Clinical Information

Ferritin is a large spherical protein consisting of 24 noncovalently linked subunits with a molecular weight of approximately 450,000 D. The subunits form a shell surrounding a central core containing variable amounts of ferric hydroxyphosphate. One molecule of ferritin is capable of binding between 4000 and 5000 atoms of iron, making ferritin the major iron storage protein for the body.
Ferritin is found chiefly in the cytoplasm of cells of the reticuloendothelial system and is a constituent of normal human serum. The concentration of ferritin is directly proportional to the total iron stores in the body, resulting in serum ferritin concentrations becoming a common diagnostic tool in the evaluation of iron status.
In most normal adults, serum ferritin concentrations vary with age and sex. There is a sharp rise in serum ferritin concentrations in the first month of life, coinciding with the depression of bone marrow erythropoiesis. Within 2 or 3 months, erythropoiesis becomes reactivated and there is a drop in the concentration of serum ferritin. By 6 months, the concentration is reduced to fairly low levels where they remain throughout childhood. There is no sex difference until the onset of puberty, at which time ferritin concentrations rise, particularly in males. There is a significant positive correlation between age and serum ferritin concentrations in females, but not in males.
Patients with iron deficiency anemia have serum ferritin concentration approximately one-tenth of normal subjects, while patients with iron overload (hemochromatosis, hemosiderosis) have serum ferritin concentrations much higher than normal. Studies also suggest that serum ferritin provides a sensitive means of detecting iron deficiency at an early stage. Serum ferritin concentrations may serve as a tool to monitor the effects of iron therapy, but results should be interpreted with caution, as these cases may not always reflect the true state of iron stores. Ferritin is a positive acute phase reactant in both adults and children, whereby chronic inflammation results in a disproportionate increase in ferritin in relation to iron reserves. Elevated ferritin is also observed in acute and chronic liver disease, chronic renal failure, and in some types of neoplastic disease.
Evaluating body iron stores may include serum iron determination, total iron binding capacity (TIBC), and percent saturation of transferrin, however are subject to diurnal variations and may be less precise. Additionally, they do not discriminate between depleted iron stores (iron deficiency) and conditions associated with defective iron release (eg, anemia of chronic disease).