Abstract
Sickle Cell Anemia (SCA), characterized by the presence of Hb S in homozygous, presents physiopathological events as hemolysis and vaso-occlusion, leading to ischemia-reperfusion injury with consequent clinical manifestations such as acute chest syndrome (ACS), crises of pain and priapism. These manifestations can be aggravated by genetic polymorphisms involved in some metabolic pathways …