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Abstract Thalassemia major (TM) is a form of hemolytic anemia requiring monthly blood transfusions from early childhood with each RBC introducing 200mg of iron to the patient system that they lack the natural mechanism to eliminate [1]. However, iron overload has been exacerbated due to both transfusion and high iron absorption [2]. Despite the use of iron-chelating agents over the last three decades hemosidrosis still remains as one of the serious leading causes of death in patients with TM [3]. Iron deposition may affect all organs such as heart, liver and pancreas [4]. The risk for developing liver fibrosis and cirrhosis has been associated to the liver iron content (LIC) and the duration of iron exposure by the liver [5]. Liver failure is the third leading cause of death, after heart failure, and infectious diseases in patients with post transfusional iron over load. [6]. The prognosis of liver iron overload is highly dependent on the one hand on both liver iron content (LIC) and the extent of liver fibrosis and on the other hand on co-factors of hepatotoxicity such as viruses and alcohol [7]. Methods to estimate total body iron stores are required, and serum ferritin acts as a reliable marker but can yield false positive results in the presence of inflammation, fever and liver disease. Iron concentration in liver is considered as the reference method for direct measurement of body iron excess [8]. Liver biopsy is considered the gold-standard method for evaluating the stage of fibrosis and to measure the liver iron content (LIC) of hepatic tissue in patients with thalassemia [9]. However, this invasive technique has many procedure-related complications, as well as wide variations in the results and sampling errors [10]. |