| disease | Iron Deficiency Anemia in Children |
| alias | Microcytic Anemia, Iron Deficiency Anemia |
Iron deficiency anemia is a common condition in children, primarily affecting infants and toddlers aged 6 months to 3 years. It is characterized by microcytic hypochromic anemia, reduced serum iron and transferrin saturation, and a favorable response to iron therapy. Since the founding of the People's Republic of China, various nutritional deficiencies have significantly decreased, yet iron deficiency anemia remains a prevalent threat to children's health. According to a 1981 nationwide survey of 8,435 children aged 29 days to 7 years across 16 provinces and cities, the prevalence of nutritional anemia (hemoglobin below 110g/L) was as high as 36.31%. Among 9,027 children aged 6 months to 6 years, the prevalence reached 43.03%. Therefore, this remains an urgent issue to address in child healthcare.
bubble_chart Etiology
During the most vigorous period of growth and development in infancy, if the iron stored in the body is depleted and the dietary iron intake is insufficient, the absorption of iron in the digestive tract cannot compensate for the increase in blood volume and red blood cells, leading to anemia. The main causes of anemia are as follows:
1. The relationship between the body's iron content at birth and anemia.
The blood volume of a normal newborn is approximately 85 ml/kg, with a hemoglobin level of about 190 g/L. During the neonatal period, over 75% of the total body iron is in hemoglobin, about 15–20% is stored in the reticuloendothelial system, and very little is used for myoglobin synthesis. The iron in enzymes amounts to only a few milligrams. Therefore, the iron content in a newborn's body mainly depends on blood volume and hemoglobin concentration. Blood volume is proportional to body weight. For example, comparing a 3.3 kg newborn with a 1.5 kg premature infant, the difference in total body iron is 120 mg.
A normal newborn has an iron content of about 70 mg/dl, while premature and low-birth-weight infants have iron levels proportional to their body weight. The iron released from physiological hemolysis after birth is stored in reticuloendothelial cells, and the stored iron is sufficient to support a doubling of body weight. Thus, the lower the birth weight, the lower the total body iron, and the higher the likelihood of anemia. Additionally, factors such as fetal blood transfusion to the mother, twin-to-twin transfusion, placental vascular rupture during childbirth, and delayed umbilical cord clamping (which can provide an extra 75 ml of blood or 40 mg of iron to the newborn) may affect the newborn's iron levels.Maternal iron-deficiency anemia during pregnancy does not have a definitive relationship with infant anemia, as the placenta can transport iron from the mother (with low serum iron levels) to the fetus (with higher serum iron levels). Regardless of maternal iron deficiency or dietary quality, about 10% of isotopically labeled iron administered to the mother enters the fetus. Therefore, at birth, there is no significant difference in hemoglobin, serum ferritin, or serum iron levels between newborns of anemic and non-anemic mothers, nor is it proportional to the mother's hemoglobin. Even if the mother has moderate or severe anemia, the infant's serum ferritin may still be within the normal range.
2. The relationship between growth rate and anemia. Infants grow rapidly, and blood volume increases quickly. A normal infant's weight doubles by 5 months, while premature infants grow even faster, increasing sixfold by 1 year. If the initial hemoglobin level is 19 g/dl, it drops to about 11 g/dl by 4.5–5 months, at which point stored iron alone can maintain levels without dietary iron supplementation. However, premature infants have much higher iron requirements than normal infants.
For a normal infant whose weight doubles, maintaining hemoglobin at 11 g/dl is achievable with stored iron. Therefore, if significant iron-deficiency anemia occurs before weight doubles, it is generally not due to dietary iron deficiency, and other causes must be investigated.3. Dietary iron deficiency. Infants primarily consume dairy-based foods, which are very low in iron. The iron content in breast milk is related to the mother's diet, typically around 1.5 mg/L, while cow's milk contains 0.5–1.0 mg/L, and other dairy products even less. The absorption rate of iron from dairy is about 2–10%, with breast milk iron being more absorbable than cow's milk (iron absorption from breast milk can increase to 50% during iron deficiency). If exclusively breastfed for the first 6 months, infants can maintain normal hemoglobin and iron stores. Therefore, when breastfeeding is not possible, iron-fortified formula should be used, and complementary foods should be introduced promptly; otherwise, anemia may occur once stored iron is depleted after weight doubles. Breastfed infants may also develop anemia if complementary foods are not introduced after 6 months. According to a survey of 39 cases of microcytic anemia at Beijing Children's Hospital, 65% were formula-fed, and partially breastfed infants lacked timely introduction of complementary foods.
