Total serum iron binding capacity (TIBC) (includes determination of iron, TIBC)

Indications for the study

Analysis for OZhSS

, as a rule, are prescribed in conjunction with other laboratory tests to determine the amount of a microelement and evaluate its relationship with proteins. The results obtained make it possible to identify iron deficiency or excess and establish the exact cause of anemia.

The test is carried out in the following cases:

• symptoms of iron excess or deficiency;
• identified deviations from normal values ​​in the results of the UAC;
• monitoring the progress of treatment.

Microelement deficiency does not manifest itself in any way over a long period of time. First of all, symptoms such as dizziness, weakness, and headaches appear. With a significant lack of iron, shortness of breath and pain in the chest appear. Unconventional food preferences may appear. When there is an excess of a microelement, symptoms such as cardiac dysfunction, pain in the abdomen or in the joint area appear.

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Interpretation of results

The following reference values ​​have been established for THC: 45.3-77.1 µmol/l. Interpretation of the results of this test is carried out taking into account data from other laboratory tests. Only a doctor can properly evaluate them; self-diagnosis and self-medication are unacceptable. An elevated reading usually indicates anemia. It may be caused by low levels of meat in the diet or significant blood loss. An increase in PVSS may also be observed in patients with acute hepatitis. In late pregnancy, an increase in levels is caused by an increase in the need for iron.

If the test results are below normal, this may indicate various diseases (for example, tuberculosis, rheumatoid arthritis). To establish an accurate diagnosis in most cases, a comprehensive examination is required.

Total iron binding capacity (TIBC)

Total iron binding capacity (IBC)

) is an indicator used to diagnose the amount of iron that the blood can carry. An increase in the level of iron-binding capacity indicates a low level of iron in the blood and is characteristic of iron deficiency anemia, which is caused by chronic blood loss, lack of iron in the diet, as well as impaired absorption in the gastrointestinal tract. Sometimes an increase in iron-binding capacity is observed in acute hepatitis.

The total iron-binding capacity of blood serum (TIBC) is the sum of serum iron and NIBC (TIBC). Determination of blood serum PVSS and LVSS (LVSS) is used in the diagnosis of anemia.

The iron-binding capacity of serum changes with disorders of iron metabolism. In iron deficiency anemia, the PVSS and LVSS increase, and the saturation of transferrin with iron decreases to 15% and below. Low values ​​of serum iron, combined with low values ​​of PVSS and NSSS, are characteristic of anemia associated with chronic diseases, malignant tumors, infections (for the differential diagnosis of anemia in these cases, the determination of ferritin is also important). Instead of determining the iron-binding capacity of serum, the determination of transferrin content in serum can be used for the same purposes.

Iron

- is an important trace element in the human body. It is part of hemoglobin, which fills red blood cells and allows them to transport oxygen from the lungs to organs and tissues. Iron is part of the muscle protein myoglobin and some enzymes. It is absorbed from food and then transported throughout the body by transferrin, a special protein that is formed in the liver.

Normally, the body contains 4–5 g of iron, about 3–4 mg (0.1% of the total amount in the body) circulates in the blood “in conjunction” with transferrin. The amount of transferrin depends on the functioning of the liver and the person’s diet. Normally, 1/3 of the transferrin binding centers are filled with iron, the remaining 2/3 remain in reserve. To determine the total iron-binding capacity of blood serum, a certain amount of iron is added to the test serum until all transferrin binding centers are filled. The total amount of iron bound to transferrin is then measured. It characterizes the degree of serum iron deficiency and actually reflects the amount of transferrin in the blood.

With iron deficiency, there is more transferrin in the body so that this protein can bind to the small amount of iron in the serum. Accordingly, transferrin “unoccupied” by iron, that is, the latent iron-binding capacity of the serum, also increases. On the contrary, with an excess of iron, almost all transferrin binding centers are occupied by this trace element, therefore the latent iron-binding capacity of the serum decreases.

The amount of serum iron can vary significantly from one day to the next and even within one day (especially in the morning), however, the normal life-value level remains relatively stable.

Indications:
When is the study prescribed?

