a1 Department of Medicine, University of Kansas Medical Center, 3901 Rainbow Boulevard, Kansas City, Kansas 66160, USA
The major liabilities of Fe lack include defects in psychomotor development in infants, impaired educational performance in schoolchildren, increased perinatal morbidity, and impaired work capacity. Few if any of the relevant investigations have demonstrated these abnormalities in the absence of anaemia. Consequently, adequate Fe nutrition can be defined as a normal haemoglobin concentration. On the other hand, optimal Fe nutrition should be regarded as sufficient body Fe to avoid any limitation in tissue Fe supply, termed Fe-deficient erythropoiesis. A variety of laboratory measurements have been used to identify this milder form of Fe deficiency, including serum ferritin, transferrin saturation, erythrocyte protoporphyrin, mean corpuscular volume, and more recently the concentration of the soluble fragment of transferrin receptor in serum. Recent studies indicate that the serum transferrin receptor is the preferred measurement, because enhanced synthesis of the transferrin receptor represent the initial cellular response to a declining Fe supply. Moreover, unlike other methods, it is not affected by chronic inflammation or infection which are often confused with Fe deficiency. In an otherwise normal healthy population the transferrin receptor: ferritin value provides a useful quantitative index of body Fe over a wide spectrum of Fe status, ranging from Fe repletion to Fe-deficiency anaemia. It is concluded that optimal Fe nutrition is best defined as a normal haemoglobin, serum ferritin and transferrin receptor concentration.