Older children often develop anemia due to poor eating habits, refusal to eat, picky eating, or inadequate nutritional intake.
4. Chronic minor blood loss In normal individuals, the stored iron accounts for 30% of the total body iron. If acute blood loss does not exceed one-third of the total blood volume, rapid recovery can occur without additional iron supplementation, and anemia will not develop. In cases of chronic long-term blood loss, every 4ml of blood loss is approximately equivalent to 1.6mg of iron loss. Although the daily blood loss may be small, the iron consumption can exceed twice the normal level, leading to anemia. Infants under one year of age experience rapid growth, and their stored iron is used to compensate for the expansion of blood volume. Even minor chronic blood loss can result in anemia. In recent years, it has been observed that infants fed large quantities (>1L) of unboiled fresh cow's milk daily may develop chronic intestinal blood loss. Antibodies against heat-labile proteins in fresh cow's milk can be detected in the blood of these infants. Some also believe that intestinal blood loss is related to the amount of unboiled fresh cow's milk consumed. If infants aged 2–12 months consume no more than 1L of fresh cow's milk daily (preferably no more than 750ml) or are given evaporated milk, the incidence of blood loss can be reduced.
Common causes of chronic blood loss also include gastrointestinal malformations, diaphragmatic hernia, polyps, ulcer disease, esophageal varices, hookworm disease, epistaxis, thrombocytopenic purpura, pulmonary hemosiderosis, and hypermenorrhea in adolescent girls.5. Other causes Chronic diarrhea and vomiting, enteritis, steatorrhea, and other conditions can impair nutrient absorption. During acute and chronic infections, reduced appetite and poor gastrointestinal absorption in children can also lead to iron-deficiency anemia.
1. Distribution and Functions of Iron in the Human Body
(1) Synthesis of Hemoglobin: The iron in hemoglobin accounts for about two-thirds of the total iron in the body, and hemoglobin constitutes over 99% of red blood cell proteins. Iron deficiency affects hemoglobin synthesis, leading to anemia.
(2) Synthesis of Myoglobin: The iron in myoglobin accounts for about 3% of the total iron in children. Myoglobin has a stronger affinity for oxygen than hemoglobin and serves as an oxygen reservoir in striated and cardiac muscles. During oxygen deprivation, it can release oxygen to meet the urgent needs of muscle contraction. The impact of iron deficiency on myoglobin levels in muscles is not yet fully understood.
(3) Formation of Essential Enzymes: A very small amount of iron constitutes essential enzymes in the body, such as various cytochrome enzymes, catalase, peroxidase, succinate dehydrogenase, and xanthine oxidase. These enzymes participate in the final stages of cellular metabolism and the generation of adenosine diphosphate (ADP), which is indispensable for cellular metabolism. In the early stages of iron deficiency, even before anemia appears, the function of these iron-containing or iron-dependent enzymes may already be affected. However, within 48–72 hours of treatment, mental state and appetite improve, indicating the recovery of enzyme function before the improvement of anemia.
(4) Storage: About 30% of iron is stored in the bone marrow and reticuloendothelial system in the form of ferritin and hemosiderin. One-third is stored in the liver (1 g of dried liver tissue in newborns contains about 15 mg of iron, decreasing to 2 mg by age 2), one-third in the bone marrow, and the remaining third in the spleen and other tissues. Ferritin can contain up to 20–25% of its weight in iron and remains in equilibrium with plasma iron, making it readily available when the body's needs increase. Hemosiderin contains about 30% iron but is less readily utilizable. For example, in children with pulmonary hemosiderosis, despite large amounts of hemosiderin deposits in the lungs, the iron cannot be used for hemoglobin synthesis. The function of hemosiderin and its relationship with ferritin are not yet fully understood.