• when any abnormalities are detected in a general blood test, analysis of hemoglobin, hematocrit, red blood cell count (together with a test for iron in serum);
• if you suspect iron deficiency or excess;
• In the early stages, iron deficiency may not show any symptoms. If a person is otherwise healthy, then the disease can make itself felt only when hemoglobin decreases below 100 g/l. Usually these are complaints of weakness, fatigue, dizziness, headaches;
• With severe iron deficiency, shortness of breath, pain in the chest and head, and weakness in the legs occur. Some people have a desire to eat unusual foods (chalk, clay), a burning sensation on the tip of the tongue, and cracks in the corners of the mouth. Children may have learning difficulties;
• OZHS and other tests reflecting iron metabolism may be prescribed if the body is suspected of overloading with iron (hemochromatosis). This condition manifests itself in different ways: for example, pain in the joints or in the abdomen, weakness, fatigue, decreased sexual desire, irregular heart rhythm;
• when monitoring the effectiveness of treatment for iron deficiency or excess.

Preparation
It is recommended to donate blood in the morning, between 8 am and 12 pm. Blood is drawn on an empty stomach, after 6–8 hours of fasting. It is allowed to drink water without gas and sugar. On the eve of the examination, food overload should be avoided.

Interpretation of results

Reference values: 45.3–77.1 µmol/l.

Interpretation of the results of the analysis on the life cycle is usually carried out taking into account other indicators that assess iron metabolism.

Reasons for increasing the life insurance ratio:

• anemia is the most common cause of low iron levels. It is usually caused by chronic blood loss or insufficient consumption of meat products;
• third trimester of pregnancy. In this case, serum iron levels decrease due to increased iron requirements;
• acute hepatitis.

Reasons for the decrease in life insurance:

• chronic diseases: systemic lupus erythematosus, rheumatoid arthritis, tuberculosis, bacterial endocarditis, Crohn's disease, etc.;
• hypoproteinemia associated with absorption disorders, chronic liver disease, burns. A decrease in the amount of protein in the body leads, among other things, to a drop in the level of transferrin, which reduces the life span;
• hereditary hemochromatosis. With this disease, too much iron is absorbed from food, the excess of which is deposited in various organs, causing their damage;
• thalassemia is a hereditary disease leading to anemia, in which the structure of hemoglobin is changed;
• liver cirrhosis, glomerulonephritis;
• multiple blood transfusions, intramuscular iron administration, inadequate dosage of prescribed iron supplements.

What can influence the result?

• Estrogens and oral contraceptives lead to an increase in life-span.
• ACTH, corticosteroids, testosterone can reduce CVV.
• Serum hemolysis makes the results unreliable.

Important notes
The amount of serum iron can vary significantly from one day to the next and even within one day (especially in the morning), but the normal life-cycle iron level remains relatively stable.

The level of transferrin can be calculated using the formula: 0.8 x TBL - 43. However, the relationship between TBL and transferrin is not linear and may not be observed in diseases that affect the binding capacity of transferrin.

Iron deficiency anemia in infants and young children

Anemia and anemic syndrome, caused by many causes, can be mentioned among the most common pathological conditions that general pediatricians have to deal with every day. This group includes various diseases and pathological conditions characterized by a decrease in the content of hemoglobin and/or red blood cells per unit volume of blood, leading to disruption of the oxygen supply to tissues. The following laboratory criteria for anemia are applied (N.P. Shabalov, 2003). Depending on the age of the children, the hemoglobin level is:

• 0–1 day of life - < 145 g/l;
• 1–14 days of life - < 130 g/l;
• 14–28 days of life - < 120 g/l;
• 1 month - 6 years - < 110 g/l.

Of all anemias, the most common is iron deficiency (IDA), which accounts for approximately 80% of all anemias. According to the World Health Organization (WHO), more than 500 thousand people worldwide suffer from IDA. The prevalence of IDA in children in Russia and developed European countries is: about 50% in young children; more than 20% - in older children.

IDA is a clinical and hematological syndrome characterized by impaired hemoglobin synthesis as a result of iron deficiency, developing against the background of various pathological (physiological) processes, and manifested by signs of anemia and sideropenia.

