Transferrin saturation

Transferrin saturation (TS), measured as a percentage, is a medical laboratory value. It is the value of serum iron divided by the total iron-binding capacity[1] of the available transferrin, the main protein that binds iron in the blood, this value tells a clinician how much serum iron is bound. For instance, a value of 15% means that 15% of iron-binding sites of transferrin are being occupied by iron. The three results are usually reported together. A low transferrin saturation is a common indicator of iron deficiency anemia whereas a high transferrin saturation may indicate iron overload or hemochromatosis.[1][2] Transferrin saturation is also called transferrin saturation index (TSI) or transferrin saturation percentage (TS%) [3]

Interpretation edit

Studies also reveal that a transferrin saturation (serum iron concentration ÷ total iron binding capacity) over 60 percent in men and over 50 percent in women identified the presence of an abnormality in iron metabolism (hereditary hemochromatosis, heterozygotes and homozygotes) with approximately 95 percent accuracy. This finding helps in the early diagnosis of hereditary hemochromatosis, especially while serum ferritin still remains low. The retained iron in hereditary hemochromatosis is primarily deposited in parenchymal cells, with reticuloendothelial cell accumulation occurring very late in the disease. This is in contrast to transfusional iron overload in which iron deposition occurs first in the reticuloendothelial cells and then in parenchymal cells. This explains why ferritin levels remain relative low in hereditary hemochromatosis, while transferrin saturation is high.[4][5]

Usual values edit

Normal reference ranges are:[citation needed]

  • Serum iron: 60–170 μg/dL (10–30 μmol/L)
  • Total iron-binding capacity: 240–450 μg/dL
  • Transferrin saturation: average 25%.[6] Reference ranges depend on multiple factors like age, sex, race and test devices. Most laboratories define “normal” as max. 30% for female and max. 45% for male persons.[7][8] Above 50% the risk of toxic non-transferrin bound iron (NTBI) rises exponentially, potentially causing organ damage.[9][10]

μg/dL = micrograms per deciliter

μmol/L = micromoles per liter

Laboratories often use different units and "normal" may vary by population and the lab techniques used. To help clinicians interpret their patients' results, laboratories are generally also required to report their normal or reference values.[citation needed]

Reference ranges for blood tests, comparing blood content of iron and related compounds (shown in brown and orange) with other constituents.

References edit

  1. ^ a b "Transferrin and Iron-binding Capacity (TIBC, UIBC)". The American Association for Clinical Chemistry. 20 April 2021.
  2. ^ Camaschella, C (May 2015). "Iron-Deficiency Anemia". New England Journal of Medicine (Review). 327 (19): 1832–43. doi:10.1056/NEJMra1401038. PMID 25946282. S2CID 17628280.
  3. ^ Transferring saturation in the blood on Retrieved June 3, 2020
  4. ^[dead link]
  5. ^ "Hemochromatosis - AASLD Hemochromatosis".
  6. ^ Iron status indicator National Report on Biochemical Indicators of Diet and Nutrition in the U.S. Population 1999-2002, CDC Summary. Retrieved December 17, 2019
  7. ^ [Fulwood R, Johnson CL, Bryner JD. Hematological and nutritional biochemistry reference data for persons 6 months–74 years of age: United States, 1976–1980. National Center for Health Statistics, Vital Health Stat Series 11(232), 1982.
  8. ^ [Alison Kelley, Dinesh Talwar: Interpreting iron studies. Department of Biochemistry, Glasgow Royal Infirmary, Glasgow, UK. BMJ 2017;357:j2513 doi: 10.1136/bmj.j2513 (Published 2017 June 15)
  9. ^ Brissot P, Ropert M, Le Lan C, Loréal O.: Non-transferrin bound iron: a key role in iron overload and iron toxicity. Biochim Biophys Acta. 2012 Mar;1820(3):403-10. doi: 10.1016/j.bbagen.2011.07.014. Epub 2011 Aug 9.
  10. ^ Meghna Patel et al.: Non Transferrin Bound Iron: Nature, Manifestations and Analytical Approaches for Estimation. Ind J Clin Biochem (Oct-Dec 2012) 27(4):322–332 DOI 10.1007/s12291-012-0250-7