(5) Transport: A very small amount of iron in the plasma binds to a β-globulin (transferrin) and is transported between tissues. For example, iron absorbed from the intestines or released from red blood cells destroyed in the reticuloendothelial system binds to transferrin in the Fe3+ form and is transported to the bone marrow. Transferrin attaches to the membranes of erythroblasts and reticulocytes, and iron enters the cells within one minute through active transport, where it is used to synthesize hemoglobin in erythroblasts. One molecule of transferrin binds two molecules of iron, rapidly carrying iron into and out of the bloodstream, with a half-life of about 20–120 minutes. Under normal conditions, plasma transferrin is similar to lactoferrin in binding. Additionally, there is a lactoferrin similar to transferrin, found in milk, various secretions, and neutrophils. It has a strong affinity for iron and exerts bacteriostatic effects by competitively depriving microorganisms of available iron. Its role in iron transport requires further study.
2. Sources and Absorption of Iron The iron in the human body primarily comes from food. Foods with the highest iron content include black fungus, kelp, and pork liver, followed by meats, legumes, eggs, etc. Cooking with iron pots can also provide a significant amount of inorganic iron salts. Additionally, when red blood cells are destroyed in the body, the iron released from hemoglobin is almost entirely reused to synthesize hemoglobin or to meet the iron needs of other tissues.
Iron absorption primarily occurs in two forms: as free iron and as heme iron. The iron in plants generally exists in the form of colloidal ferric hydroxide. Under the action of pepsin and free hydrochloric acid, non-heme iron in food is released and converted into free ferrous iron. Vitamin C can reduce ferric iron to ferrous iron, facilitating absorption. Additionally, fructose and amino acids (such as cysteine, histidine, and lysine) all have the effect of promoting iron absorption. In the alkaline environment of the small intestine, iron phosphate and iron oxalate salts are easily formed, hindering absorption. Tea and coffee beans also affect iron absorption, as the tannic acid in tea leaves forms iron tannate complexes with iron, reducing iron absorption by 75%.
The absorption of heme iron differs from that of free iron. In animal-based foods, hemoglobin and myoglobin are broken down by stomach acid and proteolytic enzymes, causing heme to separate from globin. The heme can then be directly absorbed by intestinal mucosal cells. Within the intestinal mucosal epithelial cells, Neijing heme oxygenase releases iron.
The absorption rate of iron varies depending on the type of food. The absorption rate of iron from vegetables, rice, and other plant-based foods is only about 1%, whereas iron in meat exists in the form of heme, which has a higher absorption rate of approximately 10–22%.
If fish or other meats are consumed alongside plant-based foods, the absorption rate of iron from the plant-based diet increases. However, animal-based foods like milk and eggs do not have this effect. Although the iron in eggs is poorly absorbed, eggs are still considered an important source of iron for infants due to their high iron content.
Iron absorption primarily occurs in the duodenum and is regulated by the small intestine mucosa. Intestinal mucosal cells have a lifespan of 4–6 days and serve as a temporary storage site for iron. If there is an excess of iron in the body, the iron is stored in large amounts as ferritin within the intestinal mucosal cells, with only a small amount entering the bloodstream. The excess iron is excreted as the mucosal cells shed. In cases of iron deficiency, iron is rapidly released from the mucosal cells into the bloodstream, with minimal excretion through the intestines. Although the exact regulatory mechanism is not fully understood, it primarily depends on the nature of the food, iron content, the body's iron storage status, and hematopoietic function. The lower the body's iron reserves, the higher the absorption rate. Iron absorption increases during periods of active hematopoiesis, such as after blood loss, leading to rapid recovery from anemia. In chronic hemolytic diseases like thalassemia, excessive iron absorption can occur even when iron stores are already high. Under normal hematopoietic conditions, despite significant variations in dietary iron intake, the body's iron levels remain relatively stable.
3. Iron Excretion Under normal circumstances, only a very small amount of iron is excreted daily. In children, the daily excretion is about 15 μg/kg. Approximately two-thirds of this is excreted through the intestines via shed intestinal mucosal cells, bile, and red blood cells, while the remainder is excreted through the kidneys and sweat glands. A negligible amount of iron is also lost through epidermal shedding.
bubble_chart Clinical Manifestations
The onset of the disease mostly occurs between 6 months and 3 years of age, with a generally slow progression that often goes unnoticed by parents initially. By the time medical attention is sought, most affected children already have grade II anemia. The severity of symptoms depends on the degree of anemia and the speed at which it develops.
