Diagnosing iron deficiency and iron-overload conditions
Clinical Information Discusses physiology, pathophysiology, and general clinical aspects, as they relate to a laboratory test
Ferritin is a high-molecular-weight protein that contains approximately 20% iron. It occurs normally in almost all tissues of the body but especially in hepatocytes and reticuloendothelial cells, where it serves as an iron reserve. Ferritin is also present in the serum in minute amounts, where it appears to reflect iron stores in normal individuals.
Ferritin plays a significant role in the absorption, storage, and release of iron. As the storage form of iron, ferritin remains in the body tissues until it is needed for erythropoiesis. When needed, the iron molecules are released from the apoferritin shell and bind to transferrin, the circulating plasma protein that transports iron to the erythropoietic cells.
A low serum ferritin value is thought to be the best laboratory indicator of iron depletion. Virtually all patients with low serum iron and low ferritin have iron deficiency. Serum ferritin is clinically useful in distinguishing between iron-deficiency anemia (serum ferritin levels diminished) and "anemia of chronic disease" (serum ferritin levels usually normal or elevated). Serum ferritin is a good screening test in separating erythrocyte microcytosis due to iron deficiency (low values) from microcytosis related to thalassemia minor (normal or high values). An iron-depletion state with a decreased serum ferritin value is quite common among menstruating and reproductively active females and in children.
Ferritin is an acute phase reactant. A normal serum ferritin value, therefore, cannot be used to exclude iron deficiency if a hepatic, malignant, or inflammatory condition is present.
A high serum ferritin value is seen in hemochromatosis and other iron-overload states, as well as acute hepatitis, Gaucher disease, malignancies, and chronic inflammatory disorders.
Reference Values Describes reference intervals and additional information for interpretation of test results. May include intervals based on age and sex when appropriate. Intervals are Mayo-derived, unless otherwise designated. If an interpretive report is provided, the reference value field will state this.
Males: 24-336 mcg/L
Females: 11-307 mcg/L
Hereditary hemochromatosis or other iron-overload states, acute hepatitis, and Gaucher disease are associated with very high serum ferritin levels. Slight-to-moderate elevation occurs in many malignancies and in chronic inflammatory disorders.
Iron deficiency (uncomplicated)
Males: <24 mcg/L
Females: <11 mcg/L
Males: >336 mcg/L
Females: >307 mcg/L
In hemochromatosis, ferritin is often >1,000 mcg/L
For more information about hereditary hemochromatosis testing, see Hereditary Hemochromatosis Algorithm in Special Instructions.
Cautions Discusses conditions that may cause diagnostic confusion, including improper specimen collection and handling, inappropriate test selection, and interfering substances
A normal serum ferritin value cannot be used to exclude iron deficiency if a hepatic, malignant, or inflammatory condition is present (ferritin is an acute phase reactant).
Some patients who have been exposed to animal antigens, either in the environment or as part of treatment or imaging procedure, may have circulating antianimal antibodies present. These antibodies may interfere with the assay reagents to produce unreliable results.
Clinical Reference Provides recommendations for further in-depth reading of a clinical nature
1. Fairbanks VF, Beutler E: Iron Metabolism. In Williams Hematology. Edited by E Beutler, MA Lichtman, BS Coller, et al. New York. McGraw-Hill Book Company, 2001, pp 295-304
2. Fairbanks VF, Brandhagen DJ: Disorders of iron storage and transport. In Williams Hematology. Edited by E Beutler, MA Lichtman, BS Coller, et al. New York. McGraw-Hill Book Company, 2001, pp 489-502
3. Brugnara C: Iron deficiency and erythropoiesis: new diagnostic approaches. Clin Chem 2003 Oct;49(10):1573-1578
4. Schilsky ML, Fink S: Inherited metabolic liver disease. Curr Opin Gastroenterol 2006 May;22(3):21