Haema 2012; 3(2): 134-142
by Alexandra Kourakli–Simeonidou, Argiris Simeonidis
Hematology Division, Dept of Internal Medicine, University of Patras Medical School, Patras
Abstract
Elementary iron, despite its pivotal role in many biological functions may become harmful, inducing oxidative stress. In the context of myelodysplastic syndromes (MDS), iron appears to con- tribute in the main biological features of these conditions, such as ineffective hematopoiesis, genomic instability and leukemic transformation. Intracellular excess of iron generates Reactive Oxygen Species (ROS), which have been implicated in the induction of cytotoxic, mutagenic, leukemogenic and proapoptotic effects, as it has been demonstrated in cell cultures and in many preclinical animal MDS models. Serum ferritin levels, transferring saturation, liver iron concentration and magnetic resonance imaging T2* of the heart and liver have been used as surrogate markers for the estimation of the total body iron overload. Liver biopsy is not a necessary intervention for patients with MDS. The use of iron chelating agents in iron overloaded transfusion-dependent patients with MDS, effectively prevents the induction of cellular and organ damage, whereas there is substantial evidence that hematopoiesis might also be improved, with the appearance of a reduced transfusion rate or of a complete transfusion independence, and in some cases with the inhibition of disease progression towards acute myelogenous leukemia (AML). Many official, national and international guidelines direct the application of iron chelation treatment in specific subgroups of MDS patients, aiming to improve the quality of life, prolong overall survival and reduce vital organ damage, and possibly the risk of leukemic transformation. Iron chelation has recently been proposed as an important part of supportive treatment for allotransplanted patients in the pre- and post-transplantation setting.