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Diagnose hypochromic, microcytic anemias. Decreased in iron deficiency anemia and increased in iron overload. Ferritin levels correlate with and are useful in evaluation of total body storage iron. In hemochromatosis, both ferritin and iron saturation are increased. Ferritin levels in hemochromatosis may be >1000 ng/mL.
Ferritin is an acute-phase reactant and thus may be increased in people with inflammation, liver disease, chronic infection, autoimmune disorders, and some types of cancer. Ferritin measurement is of limited usefulness during pregnancy because it diminishes late in pregnancy, even when bone marrow iron is present.
As with all tests containing monoclonal mouse antibodies, erroneous findings may be obtained from samples taken from patients who have been treated with monoclonal mouse antibodies or have received them for diagnostic purposes.1 In rare cases, interference due to extremely high titers of antibodies to streptavidin and ruthenium can occur.1
Ferritin is found in virtually all cells of the body and serves as the cellular storage repository for iron.2,3 Ferritin is a macromolecule with an average molecular weight of near 440 kD that varies depending on the iron content. Ferritin consists of a protein shell (apoferritin) of 24 subunits surrounding an iron core consisting of up to 4000 ferric iron ions. The majority of ferritin iron stores are found in the liver, spleen, and bone marrow. Ferritin is present in small concentration correlates with total-body iron stores, making its measurement valuable for the assessment of disorders of iron metabolism.
Low levels of ferritin can be found when iron stores are exhausted, well before the serum iron level has become affected. In the setting of anemia, low serum ferritin is a very specific biomarker for iron deficiency anemia. In fact, there is no clinical situation other than iron deficiency in which extremely low values of serum ferritin are seen; however, some clinical states involving infection or inflammation can cause the ferritin level in the serum of patients with iron deficiency to increase into the normal range. Ferritin is an acute-phase reactant that is thought to play a role in the body's defense against oxidative stress and inflammation. Increased ferritin values can also be observed in malignant disease, including acute leukemia; Hodgkin's disease; and carcinoma of the lung, colon, liver, and prostate. Consequently, serum ferritin in the normal range reflects iron sufficiency only in the absence of these conditions.
Patients with a serum ferritin concentration below the lower limit of the reference interval have a very high probability of being iron deficient; however, given the low sensitivity of a low ferritin level (below the lower limit of normal), a higher ferritin cutoff may be more appropriate for screening for potential iron deficiency in some populations.4-7 It is exceedingly uncommon for ferritin levels to exceed 100 ng/mL in patients with iron deficiency.6,7
An elevated ferritin level can result from iron overload due, in part, to increased hepatic ferritin synthesis.8 Iron overload can occur in hemochromatosis, other excess iron storage disorders, and in individuals who have received multiple blood transfusions. Ferritin can also become markedly elevated secondary to obesity, chronic alcohol consumption, steatohepatitis, chronic inflammation, viral hepatitis, and malignancy. The increased prevalence of obesity has likely resulted in the increased incidence of ferritin elevations, as fatty liver may be the most common cause of an elevated serum ferritin.8 Clinical assessment is required to determine whether the serum ferritin elevation is related to hemochromatosis or another underlying liver disease.9 To confirm the diagnosis of hemochromatosis, other iron tests (iron, TIBC), and genetic testing may be performed.
1. Roche Diagnostics. Ferritin. V7 Elecsys and Cobas Analyzers. Indianapolis, Ind: Roche Diagnostics; 2007-2008.
2. Fairbanks VF, Klee GG. Biochemical aspects of hematology. In: Burtis CA, Ashwood ER, eds. Tietz Textbook of Clinical Chemistry. WB Saunders Co; 1999:1642-1710.
3. Wick M, Pinggera W, Lehmann P. Ferritin in Iron Metabolism-Diagnosis of Anemias. 2nd ed. Vienna, Austria: Springer-Verlag;1995. ISBN 3-211-82525-8, ISBN 0-387-82525-8.
4. Mast AE, Blinder MA, Gronowski AM, Chumley C, Scott MG. Clinical utility of the soluble transferrin receptor and comparison with serum ferritin in several populations Clin Chem.1998 Jan; 44(1):45-51. PubMed 9550557
5. Goodnough LT, Nemeth E, Ganz T. Detection, evaluation, and management of iron-restricted erythropoiesis. Blood. 2010 Dec 2; 116(23):4754-4761. PubMed 20826717
6. Zhu A, Kaneshiro M, Kaunitz JD. Evaluation and treatment of iron deficiency anemia: A gastroenterological perspective. Dig Dis Sci. 2010 Mar; 55(3):548-559. PubMed 20108038
7. Killip S, Bennett JM, Chambers MD. Iron deficiency anemia. Am Fam Physician. 2007 Mar 1;75(5):671-678. Erratum: 2008 Oct 15; 78(8):914. PubMed 17375513
8. Adams PC. The modern diagnosis and management of haemochromatosis. Aliment Pharmacol Ther. 2006 Jun 15; 23(12):1681-1691. Review article. PubMed 16817911
9. Intragumtornchai T, Rojnukkarin P, Swasdikul D, Israsena S. The role of serum ferritin in the diagnosis of iron deficiency anaemia in patients with liver cirrhosis. J Intern Med.1998 Mar; 243(3):233-241. PubMed 9627161
Centers for Disease Control and Prevention. Iron deficiency-United States, 1999-2000 . MMWR. 2002 Oct 11; 51(40):897-899. PubMed 12425310
Centers for Disease Control and Prevention. Recommendations to prevent and control iron deficiency in the United States. MMWR. 1998 Apr 3; 47(RR-3):1-36. PubMed 9563847
Cogswell MS, Looker AC, Pfeiffer CM, et al. Assessment of iron deficiency in US preschool children and nonpregnant females of childbearing age: National Health and Nutrition Examination Survey 2003-2006. Am J Clin Nutr. 2009 May; 89(5):1334-1342. PubMed 19357218 LabCorp internal data.
World Health Organization (WHO). Iron Deficiency Anaemia. Assessment, Prevention, and Control. A guide for programme managers. Geneva: World Health Organization; 2001. (WHO/NHD/01.3) Available from: http://apps.who.int/iris/bitstream/10665/66914/1/WHO_NHD_01.3.pdf?ua=1. Accessed 2008.
