Abstract
Thalassemia is a genetic condition characterized by faulty hemoglobin synthesis and low hemoglobin concentration. Overload of iron is an unavoidable condition experienced by severe thalassemia patients as a result of excessive blood transfusions. We looked at impaired liver function in thalassemia individuals with Iraq as a result of these issues. Our findings demonstrated serum activity in hepatocytes, as well as a large rise in GOT and AIP in patients with elevated iron levels and a substantial rise in TSB. All of these elements may work together or independently to create chronic liver disease by causing damage in cells via oxidative mechanisms.
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