falciparum malaria at the erythrocytic stage may involve one or more of the following mechanisms: -Inhibition of merozoite entry into the red cell -Impairment in intracellular growth of the parasite  --------Prevention of the erythrocyte lysis that occurs at the end of parasite maturation, which leads to release of merozoites into the bloodstream.

In the circulation and tissues, DFO binds iron and the iron bound form can be excreted efficiently in the urine and bile . This is accomplished via the following steps :     Iron released by the reticuloendothelial system following catabolism of senescent RBCs is chelated by DFO and immediately excreted in the urine     Unbound DFO is internalized by hepatic parenchymal cells, interacts with the chelatable intracellular iron pool, and is excreted in bile     DFO is able to remove iron directly from myocardial cells

THE ALPHA THALASSEMIA SYNDROMES: There are four alpha-thalassemia syndromes:     Alpha thalassemia-2 trait, reflecting the loss of one of the four alpha globin genes     Alpha thalassemia-1 trait, reflecting the loss of two of the four alpha globin genes     Hemoglobin H disease, in which three of the four alpha globin loci are nonfunctional     Hydrops fetalis with Hb Barts, in which none of the four alpha globin loci is functional

THE ALPHA THALASSEMIA SYNDROMES: There are four alpha-thalassemia syndromes:     Alpha thalassemia-2 trait, reflecting the loss of one of the four alpha globin genes     Alpha thalassemia-1 trait, reflecting the loss of two of the four alpha globin genes     Hemoglobin H disease, in which three of the four alpha globin loci are nonfunctional     Hydrops fetalis with Hb Barts, in which none of the four alpha globin loci is functional