Protocol:Serum iron

Serum iron
Serum iron levels are reduced after the complete depletion of iron stores but before the haemoglobin level drops. Several manual and automated methods are available and their description is beyond the scope of this book.

Limitations associated with serum iron determination include a wide diurnal variation of serum iron concentrations, (lower in the morning as compared to the afternoon), and the diet ingested during the day before (eg. a high intake of meat may increase the serum iron levels). Serum iron has a low specificity as low levels may be found in pregnancy, during chronic infections and inflammations, pyrexia, malignancy.

Serum iron should be used in combination with serum transferrin to calculate the percentage of saturation.

Serum transferrin
Transferrin is the iron-transporting protein which can be determined using normal or automated techniques as total iron binding capacity (TIBC), that is the amount of added iron specifically bound by plasma. Alternatively transferrin can be measured as protein using immunological methods. Serum transferrin increases in iron deficiency, and is falsely reduced in acute inflammation, chronic infections, renal diseases, and malignancy. Several manual and automated methods are available and their description is beyond the scope of this book.

Transferrin saturation
Transferrin saturation is the ratio of serum iron to iron-binding capacity and is the most accurate indication of iron supply to the bone marrow. Normal values are higher than 16% in adults and higher than 10% in children.

Serum ferritin
Serum ferritin is usually measured using immunoradiometric assay (IRMA), radioimmunoassay (RIA) or by enzyme-linked immunosorbent assay (Elisa). Several manual and automated methods are available and their description is beyond the scope of this book.

The WHO reference standard is recommended. Normal values are 15 to 300 &mu;/dl in males and 15 to 200 &mu;/dl in females. Serum ferritin levels are increased in acute and chronic infections and inflammations, in liver disease, and in malignancy. Falsely reduced levels can be found in association with ascorbate deficiency.