Iron is one of the main microelements in the human body. Normally, the adult body contains 3–5 g of iron in bound form. 70% of the total amount of iron is part of hemoproteins. The iron in these compounds is bound to porphyrin. The main representative of this group is hemoglobin (58% iron); Iron is also contained in myoglobin (8%), cytochromes, peroxidases, catalases - up to 4%. Iron is also part of non-heme enzymes (xanthine oxidase, nicotinamide adenine dinucleotide (NADH) dehydrogenase, aconitase, localized in mitochondria); transport form of iron (transferrin, lactoferrin). Iron reserves in the body exist in two forms: in the form of ferritin (up to 70%) and hemosiderin (up to 30%). The peculiarity of iron distribution in young children is that they have a higher iron content in erythroid cells and less iron in muscle tissue.

Iron absorption occurs predominantly in the duodenum and proximal jejunum. The daily diet usually contains about 5–20 mg of iron, and only about 1–2 mg per day is absorbed. The degree of iron absorption depends both on its amount in food consumed and bioavailability, and on the state of the gastrointestinal tract (GIT).

Iron is more easily absorbed in heme (meat products) - 9–22%. Absorption of non-heme iron is determined by diet and gastrointestinal secretion patterns.

Iron absorption is especially active from breast milk, although its content is low - only 1.5 mg per liter; The bioavailability of iron in breast milk is up to 60%. This is facilitated by the special form in which it is presented - in the form of the iron-containing protein lactoferrin. In the lactoferrin molecule, two active binding sites for Fe3+ ions are identified. Lactoferrin is found in breast milk in saturated and unsaturated forms. The ratio of lactoferrin forms varies depending on the lactation period. During the first 1–3 months of life, the saturated iron transport form of lactoferrin predominates. The presence of specific receptors for lactoferrin on the epithelial cells of the intestinal mucosa promotes the adhesion of lactoferrin to them and its more complete utilization. In addition, lactoferrin, by binding excess iron that is not absorbed in the intestine, deprives the opportunistic microflora of the microelement necessary for its life and triggers nonspecific bactericidal mechanisms. It has been established that the bactericidal function of immunoglobulin A is realized only in the presence of lactoferrin.

Physiological losses of iron in urine, sweat, feces, through the skin, hair and nails do not depend on gender and amount to 1-2 mg per day, in women during menstruation - 2-3 mg per day. In children, iron loss is 0.1–0.3 mg per day, increasing to 0.5–1.0 mg per day in adolescents.

The daily requirement of a child's body for iron is 0.5–1.2 mg per day. In young children, due to rapid growth and development, there is an increased need for iron. During this period of life, iron reserves are quickly depleted due to increased consumption from the depot: in premature infants by the 3rd month, in full-term infants by the 5th–6th month of life. To ensure the normal development of a child, the daily diet of a newborn should contain 1.5 mg of iron, and for a child 1–3 years old - at least 10 mg.

Iron deficiency in children leads to an increase in infectious diseases of the respiratory system and gastrointestinal tract. Iron is necessary for the normal functioning of brain structures; if it is insufficient, the child’s neuropsychic development is disrupted. It has been established that in children who had iron deficiency anemia in infancy, at the age of 3–4 years, disturbances in the transmission of nerve impulses from the centers of the brain to the organs of hearing and vision are determined due to impaired myelination and, as a consequence, impaired nerve conduction.

The causes of iron deficiency in children are very diverse. The main cause of IDA in newborns is considered to be the presence of IDA or hidden iron deficiency in the mother during pregnancy. Antenatal causes also include complicated pregnancy, impaired uteroplacental circulation, fetomaternal and fetoplacental bleeding, fetal transfusion syndrome in multiple pregnancies. Intrapartum causes of iron deficiency are: fetoplacental transfusion, premature or late ligation of the umbilical cord, intrapartum bleeding due to traumatic obstetric care or abnormal development of the placenta or umbilical cord. Among the postnatal causes of sideropenic conditions, the first place is taken by insufficient intake of iron from food. In this case, newborns who are bottle-fed with unadapted milk formulas, cow's and goat's milk suffer the most. Other postnatal causes of IDA are: increased body need for iron; iron losses exceeding physiological ones; gastrointestinal diseases, malabsorption syndrome; deficiency of iron stores at birth; anatomical congenital anomalies (Meckel's diverticulum, intestinal polyposis); consumption of foods that inhibit iron absorption.

Premature children and children born with a very large weight, children with a lymphatic-hypoplastic type of constitution are always at risk.

