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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.
Iron overload (also known as haemochromatosis or hemochromatosis) is the abnormal and increased accumulation of total iron in the body, leading to organ damage. [1] The primary mechanism of organ damage is oxidative stress, as elevated intracellular iron levels increase free radical formation via the Fenton reaction.
Transferrin and TIBC Percent transferrin saturation; Iron deficiency anemia: Low High. The liver produces more transferrin, presumably attempting to maximize use of the little iron that is available. Low, as there is insufficient iron. Anemia of chronic disease: Low, as the body holds iron intracellularly with ferritin. Low.
Fasting transferrin saturation is a better test to detect HH. [14] [55] Transferrin saturation greater than 62% is suggestive of homozygosity for mutations in the HFE gene. [56] Ferritin, a protein synthesized by the liver, is the primary form of iron storage within cells and tissues.
Diagnosis is based upon identification of symptoms, medical history, family history, and laboratory tests. Blood tests may show high levels of ferritin and low, normal, or high levels of transferrin saturation, depending on the form of hemochromatosis. The diagnosis must be confirmed by genetic testing for SLC40A1 mutations. [14]
Serum Iron: high; increased ferritin levels; decreased total iron-binding capacity; high transferrin saturation; Hematocrit of about 20-30%; The mean corpuscular volume or MCV is usually normal or low for congenital causes of sideroblastic anemia but normal or high for acquired forms.
Transferrin glycoproteins bind iron tightly, but reversibly. Although iron bound to transferrin is less than 0.1% (4 mg) of total body iron, it forms the most vital iron pool with the highest rate of turnover (25 mg/24 h). Transferrin has a molecular weight of around 80 kDa and contains two specific high-affinity Fe(III) binding sites.
Excess hepatic iron in dietary iron overload is typically associated with serum ferritin saturation of greater than 700pg/L and transferrin saturation of greater than 55%. [13] Increased hepatic iron generates chronic oxidative stress by disrupting the redox balance of the cell, which damages DNA, protein, hepatocytes and lipids.