Serum iron and iron-binding capacity
The serum iron and, more particularly, the saturation of the total iron-binding capacity of transferrin (TIBC) give a measure of the iron supply to the tissues. In normal subjects, the serum iron shows a diurnal rhythm, with values being lower in the morning than in the evening. In iron deficiency and iron overload, however, values stabilize at low or high levels respectively. A serum transferrin saturation (serum iron/TIBC X 100) that is persistently less than 15% is insufficient to support normal erythropoiesis. A rise in TIBC is characteristic of iron deficiency (i.e. an absence of storage iron). A reduced serum iron con centration with a normal or reduced TIBC is a characteristic response to infection and inflammation. A sustained increase in transferrin saturation to more than 50% is an early change in the development of parenchymal iron loading (Chapter 4).
Plasma concentrations reflect both the number of erythroid precursors and iron supply to the bone marrow. In clinical practice, these two factors must be considered in interpreting transferrin receptor levels. Increased erythropoiesis from any cause results in high serum concentrations so the assay has been used as a replacement for ferrokinetic procedures as a means of identifying increased erythropoiesis. In the anaemia of chronic diseases, the assay provides a valuable indicator of deficiency of body iron stores. Serum transferrin receptor levels only increase in this situation in the absence of storage iron. Further improvement in sensitivity and specificity has been described using various ferritin-transferrin receptor ratios. At the moment, several units and reference ranges are in use and the assay is therefore method specific. In general hospital practice, some consider that the serum transferrin receptor assay adds little to the diagnostic information provided by the ferritin assay.
When iron supply to the erythron is limited, iron incorporation into haem is restricted, leading to accumulation of the immediate precursor, protoporphyrin IX. This is lost only slowly from circulating red cells; concentrations greater than the normal upper limit of 80 |mol/mol haemoglobin therefore indicate that a reduction in iron supply has been present over the previous few weeks. Protoporphyrin levels may also increase in patients with side-roblastic anaemias and lead poisoning. Convenient analysers measure zinc protoporphyrin - the form in which most of the protoporphyrin exists in iron deficiency.
Red cell ferritin
The ferritin in the circulating erythrocyte is but a tiny residue of that present in its nucleated precursors in the bone marrow
and only about 10 ag/cell (10-18 g/cell) remains in the erythrocyte. In general, red cell ferritin levels reflect the iron supply to the erythroid marrow and tend to vary inversely with red cell protoporphyrin levels. Despite some advantages over serum ferritin as a measure of storage iron (e.g. not affected by release of ferritin from damaged liver cells) the assay of red cell ferritin has seen little routine application. This is largely because it is necessary to prepare red cells free of white cells (which have much higher levels of ferritin).
As iron supply to the erythron diminishes, the new red cells produced are increasingly hypochromic. Assessment of the haemoglobin content of individual red cells, which is possible using some automated cell counters, allows measurement of the percentage of hypochromic cells. Values rising to above 6% may help in the early identification of impaired iron supply in patients with chronic renal failure who are receiving treatment with recombinant erythropoietin, when associated inflammatory disease means that other measures of iron status can be misleading.
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