Novel approach to reactive oxygen species in nontransfusion-dependent thalassemia.

摘要: The term Nontransfusion dependent thalassaemia (NTDT) was suggested to describe patients who had clinical manifestations that are too severe be termed minor yet mild major. Those not entirely on transfusions for survival. If left untreated, three main factors responsible the sequelae of NTDT: ineffective erythropoiesis, chronic hemolytic anemia, and iron overload. Reactive oxygen species (ROS) generation in NTDT is caused by 2 major mechanisms. first one hypoxia resulting from anemia erythropoiesis leading mitochondrial damage second overload also due tissue increase intestinal absorption thalassemic patients. Oxidative reactive (generated free globin chains labile plasma iron) believed contributors cell injury, damage, hypercoagulability with thalassemia. Independently increased ROS has been linked a myriad pathological outcomes such as leg ulcers, decreased wound healing, pulmonary hypertension, silent brain infarcts, thrombosis count few. Interestingly many those complications overlap found