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Iron 

  • Author: Bishnu Prasad Devkota, MD, MHI, FRCS(Edin), FRCS(Glasg), FACP; Chief Editor: Eric B Staros, MD  more...
 
Updated: Jan 17, 2014
 

Reference Range

The amount of circulating iron bound to transferrin is reflected by the serum iron level.

The serum iron reference range is 55–160 µg/dL in men and40–155 µg/dL in women.[1]

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Interpretation

Increases in serum iron level are associated with the following:[1, 2, 3]

Decreases in the serum iron level are associated with the following:[1, 2, 3]

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Collection and Panels

Collection - Tiger-top or red-top tube

Panel - Iron panel

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Background

Description

The metabolism of all living organisms requires iron. Iron is a part of heme, which is the active site of peroxidases that protect cells from oxidative injury by reducing peroxides to water. Heme is also the active site of electron transport in cytochromes.[3] When iron levels are insufficient, proliferation of bacteria or nucleated cells stops.[3]

Iron deficiency anemia may cause pallor, stomatitis, glossitis (smooth red tongue), angular cheilitis, and koilonychias. Patients with Plummer-Vinson syndrome may experience esophageal webs, dysphagia, and iron deficiency anemia.[4] Retinal hemorrhages and exudates may also be observed, especially in individuals with severe anemia. Although rare, splenomegaly in individuals with iron deficiency anemia likely results from other causes.[5, 3, 6]

The following is observed in patients with severe uncomplicated iron deficiency anemia

  • RBCs are hypochromic and microcytic.
  • The plasma iron concentration is decreased.
  • The iron-binding capacity is increased.
  • The serum ferritin concentration decreases.
  • The serum transferrin receptor and erythrocyte zinc protoporphyrin concentrations are increased.
  • The bone marrow is depleted of stainable iron.

The classic combination of these laboratory findings is observed only in severe and uncomplicated iron deficiency anemia that presents in patients without infection or malignancy who are not receiving blood transfusions or iron therapy.[3] Serum iron levels are often low in untreated iron deficiency anemia; however, levels may be normal.[7, 8]

If patients with iron deficiency anemia receive iron medication before blood is drawn, normal or high concentrations are typically noted. Even multivitamins with low (18 mg) elemental iron may produce this result. Thus, 24 hours before a blood draw for serum iron, all oral iron mediation should be stopped. Parenteral injection of iron dextran may result in high serum iron levels (eg, 500-1000 µg/dL) for several weeks.[9] Infusion of sodium ferric gluconate or iron sucrose causes increases in iron levels that last much shorter;[10, 11] these infusions are unlikely to interfere with serum iron testing.[10, 11, 3]

Deterministic factors for plasma iron concentration include the following:[3]

  • Absorption from the intestine
  • Storage in the intestine, liver, spleen, bone marrow
  • Rate of breakdown or loss of hemoglobin
  • Rate of synthesis of new hemoglobin

When screening for hereditary hemochromatosis, serum iron, iron-binding capacity, and transferrin saturation may be helpful.

Recent transfusions influence test findings.

The amount of circulating iron bound to transferrin is the serum iron level. The circulating transferrin is indirectly measured by the total iron-binding capacity (TIBC). Transferrin saturation in excess of 50% suggests a disproportionate amount of iron bound to transferrin is being delivered to nonerythroid tissues. If this continues for an extended time, tissue iron overload may be observed.[12]

Indications/Applications

Serum iron testing is indicated for the following:

  • Diagnosis of blood loss
  • Differential diagnosis of anemia
  • Diagnosis of hemosiderosis and hemochromatosis
  • Evaluation of iron deficiency
  • Diagnosis of acute iron toxicity particularly in children
  • Evaluation of thalassemia and sideroblastic anemia
  • Monitoring the response to therapy of anemia [2]

Considerations

Serum iron testing does not reliably determine iron deficiency or identify hemochromatosis or other iron overload states. TIBC, transferrin saturation percentage, and ferritin levels are recommended measurements in these settings. Oral contraceptives increase the iron level. Iron dextran elevates serum iron levels several weeks. Ingestion of even small amounts of iron may transiently increase serum iron levels. Patients undergoing iron chelation therapy (deferoxamine) may have inaccurate serum iron test results.