(1) General manifestations: Early symptoms often include dysphoria, restlessness, or listlessness, reduced activity, decreased appetite, and pallor of the skin and mucous membranes, most notably in the lips, oral mucosa, nail beds, and palms. Preschool and school-aged children may complain of fatigue and weakness.
(2) Manifestations of hematopoietic organs: Due to extramedullary hematopoietic reactions, the liver, spleen, and lymph nodes are often grade I enlarged. The younger the child, the more severe the anemia, and the longer the duration of the disease, the more pronounced the hepatosplenomegaly becomes, though it rarely exceeds grade II.
Apart from changes in the hematopoietic system, iron deficiency affects various metabolic processes. From a cytological perspective, it can lead to deficiencies in the cytochrome enzyme system; reduced activity of enzymes such as catalase, glutathione peroxidase, succinate dehydrogenase, monoamine oxidase, aconitase, and α-glycerophosphate dehydrogenase; and impaired DNA synthesis. Due to metabolic disturbances, symptoms like loss of appetite, slowed weight gain, atrophy of tongue papillae, reduced gastric acid secretion, and small intestine mucosal dysfunction may occur. Pica is more common in adults and relatively rare in children.
Neurological and psychological changes are increasingly gaining attention. It has been observed that even before anemia becomes severe, symptoms such as dysphoria and disinterest in the surroundings may appear. Intelligence tests reveal that affected children have poor concentration, reduced comprehension, and slower reactions. Infants and toddlers may experience episodes of breath-holding spells (breath bolding spells). School-aged children may exhibit abnormal behaviors in class, such as restlessness or constant fidgeting. The relationship between these phenomena and iron supplementation is not entirely clear, but recent experiments have shown that norepinephrine levels in the urine of patients with iron-deficiency anemia are elevated and normalize rapidly after iron treatment, suggesting that neurological and psychological changes may be linked to norepinephrine degradation metabolism. Increased urinary norepinephrine may result from monoamine oxidase deficiency, an iron-dependent enzyme that plays a critical role in neurochemical reactions in the central nervous system. It has been measured that platelet monoamine oxidase activity is reduced in iron-deficiency anemia patients and quickly returns to normal after iron supplementation. To further confirm the relationship between iron deficiency and neuropsychological symptoms, more animal experimental studies should be conducted in the future.
Children with iron-deficiency anemia are more prone to infections. In these patients, both E rosette formation and active E rosette formation rates are reduced, and skin test responses to PHA are significantly lower than normal, indicating weakened T lymphocyte function. Some reports indicate that peripheral blood T lymphocyte subsets CD3 and CD4 lymphocytes are reduced, with a decreased OKT4/OKT8 ratio. Other studies have reported that NBT test results in patients are lower than normal, possibly due to reduced iron-containing myeloperoxidase, leading to impaired granulocyte killing capacity. After iron treatment, granulocyte bactericidal function typically returns to normal within 4 to 7 days.
When hemoglobin levels drop below 70g/L, cardiac enlargement and murmurs may occur, which are general manifestations of anemia rather than specific signs of iron-deficiency anemia. Due to the slow progression of iron-deficiency anemia, the body's tolerance is high, and even when hemoglobin levels fall below 40g/L, signs of cardiac insufficiency may not appear. However, concurrent respiratory infections can increase cardiac workload and may trigger heart failure.
