Ann Hematol 2013 May;92(5):577-86
The management of iron overload in allogeneic hematopoietic stem cell transplant (alloHSCT) recipients: where do we stand?
Sivgin S, Eser B.
Iron overload (IO), primarily related to multiple red blood cell transfusions, is a relatively common complication in hematopoietic stem cell transplant (HSCT) recipients. Elevated pretransplant ferritin levels have been reported to increase the risk of non-relapse mortality following HSCT and might influence the risk of acute and chronic graft versus host disease. IO has been shown to be an important cause of mortality and morbidity in patients who have undergone alloHSCT (Armand et al., Blood 109:4586-4588, 2007; Kim et al., Acta Haematol 120:182-189, 2008; Kataoka et al., Biol Blood Marrow Transplant 15:195-204, 2009). We know that excessive iron accumulation results in tissue damage and organ failure, mainly as a result of the generation of free radicals that cause oxidative damage and organ dysfunction (e.g., hepatotoxicity, cardiotoxicity, and endocrine dysfunction) (Altes et al., Bone Marrow Transplantation 29: 987-989, 2002; Papanikolaou et al., Toxicol Appl Pharmac 202:199-211, 2005). In the last decade, efforts have been directed toward identifying alternative treatment for IO in alloHSCT recipients to maintain improved transplant outcomes.
, primarily related to multiple red blood cell transfusions, is a relatively common complication in hematopoietic stem cell transplant (HSCT) recipients. Elevated pretransplant ferritin levels have been reported to increase the risk of non-relapse mortality following HSCT and might influence the risk of acute and chronic graft versus host disease. IO has been shown to be an important cause of mortality and morbidity in patients who have undergone alloHSCT (Armand et al., Blood 109:4586-4588, 2007; Kim et al., Acta Haematol 120:182-189, 2008; Kataoka et al., Biol Blood Marrow Transplant 15:195-204, 2009). We know that excessive iron accumulation results in tissue damage and organ failure, mainly as a result of the generation of free radicals that cause oxidative damage and organ dysfunction (e.g., hepatotoxicity, cardiotoxicity, and endocrine dysfunction) (Altes et al., Bone Marrow Transplantation 29: 987-989, 2002; Papanikolaou et al., Toxicol Appl Pharmac 202:199-211, 2005). In the last decade, efforts have been directed toward identifying alternative treatment for IO in alloHSCT recipients to maintain improved transplant outcomes.