Ferritin is a high-molecular weight iron-containing protein that functions in the body as an iron storage compound. Each ferritin molecule is thought to consist of a spherical protein shell of molecular weight about 460,000 daltons made up of 24 subunits with a variable amount of iron as a core of ferricoxide-phosphate. It has been demonstrated that the ferritin molecule, when fully saturated, may consist of over 20% iron by weight.
Approximately 25% of the iron in a normal adult is present in various storage forms. About two-thirds of the iron stores in the human body exist in the form of ferritin. The remaining iron stores are contained in insoluble hemosiderin, which most likely represents a form of denatured ferritin. The availability of sensitive methods for measuring serum ferritin have significantly advanced the ability to detect iron deficiency and overload. Since iron deficiency is present before the onset of anemia, detection of an iron depleted state is important for the control of nutritional anemia. The clinical assessment of iron stores has historically relied on the determination of serum iron, total ironbinding capacity (TIBC) and percent transferrin (ratio of serum iron and TIBC) or direct examination of bone marrow. The estimation of stainable iron in the bone marrow is the traditional method for
assessing body iron stores. This biopsy method provides a sensitive index of iron deficiency but has the disadvantage of being subjective and semiquantitative. Low hemoglobin concentration is the most readily available sign of anemia, but a significant fall in circulating hemoglobin cannot be detected until the final stage of iron deficiency anemia. Serum iron, TIBC and percent transferrin saturation do not distinguish iron deficiency as a progressive disease. Also, these measurements are affected by diurnal variation and may not discriminate between depleted iron stores and conditions associated with defective reticuloendothelial release of iron (e.g., anemia of chronic disease). Recent literature suggests that ferritin provides a more sensitive, specific and reliable measurement for determining iron deficiency at an early stage. In patients being given iron orally, serum ferritin measurements have been shown to be useful for monitoring the reaccumulation of iron stores and determining when therapy can be discontinued. In chronic inflammatory disorders, infections, and in chronic renal failure, there is a disproportionate increase in serum ferritin levels in relation to iron stores. The correlation of serum ferritin to body iron stores still exists, however, it is set at a higher level of serum ferritin. Numerous studies in the literature demonstrate the usefulness and necessity of serum ferritin measurements in combination with other parameters in determining the rate and degree of body iron overload in such disorders as thalassemia, sideroblastic anemia and in determining the response of patients treated with iron chelating agents. Specifically, the combined use of serum ferritin levels and mean corpuscular volume (MCV) has made differentiation between iron deficiency, beta-thalassemia trait and normal subjects possible at a very high level of accuracy.
1. Manufacturer’s Reagent package inserts Architect Ferritin, November 2015, Abbott Ireland, Diagnostic Division Lisnamuck Longford Co., Ireland.
2. (*) Reference intervals (normal values) : Method Validation/Verification Reference Range Establishment for Architect System (Retrieved: Year 2014)