Blood Res  
Role of redox iron towards an increase in mortality among patients: a systemic review and meta-analysis
Sankalp Sharma
Department of Transfusion Medicine and Blood Bank, All India Institute of Medical Sciences, Chhattisgarh, India
Correspondence to: Sankalp Sharma, M.D.
Department of Transfusion Medicine and Blood Bank,
Gate Number 1, Hospital Block – A, GE Road,
All India Institute of Medical Sciences, Raipur, Raipur Chhattisgarh, India
Published online: April 11, 2019.
© The Korean Journal of Hematology. All rights reserved.

An increase in non-transferrin bound iron (NTBI) was evaluated with the following objectives: (a) Iron overload conditions and redox iron (ROS) imbalance mediated mortality (b) Intervention with iron and iron
containing drugs in context to redox iron levels and mortality.
The citations were accessed with the URL: ascending; Protocol registration ID: CRD42018093657 Prospero.
Redox iron levels are increased during dyserythropoiesis and among transfusion recipient population and are re
sponsive to iron-chelation therapy. Near expiry ‘stored blood units’ showed a significant rise in the ROS levels. Iron
mediated ROS damage may be estimated by the serum antioxidant level, and showed reduction in toxicity with high antioxidant, low pro-oxidant levels. Iron drug therapy causes a significant increase in NTBI and labile iron levels. However, hospitalized patients on iron therapy showed lower mortality. Serum ferritin is a mortality indicator among the high-dose iron therapy and transfusion dependent population.
The cumulative difference of pre-chelation to post chelation ROS iron level was 0.97 (0.62; 1.32; N=261) among the
transfusion dependent subjects and 1.09 (0.73-1.45; N= 80) in the post iron therapy ‘iron ROS’ group. In conclusion,
iron mediated mortality can be determined by serum ferritin levels rather than the redox iron among multi-transfused
and iron overloaded patients.
Keywords: Chelation Antioxidants, Hepcidin, Non Transferrin Bound Iron, Pro-oxidant effect, Serum Ferritin,
Transferrin Saturation


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