Background: Beta-thalassemia is a hereditary haemoglobinopathy caused by defective hemoglobin (Hb) β-globin synthesis, leading to excess α-globin chains that cause hemolysis and impair erythropoiesis. Ischemia modified albumin (IMA) is not a signal protein and not generated in pro-inflammatory state alone but rather an end product of oxidative stress. Objectives: The aim of the study was to evaluate ischemia modified albumin (IMA) and C-reactive protein (CRP) in children with β-thalassemia major and its relation to differ