In children of the first year of life, iron deficiency is most often caused by an unbalanced diet, in particular, feeding exclusively with milk, vegetarianism, and insufficient consumption of meat products.

Bleeding of various etiologies can lead to sideropenia. The source of this may be: hiatal hernia, esophageal varices, gastrointestinal ulcers, tumors, diverticula, ulcerative colitis, hemorrhoids, as well as bleeding from the genitourinary tract and respiratory tract. Taking certain medications, such as nonsteroidal anti-inflammatory drugs, salicylates, coumarins, and glucocorticosteroids, can also lead to iron loss. Iron deficiency always accompanies diseases accompanied by impaired intestinal absorption (enteritis, Crohn's disease, parasitic infestations, etc.). Intestinal dysbiosis also interferes with normal digestion of food and thereby reduces the body's ability to absorb iron. In addition, there may be a disruption in iron transport due to insufficient activity and decreased transferrin levels in the body.

It is extremely important to recognize the cause of the development of IDA in each specific case. Focus on nosological diagnosis is necessary, since in most cases, when treating anemia, it is possible to influence the underlying pathological process.

IDA manifests itself with general symptoms. One of the main and visible signs is pallor of the skin, mucous membranes, and conjunctiva of the eyes. Noteworthy are general lethargy, moodiness, tearfulness, easy excitability of children, decreased overall body tone, sweating, lack or decreased appetite, shallow sleep, regurgitation, vomiting after feeding, decreased visual acuity. Changes in the muscular system are detected: the child has difficulty overcoming physical activity, weakness and fatigue are noted. In children of the first year of life, regression of motor skills may be observed.

In the second half of life and in children older than one year, signs of damage to epithelial tissue are observed - roughness, dry skin, angular stomatitis, painful cracks in the corners of the mouth, glossitis or atrophy of the oral mucosa, fragility and dullness of hair, hair loss, dullness and brittleness of nails, tooth decay (caries), retardation in physical and psychomotor development.

Depending on the severity of the disease, symptoms of damage to organs and systems are identified: cardiovascular - in the form of a functional heart murmur, tachycardia; nervous system - in the form of headaches, dizziness, fainting, orthostatic collapse. Possible increase in the size of the liver and spleen. From the gastrointestinal tract, there is difficulty swallowing, bloating, diarrhea, constipation, perversion of taste - the desire to eat clay, earth.

The diagnosis of IDA is made based on the clinical picture, laboratory signs of anemia and iron deficiency in the body: hypochromic (color index < 0.85) anemia of varying severity, hypochromia of erythrocytes, decrease in the average hemoglobin concentration in erythrocytes (less than 24 pg), microcytosis and poikilocytosis of erythrocytes (in peripheral blood smear); decrease in the number of sideroblasts in bone marrow aspirate; decrease in iron content in blood serum (<12.5 µmol/l); an increase in the total iron-binding capacity of serum (TIBC) of more than 85 µmol/l (an indicator of “starvation”); an increase in the level of transferrin in the blood serum, with a decrease in its saturation with iron (less than 15%); decreased serum ferritin levels (<15 µg/L).

Treatment of IDA

Treatment of IDA in young children should be comprehensive and based on four principles: normalization of the child’s regimen and nutrition; possible correction of the cause of iron deficiency; prescription of iron supplements; concomitant therapy.

The most important factor in correcting iron deficiency is a balanced diet, and primarily breastfeeding. Breast milk not only contains iron in a highly bioavailable form, but also increases the absorption of iron from other foods consumed at the same time. However, intense metabolic processes in infants lead to the fact that by the 5th–6th month of life, antenatal iron reserves are depleted even in children with a good perinatal history and babies fed with breast milk.

Among other foods, the greatest amount of iron is found in pork liver, beef tongue, veal kidneys, egg yolk, oysters, beans, sesame seeds, seaweed, wheat bran, buckwheat, pistachios, chick peas, peaches, oatmeal, spinach, hazelnuts and etc. (table).

Iron absorption is inhibited by tannins contained in tea, carbonates, oxalates, phosphates, ethylenediaminetetraacetic acid used as a preservative, antacids, and tetracyclines. Ascorbic, citric, succinic and malic acids, fructose, cysteine, sorbitol, nicotinamide enhance iron absorption.

