Transition of Thalassaemia and Friedreich ataxia from fatal to chronic diseases

Figure 1 The organisational health structure and the chronological development of Thalassaemia in Cyprus. WHO: World Health Organization.

Figure 2 The mode of chelating and antioxidant activity of deferiprone in Friedreich Ataxia. Deferiprone can chelate intracellular and intramitochondrial iron deposits and labile low molecular weight (LMwt) iron, which are responsible for the catalytic formation of toxic free radicals and toxic byproducts. It can inhibit iron toxicity related damage to the heart and brain of Friedreich ataxia patients.

Figure 3 The chemical structure of the iron chelating drug deferiprone (L1). Deferiprone can bind iron through the two molecules of oxygen. It is a bidentate chelator and at physiological pH three molecules of L1 are used for binding one molecule of iron.