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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.
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.
This explains why ferritin levels remain relative low in Hereditary hemochromatosis, while transferrin saturation is high. [ 23 ] [ 24 ] Transferrin and its receptor have been shown to diminish tumour cells when the receptor is used to attract antibodies .
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.
In iron deficiency anemia (IDA) ferritin is low. [6] Total iron-binding capacity is high in iron deficiency, reflecting production of more transferrin to increase iron binding; TIBC is low or normal in anemia of chronic inflammation.
Ferritin genes are highly conserved between species. All vertebrate ferritin genes have three introns and four exons. [8] In human ferritin, introns are present between amino acid residues 14 and 15, 34 and 35, and 82 and 83; in addition, there are one to two hundred untranslated bases at either end of the combined exons. [9]
Serum ferritin falls to less than 20 ng/mL. Increased iron absorption, a compensatory change, results in an increased amount of transferrin and consequently increased iron-binding capacity. [4] Stage 2 – Erythropoiesis is impaired. In spite of an increased level of transferrin, serum iron level is decreased along with transferrin saturation.
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