Iron deficiency (ID) and iron deficiency anemia (IDA) continue to be of worldwide concern. ID is the most common single nutrient deficiency among children in developing countries . In developed nations, despite a marked decline in prevalence, IDA remains a common cause of anemia in young children . However, the more significant than anemia itself is the more common ID without anemia that also adversely affects neurodevelopment and behavior, and some of these effects may be irreversible .
Iron is a trace element that is essential for numerous cellular metabolic functions . The body requires iron for the synthesis of its oxygen transport proteins, in particular hemoglobin and myoglobin, and for the formation of heme enzymes and other iron-containing enzymes involved in electron transfer and oxidation–reduction .
Approximately 70% of the total body iron is contained in heme compounds (e.g., hemoglobin and myoglobin), 29% is stored as ferritin and hemosiderin, < 1% is incorporated into heme-containing enzymes (e.g., cytochromes, catalase, and peroxidase), and < 0.2% is found circulating in the plasma bound to transferrin .
There is no physiological mechanism for iron excretion, and only 1–2 mg of iron is lost each day due to sloughing of cells (i.e., from the mucosal lining of the gastrointestinal tract, skin, and renal tubules). Hence, iron loss and gain is generally in balance, with the amount lost daily being equal to the amount absorbed daily.
Hepcidin is the principal regulator of plasma iron concentrations. It acts by binding to ferroportin on cell surfaces, inducing ferroportin internalization and degradation, and thereby blocking iron efflux into the plasma from professional iron-exporting cells, including hepatocytes, duodenal enterocytes, splenic and other macrophages, and syncytiotrophoblasts .
The symptoms of ID are not unique to iron deficiency (i.e., not pathognomonic). The signs of ID may include brittle nails, swelling or soreness of the tongue, cracks in the sides of the mouth, an enlarged spleen, and frequent infections .
Structural studies from autopsies and MRI scanning have demonstrated that iron distribution in the adult brain is heterogeneous and dependent on the stage of development. The basal ganglia, substantia nigra, and deep cerebellar nuclei contain the highest concentrations of iron in the adult brain. However, in children and adolescents, the maximum iron concentrations are found in the globus pallidus, caudate nucleus, putamen, and substantia nigra, with the highest concentrations being found at birth .
Therefore, the timing of ID is of great significance, and it is important to consider the “critical periods” of development that absolutely require adequate iron nutrition for “normal” development. In early life, there are three peak times for the risk of developing ID, based on the balance of iron supply and demand, which are perinatal, toddlerhood, and adolescence, with the latter being particularly in females. Unfortunately, several human infant studies have demonstrated that the effects of “early” ID on biological neural functioning are potentially irreversible .
There are three stages of ID. The first stage is known as iron depletion, during which iron stores are low and serum ferritin concentrations decrease. IDA is the third and most severe stage of iron deficiency and is characterized by low hemoglobin and hematocrit levels .
There is no single reliable marker of iron status, except at the extremes of deficiency and excess . A low serum ferritin level is widely considered as the best single laboratory indicator of iron depletion; the result must be interpreted with caution in any patient with an underlying inflammatory process, because ferritin is an acute phase reactant, and its level is increased in the presence of an acute or chronic inflammatory process .
Transferrin saturation of < 15% is indicative of an ID state, either latent ID or true ID, where a decrease in serum iron level is associated with an increase in transferrin level .
Screening of infants with one or more risk factors for ID would allow treatment of ID in the pre-anemic stage, thereby preventing its associated mental, motor, and behavior effects .
Aim of the study
The aim of our study was to evaluate iron status among apparently healthy toddlers and preschool children (aged 1–6 years) with normal hemoglobin levels to determine the proportion of children who have ID without anemia or evident clinical manifestations.