bubble_chart Auxiliary Examination
1. Generation and transformation test: A series of changes in generation and transformation occur before the onset of anemia. When iron is deficient, the body first mobilizes stored iron to meet the needs of iron metabolism, leading to a decrease in ferritin and hemosiderin content in the liver and bone marrow. Subsequently, serum ferritin levels decrease. The normal value of serum ferritin is 35 ng/ml; if it drops below 10 ng/ml, generation and transformation or clinical signs of iron deficiency may appear. Thereafter, serum iron levels fall below 50 μg/dl, sometimes even below 30 μg/dl, while the total iron-binding capacity increases to over 350 μg/dl, and transferrin saturation drops below 15%. When transferrin saturation is below 15%, hemoglobin synthesis decreases, and free erythrocyte protoporphyrin (FEP) may accumulate to levels as high as 60 μg/dl of whole blood. In infants and young children, an increase in the ratio of free erythrocyte protoporphyrin to hemoglobin (FEP/Hgb) is more significant for diagnosing iron deficiency anemia than a decrease in transferrin saturation. A ratio >3 μg/g is considered abnormal, and if it falls between 5.5–17.5 μg/g, iron deficiency anemia can be diagnosed after excluding lead poisoning. Serum copper levels may rise to 146 μg/dl. If iron deficiency progresses further, changes in blood parameters will appear.
2. Blood parameters: Both red blood cells and hemoglobin are reduced, with hemoglobin showing a more pronounced decrease. Hematocrit levels decrease accordingly. The mean corpuscular volume (MCV) is less than 80 fl and may drop as low as 51 fl; the mean corpuscular hemoglobin (MCH) is below 26 pg, with a minimum of 11.1 pg; the mean corpuscular hemoglobin concentration (MCHC) is below 0.30 and may drop to 0.20. Based on measurements from a few cases, the mean corpuscular weight may be as low as 70 pg. On smears, red blood cells appear smaller, with most diameters less than 6 μm, and sometimes show size variation, with smaller cells predominating. The Price-Jones curve shifts to the left and widens at the base. Red blood cells stain lightly, with an enlarged central pale area. In severe cases, red blood cells may appear ring-shaped. The reticulocyte percentage is normal, but the absolute count is below normal, and red cell fragility is reduced. Nucleated red blood cells are rarely seen in peripheral blood smears.
White blood cell morphology and counts are normal, but in severe cases, the white blood cell count may decrease, accompanied by a relative increase in lymphocytes. Platelet counts are mostly within the normal range, though they may slightly decrease in severe cases, but rarely to a degree that causes bleeding.
3. Bone marrow findings: The bone marrow shows hyperplasia, with a slight increase in bone marrow cell counts and a normal number of megakaryocytes. According to statistics from Beijing Children's Hospital, bone marrow cell counts mostly range between 150,000–400,000/mm3, averaging 300,000/mm3. Megakaryocyte counts typically range between 25–125/mm3, averaging about 70/mm3.
In bone marrow differential counts, the ratio of granulocytes to nucleated red blood cells indicates an increase in nucleated red blood cells, reflecting active erythropoiesis. Granulocyte morphology remains unchanged, though neutrophil counts may be slightly elevated in differential counts. Among erythroid precursors, polychromatic and orthochromatic normoblasts increase, with orthochromatic normoblasts showing a more significant rise. Early, intermediate, and late normoblasts exhibit scant cytoplasm with minimal hemoglobin content, indicating delayed cytoplasmic maturation compared to nuclear maturation. The cytoplasmic edges appear irregular. Prussian blue staining reveals a decrease or absence of sideroblasts, and blue-stained ferritin or hemosiderin particles are absent in smear fragments.
4. Other tests: If chronic intestinal blood loss is present, stool occult blood tests may be positive. In severe and prolonged cases, skull X-rays may show radial striations similar to those seen in hemoglobinopathies.
Early diagnosis is not easy based solely on symptoms. A detailed medical history should be carefully obtained, with particular attention to disease cause analysis, which can provide early diagnostic clues, such as birth weight, whether there was transplacental blood loss or placental abruption, postnatal weight gain rate, the child's dietary habits, and daily intake of fresh milk. For older children, chronic blood loss and Chinese Taxillus Herb infestation should be considered. For adolescent girls, menstrual history should be noted. In cases of diagnostic difficulty, a therapeutic trial with iron supplements may be used.
bubble_chart Treatment Measures
The principle is to supplement iron and remove the disease cause.
