassemia) may ameliorate or exacerbate disease severity in β-thalassemia, resulting in some phenotypic variation.

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