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AbstractIntroduction. Cardiovascular involvement represents a well-known complicationand theprimary cause of mortality, both in transfusion-dependent beta thalassemia major (β-TM) and intransfusion-independent beta thalassemia intermedia (β-TI). In β-TM, heart iron overload isconsidered the main cause of this complication. This is likely due to poor adherenceto iron-chelating therapy, resulting in the inability of the body to efficiently remove iron excess derivedfrom transfused red blood cell breakdown. Different clinical pictures may instead be evoked incardiovascular involvement occurring in β-TI; however, until now, no factor has emerged as themajor one responsible for these complications. Design and Methods. In the present study, iron status, and lipid profiles in serum, as well aslipid content in peripheral blood mononuclear cells (PBMCs) were evaluated in 70 adult β-TMand in 22 adult β-TI patients. Ninety-two age-matched blood donors, free from any form ofthalassemia,were utilized as controls. The mRNA levels of genes involved in the regulation ofiron metabolism, such as interleukine 1 alfa (IL1α), tumor necrosis factor alfa (TNFα), as wellas those involved in cholesterol homeostasis, such as acetyl-coenzymeA: cholesterolacyltransferase (ACAT-1), neutral cholesterol ester hydrolase (nCEH), and ATP bindingcassette-A (ABCA1), were also evaluated in PBMCs from the above subjects.

Chronic hyperplastic anemia as an independent risk factor for atherosclerotic lesions: a lesson from thalassemia intermedia