1. Iron therapy: Iron is the specific treatment for iron-deficiency anemia, with many types available. Generally, oral inorganic iron salts are the most economical, convenient, and effective method. Ferrous iron is more easily absorbed than ferric iron, so it is commonly used. Examples include ferrous sulfate (20% iron content) and ferrous fumarate (30% iron content). For infants, a 2.5% ferrous sulfate solution is often prepared for ease of administration (ferrous sulfate 2.5g, dilute hydrochloric acid 2.9ml, glucose 12.5g, chloroform water 100ml). The dose should be calculated based on the iron content. Studies suggest 4.5–6mg/kg/day divided into three doses (equivalent to ferrous sulfate 0.03g/kg/day, ferrous fumarate 0.02g/kg/day, or 2.5% ferrous sulfate solution 1.2ml/kg/day). This dose achieves maximum absorption; exceeding it reduces absorption and increases gastric mucosal irritation. Excessive doses may cause toxicity. Administering iron between meals minimizes gastric irritation and enhances absorption. Avoid taking iron with large amounts of milk, as high phosphorus content in milk can inhibit iron absorption.
Vitamin C reduces ferric iron to ferrous iron, improving solubility and maintaining iron in a dissolved state even at higher pH levels in the small intestine. For example, adding 60mg of vitamin C to rice can triple iron absorption. Therefore, vitamin C is recommended alongside iron therapy. However, taking vitamin C four hours before iron does not have this effect.
For the rare cases of children with severe reactions, switching to less irritating ferrous gluconate or reducing the iron dose by half until symptoms like nausea, vomiting, diarrhea, or gastric discomfort subside is advisable. Only consider injectable iron for children who cannot tolerate oral iron, have severe diarrhea, or significant anemia. Common iron injections include iron dextran (50mg iron per ml, intramuscular) and iron saccharate (20mg iron per ml, intravenous). Intramuscular iron may cause local pain, urticaria, fever, arthralgia, headache, or lymphadenopathy. Intravenous iron can lead to thrombophlebitis. Injectable iron is not faster-acting than oral iron, so it should be used cautiously.
Iron therapy should continue for at least 6–8 weeks after red blood cells and hemoglobin return to normal levels. Iron-deficiency anemia depletes both hemoglobin and stored iron. Due to children’s ongoing growth and expanding blood volume, dietary iron alone may not suffice. The goal is not only to correct anemia but also to replenish iron stores for future needs. Vitamin B12, folic acid, or liver extract are ineffective for iron-deficiency anemia and should not be misused.
2. Etiological treatment: Most cases stem from poor diet, so dietary improvement and proper feeding are essential. Some mild cases can be resolved with dietary adjustments alone. When modifying the diet, age-appropriate foods should be introduced. Since affected children often have poor digestion, introducing or changing complementary foods must be done carefully. Typically, after a few days of medication and clinical improvement, complementary foods can be gradually added to avoid digestive issues. For infants around one year old, egg yolk, vegetable puree, liver, and minced meat can be introduced. Older children should correct picky eating habits and consume iron-rich, vitamin C-rich, and protein-rich foods.
For chronic intestinal blood loss caused by excessive fresh milk intake, reduce milk to below 500ml daily or switch to powdered milk, evaporated milk, or milk substitutes. Surgical intervention or deworming is necessary for intestinal malformations or hookworm disease after anemia is corrected.
3. Blood Transfusion Due to the slow progression of the disease and the strong compensatory capacity of the body, blood transfusion is generally not required. Severe anemia, combined with serious infection, or the urgent need for surgical intervention are the indications for blood transfusion. For patients with hemoglobin levels below 30g/L, immediate blood transfusion is necessary, but it must be administered in small, frequent doses or as concentrated red blood cells, at 2–3 ml/kg per session. Rapid or excessive transfusion may lead to heart failure. In cases of severe heart failure, exchange transfusion can be performed, replacing whole blood with concentrated red blood cells. Digitalis therapy is usually not required.
Post-treatment response Within 12 to 24 hours after iron supplementation, iron-containing enzymes in cells begin to recover, leading to initial clinical symptom improvement, such as reduced dysphoria and other mental symptoms, as well as increased appetite. After 36 to 48 hours, bone marrow shows signs of erythroid hyperplasia. Reticulocyte counts start to rise 48 to 72 hours after medication, peaking between 4 to 11 days. During this period, hemoglobin levels increase rapidly, and anemia is typically corrected within 3 to 4 weeks of treatment. Heart murmurs diminish or disappear after 2 to 3 weeks, and the spleen gradually shrinks. After 1 to 3 months of medication, iron stores return to normal levels.
