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Transfusion Medicine / Iron Overload

Platelet Transfusion

RBC Transfusion

Iron Overload 

Figure C (below): 
  • Non-transferrin bound Iron that eventually spills in due to less transferrin is the major mediator of extra hepatic tissue damage
  • Such non-trasnferrin bound Iron enters specific cells that includes hepatocytes, cardiomyocytes, anterior pituitary cells, and pancreatic beta- cells. In these cells, iron accumulation leads to the generation of reactive oxygen species, result- ing in damage to lipids, proteins, DNA, and subcellular organelles, including lysosomes and mitochondria. This injury may result in cellular dysfunction, apoptosis, and necrosis 
Figure D (Below)
  1. Therapy with chelating agents that form a complex with iron and promote its excretion can clear plasma non–transferrin-bound iron, remove excess iron from cells, and maintain or return body iron to safe levels  

Two iron-chelating agents are approved for use in North America: 

  • parenteral deferoxamine mesylate (Desferal, Novartis) and 
  • oral deferasirox (Exjade, Novartis). 

Ideally, iron-chelating therapy should be initi- ated prophylactically, before clinically significant iron accumulation has occurred. Treatment should begin when patients have received between 10 and 20 red-cell transfusions.

Evaluation of the patient before the initiation or adjustment of iron-chelating therapy includes a detailed characterization of the underlying dis- order, with thorough documentation of the his- tory of transfusion and chelation; determination of the body iron load by measurement of the hepatic iron and serum ferritin concentrations; estimation of the rate of transfusional iron load- ing; and assessment of cardiac iron deposition  

The dose of an iron-chelating agent is deter-mined by three principal factors: the presence or absence of cardiac iron overload, the rate of transfusional iron loading, and the body iron burden 

Transfusion Medicine and Clinical Immunology