Abstract
Children with β- thalassemia major experience significant cellular oxidative injury predominantly due to excessive breakdown of uncoupled globin chain and secondary iron overload. These processes contribute to cellular oxidative hassle damage affecting platelets & RBCs, potentially exacerbating ineffective erythropoiesis, the increase of risk of thromboembolic actions. Present study aimed to judge malondialdehyde (MDA), iron, vitamin E, Erythrocyte superoxide dismutase (ESOD), and consequence of 24 weeks of vitamin E supplementation in transfusion dependant β- thalassemia major. A prospective cross sectional before and after comparison study was conducted among 120 subjects were between age group 4 to 11 years. Six homozygous beta thalassemia cases were assessed at baseline and afterwards with vitamin E tablet (10U/kg/day) for 24 weeks with regular standard treatment, and they were compared with 60 age and sex matched controls. The intensities of MDA, ESOD and iron in serum were found to be significantly elevated (p<0.001) and the vitamin E level was significantly reduced (p< 0.001) in the cases as compared to controls. After the supplementation of the vitamin E orally for 24 weeks, significantly lowered (p<0.001) mean standards of MDA, iron and ESOD in blood, non- significantly Hb although vitamin E was significantly advanced (p<0.001), as compared to baseline. Recurrent blood transfusions consequence in undue free iron load in the blood, which indications to substantial generation of huge free radicals, ROS. Vitamin E orally can be harmless effective supplement to recover oxidative harm in thalassemic children. Besides it appears that a extended period of consuming antioxidant supplementations prerequisite to mark medical haematological expansion in β- thalassemia major children.
Keywords: Homozygous β- thalassemia, Vitamin E, Iron overload, Oxidative hassle