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Ferritin is an intracellular iron storage molecule that stores iron in a form readily accessible to cells, and then releases it in a controlled fashion in response to the body's needs. Therefore ferritin can act as a "buffer" against iron storage problems by releasing more if the body is iron deficient, or to some extent, by storing excess iron if the blood and body tissues are iron overloaded (1). The ferritin molecule forms a hollow sphere capable of holding as many as 4500 ferric (Fe³⁺) iron atoms (2). Ferritin is found in measurable quantities within the blood as serum ferritin, but is located predominantly within reticuloendothelial macrophages and hepatocytes. Presumably, most other cells synthesize ferritin as well.

Ferritin

Under steady-state conditions, serum ferritin levels correlate with total body iron. Increasing serum ferritin levels may be one of the first clinical signs of iron overload. As cellular iron storage capacity is exceeded, excess ferritin-bound iron is released into the bloodstream.

Normal serum ferritin levels differ for males (<300 ng/mL) and females (<150 ng/mL). Mild-to-moderate iron overload is indicated by serum ferritin levels of 300-2500 ng/mL, while levels >2500 ng/mL are associated with an increased risk of cardiac disease (3). Serum ferritin >1000 has been shown to be associated with adverse outcomes in both primary and secondary iron overload.

Ferritin is an acute-phase reactant, so can be naturally elevated during the course of disease. Inflammation and infections, ascorbate levels, abnormal liver function, and increased erythropoiesis can influence circulating ferritin levels. As such, a single measure of ferritin is not clinically useful; however, serial assessment is convenient, and is valuable for estimating body iron stores and for monitoring chelation therapy.