Diurnal variation is observed with serum iron testing; normal values are found in the mid-morning, low values are found in mid-afternoon, and even lower values are found near midnight. Diurnal variation disappears at values below 45 µg/dL.[2]

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Contributor Information and Disclosures
Author

Bishnu Prasad Devkota, MD, MHI, FRCS(Edin), FRCS(Glasg), FACP Associate Professor of Medicine, St Louis University School of Medicine

Bishnu Prasad Devkota, MD, MHI, FRCS(Edin), FRCS(Glasg), FACP is a member of the following medical societies: American College of Physicians, American Medical Informatics Association, Royal College of Physicians and Surgeons of Glasgow, Royal College of Surgeons of Edinburgh, Healthcare Information and Management Systems Society

Disclosure: Nothing to disclose.

Chief Editor

Eric B Staros, MD Associate Professor of Pathology, St Louis University School of Medicine; Director of Clinical Laboratories, Director of Cytopathology, Department of Pathology, St Louis University Hospital

Eric B Staros, MD is a member of the following medical societies: American Medical Association, American Society for Clinical Pathology, College of American Pathologists, Association for Molecular Pathology

Disclosure: Nothing to disclose.

References
  1. Gomella LG HS. Laboratory Diagnosis: Chemistry, Immunology, Serology. Gomella LG HS, ed. Clinician's Pocket Reference: The Scut Monkey. 11 ed. New York: McGraw-Hill; 2007.

  2. Williamson MA, Snyder LM, Wallach JB. Wallach's interpretation of diagnostic tests. 9th ed. Wolters Kluwer/Lippincott Williams & Wilkins Health: Philadelphia; 2011.

  3. Beutler E. Disorders of Iron Metabolism. Prchal JT KK, Lichtman MA, Kipps TJ, Seligsohn U, ed. Williams Hematology. 8th ed. New York: McGraw-Hill; 2010.

  4. Atmatzidis K, Papaziogas B, Pavlidis T, Mirelis Ch, Papaziogas T. Plummer-Vinson syndrome. Dis Esophagus. 2003. 16(2):154-7. [Medline].

  5. Leonard BJ. Hypochromic anaemia in R.A.F. recruits. Lancet. 1954 May 1. 266(6818):899-902. [Medline].

  6. Aksoy M, Erdem S, Baserer G. On the pathogenesis of the hepatosplenomegaly in chronic iron deficiency anaemia. Astudy in five patients with a syndrome of chronic iron deficiency anaemia, hepatosyplenomegaly, hypogonadism and dwarfism. Acta Hepatosplenol. 1968 Jul-Aug. 15(4):241-51. [Medline].

  7. Hershko C, Bar-Or D, Gaziel Y, Naparstek E, Konijn AM, Grossowicz N. Diagnosis of iron deficiency anemia in a rural population of children. Relative usefulness of serum ferritin, red cell protoporphyrin, red cell indices, and transferrin saturation determinations. Am J Clin Nutr. 1981 Aug. 34(8):1600-10. [Medline].

  8. Beutler E. The red cell indices in the diagnosis of iron-deficiency anemia. Ann Intern Med. 1959 Feb. 50(2):313-22. [Medline].

  9. Seligman PA, Schleicher RB. Comparison of methods used to measure serum iron in the presence of iron gluconate or iron dextran. Clin Chem. 1999 Jun. 45(6 Pt 1):898-901. [Medline].

  10. Pai AB, Boyd AV, McQuade CR, Harford A, Norenberg JP, Zager PG. Comparison of oxidative stress markers after intravenous administration of iron dextran, sodium ferric gluconate, and iron sucrose in patients undergoing hemodialysis. Pharmacotherapy. 2007 Mar. 27(3):343-50. [Medline].

  11. Warady BA, Seligman PA, Dahl NV. Single-dosage pharmacokinetics of sodium ferric gluconate complex in iron-deficient pediatric hemodialysis patients. Clin J Am Soc Nephrol. 2007 Nov. 2(6):1140-6. [Medline].

  12. JW A. Iron Deficiency and Other Hypoproliferative Anemias. Longo DL FA, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, ed. Harrison's Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2012.

 
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