Long walks in the fresh air, normalization of sleep, a favorable psychological climate, prevention of acute respiratory viral infections (ARVI), and limitation of physical activity are necessary. The child's diet should be balanced and include foods rich in iron and substances that enhance its absorption in the intestines. Children suffering from IDA need to be introduced to complementary foods 2–4 weeks earlier than healthy ones. It is advisable to start introducing meat complementary foods at 6 months. You should avoid introducing cereals such as semolina, rice, and bearberry into your child’s diet, giving preference to buckwheat, barley, and millet.

However, these measures are insufficient and do not lead to the cure of IDA, so the basis of therapy is iron supplements. The main ones used orally include: ferric iron compounds - hydroxide-polymaltose complex (iron polymaltose), maltofer, maltofer foul, ferrum lek and iron-protein complex (iron protein succinylate) - ferlatum; divalent iron compounds - actiferrin, ferroplex, tardiferon, hemofer, totema, ferrous fumarate, ferronate.

Therapy should be started with drugs for oral administration and only if they are poorly tolerated (nausea, vomiting, diarrhea), malabsorption syndrome, resection of the small intestine, etc. - iron supplements are prescribed parenterally. When prescribing oral forms, preference should be given to nonionic iron compounds - protein (ferlatum) and hydroxide-polymaltose Fe3+ complexes (maltofer, maltofer foul, ferrum lek). These compounds have a large molecular weight, which makes it difficult for them to diffuse across the intestinal mucosal membrane. They enter the blood from the intestines as a result of active absorption. This explains the impossibility of overdosing on drugs, unlike iron salt compounds, the absorption of which occurs along a concentration gradient. There is no interaction between them and food components and medications, which allows the use of non-ionic iron compounds without disturbing the diet and treatment of concomitant pathologies. Their use significantly reduces the incidence of side effects usually observed when prescribing oral iron supplements (nausea, vomiting, diarrhea, constipation, etc.). In addition, in young children, the dosage form of the drug is of great importance. At this age, it is convenient to use drops and syrups, which also provides the possibility of precise dosing of drugs and does not cause a negative attitude from the child.

When prescribing any iron supplements, it is necessary to calculate the individual need for it for each patient, based on the fact that the optimal daily dose of elemental iron is 4–6 mg/kg. The average daily dose of iron in the treatment of IDA is 5 mg/kg. The use of higher doses does not make sense, since the amount of iron absorption does not increase.

The use of parenteral iron supplements is indicated to quickly achieve an effect in severe anemia; gastrointestinal pathology combined with malabsorption; nonspecific ulcerative colitis; chronic enterocolitis; with severe intolerance to oral forms of drugs. Today in the Russian Federation, only one drug is approved for intravenous administration - venofer (iron sucrose), while ferrum lek can be used for intramuscular administration.

It must be remembered that in young children, iron deficiency is never isolated and is often combined with a deficiency of vitamins C, B12, B6, PP, A, E, folic acid, zinc, copper, etc. This is due to the fact that nutritional deficiency and impaired intestinal absorption, leading to iron deficiency, also affects saturation with these micronutrients. Therefore, it is necessary to include multivitamin preparations in complex therapy for IDA.

The effectiveness of IDA therapy can be judged after 7–10 days by an increase in reticulocytes by 2 times compared to the initial number (the so-called reticulocyte crisis). The increase in hemoglobin is also assessed, which should be 10 g/l or more per week. Accordingly, achievement of the target hemoglobin level is observed on average 3–5 weeks from the start of therapy, depending on the severity of anemia. However, treatment with iron supplements should be carried out in sufficient doses and for a long time (at least 3 months) even after normalization of hemoglobin levels in order to replenish iron reserves in the depot.

If within 3-4 weeks there is no significant improvement in hemoglobin levels, then it is necessary to find out why the treatment was ineffective. Most often we are talking about: an inadequate dose of iron supplement; ongoing or unknown blood loss; the presence of chronic inflammatory diseases or neoplasms; concomitant vitamin B12 deficiency; incorrect diagnosis; helminthic infestation and other parasitic infections.