The prognosis is good, and most cases can be cured with iron therapy. If dietary improvements are made and the disease cause is eliminated, recurrence is rare. For extremely severe cases, death may occur if timely rescue is deficient. Severe infections and digestive disorders are often fatal causes. For children treated late, although anemia may fully recover, physical and intellectual development will be affected.
First, infant feeding guidance should be well implemented. Although the iron content in breast milk is insufficient, its absorption is relatively good. If breastfeeding is not possible, iron-fortified formula should be chosen for feeding. Alternatively, iron should be added to food early, and the food industry should be encouraged to produce iron-fortified infant and toddler foods on an industrial scale. Iron sulfate can be added to milk, cereals, and flour. For example, adding 0.06g of iron sulfate to 1000ml of milk equals 12mg of pure iron, which can meet the needs of infants. Assuming an iron absorption rate of 10%, the recommended daily intake during childhood is 10–15mg, while adolescent girls require 18mg/day.
Regarding iron-fortified diets, full-term infants should start from 4–6 months (no later than 6 months), while premature and low-birth-weight infants should start from 3 months. The simplest method is to add iron sulfate to formula or complementary foods. For breastfed infants, iron-fortified cereals can be added once or twice daily. Alternatively, iron sulfate drops can be used alternately, with full-term infants not exceeding 1mg/kg/day of pure iron (2.5% FeSO4 0.2ml/kg/day), and premature infants not exceeding 2mg/kg/day. The maximum total daily dose is 15mg, and home use should not exceed 1 month to avoid iron toxicity.
For formula-fed infants after 6 months, if non-iron-fortified milk is used, the total amount should not exceed 750ml; otherwise, it will displace iron-rich foods.
For children and adults, it is best to add 13–16mg of iron per pound of flour. In rural areas of China, where diets are primarily cereal- and starch-based, and some regions are endemic for hookworm disease, this issue must be taken seriously. At the same time, efforts should be made to increase the intake of animal-based foods, as even if iron is added to cereals, its absorption is not as efficient as that from animal-based foods.
Regular health check-ups and anemia screenings should be conducted to enable early treatment of mild cases. For infants with hemoglobin levels at the lower normal limit of 110g/L, iron supplements at 3mg/kg/day should also be administered for 3 months. Studies have shown that in some of these infants, hemoglobin levels increase by grade I after iron supplementation, indicating that grade I iron deficiency also exists in this group and must be promptly corrected.
The diagnosis relies on the aforementioned laboratory tests, excluding the following hypochromic microcytic anemias:
1. Thalassemia: There is a family history, with a notable regional distribution. Characteristic facial features and significant hepatosplenomegaly are present. Blood smears show target cells and nucleated red blood cells. Hemoglobin electrophoresis reveals increased A2 and F, or the presence of hemoglobin H or Bart's. Serum iron levels are elevated, and bone marrow shows increased sideroblasts.
2. Pulmonary hemosiderosis: Manifested as episodic pallor, weakness, cough, blood in sputum, and hemosiderin-laden cells found in sputum and gastric fluid. Reticulocyte count is elevated. Chest X-rays show reticulonodular shadows in the lung fields.
3. Sideroblastic anemia: Bone marrow smears reveal a marked increase in extracellular iron, with iron granules arranged in a ring around the nuclei of intermediate and late erythroblasts. Serum iron levels are elevated. Iron therapy is ineffective, but some patients respond well to vitamin B6 treatment.
4. Anemia of chronic infection: Typically presents as normochromic microcytic anemia, occasionally hypochromic. Both serum iron and iron-binding capacity are reduced, with increased sideroblasts in the bone marrow. Iron therapy is ineffective.
5. Lead poisoning: Basophilic stippling is observed in red blood cells, serum lead levels are elevated, and erythrocyte and urinary protoporphyrin levels are significantly increased. FEP/Hgb may exceed 17.5 μg/g.
