Коэффициент насыщения трансферрина железом (TSAT)

Transferrin (also known as siderophilin) quantification supports the evaluation of iron metabolism when interpreted alongside serum iron and measures of total and unsaturated iron‑binding capacity, from which percent transferrin saturation is calculated. The test helps differentiate iron‑deficiency anemia from anemia due to chronic disease or vitamin B12 deficiency, provides an estimate of iron stores, and serves as an indicator of hepatic synthetic function; transferrin concentrations typically increase in iron deficiency and decline with impaired liver synthesis.

Transferrin is the principal iron‑transport protein in plasma. It is synthesized in the liver from amino acids absorbed during digestion and binds iron derived from dietary intake or erythrocyte turnover, delivering it to tissues such as the liver and spleen. Transferrin demonstrates a high iron‑binding capacity relative to its own mass. Iron is an essential micronutrient incorporated into hemoglobin, which enables erythrocytes to transport oxygen, and into the muscle protein myoglobin. Total body iron is typically 4–5 g, of which approximately 3–4 mg (0.1% of the total) circulates bound to transferrin. Under physiological conditions, roughly one‑third of transferrin iron‑binding sites are occupied and two‑thirds remain available as reserve. The degree of binding site occupancy is reflected by total iron‑binding capacity, unsaturated iron‑binding capacity, and percent transferrin saturation. In iron deficiency, transferrin concentration rises to maximize binding of the limited circulating iron. Transferrin levels are influenced by hepatic function, nutritional protein intake, and intestinal absorption. Diminished hepatic synthetic capacity due to advanced fibrosis or cirrhosis lowers transferrin concentrations. Inadequate protein nutrition or malabsorption from intestinal inflammation similarly reduces transferrin synthesis.