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Increased in iron deficiency anemia. It is decreased in chronic inflammatory states, hereditary atransferrinemia, some instances of acquired liver disease, neoplasia, and renal disease. Transferrin is an index of nutritional status.
Increased in patients on oral contraceptives and in late pregnancy. May not be elevated in iron-deficient states in which there is severe protein malnutrition (eg, kwashiorkor).
Transferrin is responsible for 50% to 70% of the iron binding capacity of serum. Since other proteins may bind iron, transferrin is not the same as TIBC. Transferrin is an iron transport protein receiving and binding iron for delivery to receptors at recipient cells. The human transferrin gene, responsible for production of this single chain, 77 kilodalton polypeptide resides on chromosome 3, band q21-25. Transferrin has two iron-binding sites and is largely but not exclusively synthesized by the liver. There are over 20 genetic variants, largely single amino acid substitutions. Transferrin levels rise with iron deficiency and fall in cases of iron overload. Transferrin is normally only about one-third saturated and is responsible for circadian variation in serum iron (peak in AM) due to variable activity of the reticuloendothelial system. Recent studies have indicated that the serum transferrin receptor levels can be used as an index of iron deficiency anemia.
