Editorial Retrospective

Abstract

The more severe forms of β-thalassemia, which are among the commonest single-gene disorders in the world, are particularly distressing, because affected children who receive adequate transfusions grow and develop normally, only to die of cardiac failure secondary to iron loading of the myocardium toward the end of the second decade.¹ Although chelating agents, such as deferoxamine, were introduced in the early 1960s to treat iron loading in thalassemia,² early experiences were disappointing, and their use was largely abandoned. However, in 1974 a small study carried out in London showed that patients with β-thalassemia who had received regular bolus injections of . . .