Serum Ferritin: Which Reference Range Do I Use?

Presently, normal ranges for serum ferritin (SF) vary from lab to lab. SF ranges also differ by gender, ethnicity and age. Such variations limit the consistency with which a healthcare provider can determine abnormal iron levels. Standardizing ranges for serum ferritin is a slow and complex process. In 2010, the Iron Disorders Institute’s Scientific & Medical Advisory Board took the first steps toward standardization and issued an Opinion Statement that the ideal serum ferritin range for adults is 50-150ng/mL.

We know this ideal range has limitations. The 50-150ng/mL range applies mostly to adults undergoing therapeutic phlebotomy for hemochromatosis related iron overload. These individuals are healthy or patients whose iron reduction therapy has achieved a one time target of SF ≤50ng/mL. Iron Disorders Institute board members also concluded that there is no known benefit to a serum ferritin below 10ng/mL. However, they note that lower ferritin levels, even mild iron deficiency provides an advantage to life span.

Ferritin is the only iron test that can distinguish between iron deficiency and anemia of inflammatory response because it is the only test that demonstrates the amount of iron one has in storage. Other tests such as transferrin-iron saturation percentage (TS%), serum transferrin receptor (STfr), reticulocyte content hemoglobin (CHr) or C-reactive Protein (CRP) are helpful tests to determine why ferritin is elevated or depleted.

For now, we recognize serum ferritin lower than 20ng/mL as iron deficiency and a serum ferritin elevated above 150ng/mL as potential iron overload. For both conditions, TS% and hemoglobin are important to determine anemia.

What is Ferritin?

Ferritin is protein produced by nearly every cell of the body. Ferritin molecules are huge; each molecule can hold 4,500 atoms of iron. The greatest concentrations of ferritin are in the brain and the liver.  One function of ferritin is to serve as the primary iron reservoir from which iron can be mobilized and used in the production of new red blood cells to circulate in hemoglobin. Another function of ferritin is to contain iron as part of the Iron Withholding Defense System. Free iron, a powerful oxidant, can severely damage healthy tissues and alter DNA. Functioning in a defensive mode, ferritin keeps iron away from invading cancer and pathogenic microorganisms. These invaders need iron in order to multiply and grow. For this reason, ferritin rises when inflammation is present even though hemoglobin or serum iron might drop slightly. Were it not for this sequestering function, iron would be free to nourish and increase the growth of cancer cells as well as harmful and opportunistic bacteria. When serum ferritin is elevated along with an elevated gamma-glutamyl transpeptidase (GGT) the risk of disease and premature death is increased.

Serum ferritin is a good measure of iron stores, especially for someone who is iron-deficient. Serum ferritin can be elevated in people with iron overload, hemochromatosis, Wilson’s disease (copper overload); aceruloplasminemia, porphyria cutanea tarda (PCT), African siderosis, fatty liver disease (non-alcoholic steatohepatitis [NASH]), alcoholic liver disease, dysmetabolic iron overload syndrome (DIOS); or from excessive consumption of supplemental iron. SF can also be elevated in conditions where both iron overload and anemia are present, generally seen in patients with red blood cell production abnormalities (thalassemia, sickle cell disease, sideroblastic anemia). Often these individuals require long term red blood cell transfusions to correct anemia and to sustain life. Additionally, ferritin can be elevated in chronic renal (kidney) insufficiencies, infections, chronic inflammation, some forms of leukemia and cancers.

Elevated SF can also be seen in patients as a response to medication or hormone replacement therapy or in chronic users of nicotine gums or alcohol. Serum ferritin can be highly elevated in conditions not categorized as iron overload: inflammatory bowel disease, thyroid disease, rheumatoid arthritis or hereditary hyperferritinemia-cataract syndrome (HFCS). HFCS is a disorder that results in early onset cataracts; SF will be dramatically increased in these individuals. Phlebotomy is not warranted and could actually do harm if performed therapeutically to lower serum ferritin in a person with HFCS.

Tips to discuss with your healthcare provider: 

If you’re iron deficient; boost your ferritin with these approaches: Consume meals rich in vitamin C and lean cuts of red meat avoid calcium supplements, coffee or tea 2 hours before & after meat meals. If iron supplements are recommended, take them with vitamin C-rich foods or beverages.

If you have elevated body iron, lower your ferritin with these approaches: Donate blood.  For others, iron chelation therapy, consuming calcium rich foods, drinking coffee and tea at mealtime, and limiting supplemental vitamin C at mealtime can help.

Lifesaver tip from HealtheIron: Lower GGT and protect against oxidative stress by consuming foods rich in antioxidants.


KEY RESOURCES:

—McLaren CE, Barton JC, Eckfeldt JH, McLaren GD, Acton RT, Adams PC, Henkin LF, Gordeuk VR, Vulpe CD, Harris EL, Harrison BW, Reiss JA, Snively BM. Heritability of serum iron measures in the hemochromatosis and iron overload screening (HEIRS) family study. American Journal of Hematology. 2010 85(2):101-5.

—Bacon BR, Olynyk JK, Brunt EM, Britton RS, Wolff RK HFE genotype in patients with hemochromatosis and other liver diseases. Annals of Internal Medicine. 1999 130(12):953-62.

—Phatak P, Brissot P, Wurster M, Adams PC, Bonkovsky HL, Gross J, Malfertheiner P, McLaren GD, Niederau C, Piperno A, Powell LW, Russo MW, Stoelzel U, Stremmel W, Griffel L, Lynch N, Zhang Y, Pietrangelo A. A phase 1/2, dose-escalation trial of deferasirox for the treatment of iron overload in HFE-related hereditary hemochromatosis. Hepatology. 2010 52(5):1671-779.

—Ghaziani T, Alavian SM, Zali MR, Shahraz S, Agah M, Jensen KP, Ansari S, Sendi H, Lambrecht RW, Covault J, Bonkovsky HL. Serum measures of iron status and HFE gene mutations in patients with hepatitis B virus infection. Hepatology Research 2007 37(3):172-8.

—Olynk J, Cullen D, Aquilia S, Rossi E, Summerville L, Powell L. A Population-based study of the clinical expression of the hemo-chromatosis gene. New England Journal of Medicine 1999; 341:718–724.

—McLaren C, McLachlan G, Halliday J. Distribution of transferrin saturation in an Australian population: relevance to the early diagnosis of hemochromatosis. Gastroenterology 1998; 114:543–549.

—Fargion S, Mattioli M, Fracanzani A, et al. Hyperferritinemia, iron overload, and multiple metabolic alterations identify patients at risk for nonalcoholic steatohepatitis. American Journal of Gastroenterology 2001; 96:2448–2455.

—Lim M, Lee C, Ju Y, et al. Serum ferritin as a serologic marker of activity in systemic lupus erythematosus. Rheumatology International 2001; 20:89–93.

—Harrison, S.A, B. R. Bacon. Hereditary hemochromatosis: Update for 2003. Journal of Hepatology 38 (2003): S14-S23.


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