Contraindications to the use of iron supplements are:

• lack of laboratory confirmation of iron deficiency;
• sideroachrestic anemia;
• hemolytic anemia;
• hemosiderosis and hemochromatosis;
• infection caused by gram-negative flora (enterobacteria, Pseudomonas aeruginosa, Klebsiella).

With the development of severe anemia, accompanied by inhibition of erythropoiesis and a decrease in erythropoietin production, the administration of recombinant human erythropoietin (rhEPO) preparations is indicated. The use of rhEPO is of particular importance in the development of early anemia of prematurity, which develops in the second month of life and occurs, according to various authors, in 20–90% of cases. The administration of rhEPO drugs (Recormon, Eprex, Epocrine) leads to a sharp activation of erythropoiesis and, as a consequence, to a significant increase in iron requirements.

Therefore, the use of rhEPO is an indication for the administration of iron supplements, usually parenteral. Currently, a- and b-epoetins are approved for use in the Russian Federation and are included in the list of additional medicinal products. Prescribing rhEPO allows, in most cases, to avoid blood transfusions, in which there is a high probability of complications (transfusion reactions, sensitization, etc.). The preferred route of administration of rhEPO preparations, especially in early childhood, is subcutaneous. The subcutaneous route of administration is safer and more economical, since smaller doses are required to achieve an effect than with intravenous administration. Until recently, in the countries of the European Union and in the Russian Federation, mainly β-erythropoietins were used for the treatment of hyporegenerative anemia in children, which, when administered subcutaneously, did not cause significant adverse reactions, unlike a-erythropoietins, when administered subcutaneously, there was a high risk of developing red cell aplasia. The most widely used drug among β-erythropoietins is Recormon (F. Hoffmann-La Roche), which is easy to use and leads to a rapid increase in the level of erythrocytes and reticulocytes without affecting leukopoiesis, increases the level of hemoglobin, as well as the rate of incorporation of iron into cells.

Since 2004, European countries have allowed subcutaneous administration of a-erythropoietins, among which in our country the most commonly used are Eprex (Jansen-Silag) and Epocrine (Sotex-GosNII OCHB).

The goal of rhEPO treatment is to achieve hematocrit levels of 30–35% and eliminate the need for blood transfusions. The target hemoglobin concentration values ​​may vary depending on the days and months of the child’s life, but cannot be lower than 100–110 g/l. Depending on the dose, target hemoglobin concentrations and hematocrit are achieved after approximately 8–16 weeks of rhEPO treatment.

To prevent iron deficiency anemia, rhEPO is prescribed to premature newborns born weighing 750–1500 g before the 34th week of pregnancy.

Treatment with erythropoietin should begin as early as possible and continue for 6 weeks. The drug Recormon is administered subcutaneously at a dose of 250 IU/kg 3 times a week. However, it must be taken into account that the younger the child is, the higher doses of erythropoietin he requires, so the dose can be increased.

As mentioned above, rhEPO therapy leads to a sharp increase in iron intake, therefore, in most cases, especially in premature infants, along with an increase in hematocrit, serum ferritin levels decrease. Rapid depletion of iron reserves in the body can lead to IDA. Therefore, all patients receiving rhEPO therapy are prescribed iron supplements. Therapy with iron supplements should continue until serum ferritin levels are normalized (at least 100 mcg/ml) and transferrin saturation (at least 20%). If serum ferritin concentration remains persistently below 100 mcg/ml or there are other signs of iron deficiency, the dose of iron should be increased, including the use of parenteral drugs.

Prevention of IDA in young children includes: antenatal (correct regimen and nutrition of the pregnant woman, timely detection and treatment of anemia in the pregnant woman, preventive administration of iron supplements to women at risk for developing IDA); postnatal (observance of hygienic living conditions for the child, long-term breastfeeding and timely introduction of complementary foods, adequate choice of formula for children on mixed and artificial feeding, prevention of the development of rickets, malnutrition and ARVI in the child). The following people need prophylactic administration of iron supplements:

• women of reproductive age suffering from heavy and prolonged menstrual bleeding;
• regular donors;
• pregnant women, especially repeat pregnancies following a short interval;
• women with iron deficiency during lactation.

Preventive administration of iron supplements is indicated for children at risk for developing IDA:

• premature babies (from 2 months of age);
• children from multiple pregnancies, complicated pregnancies and childbirths;
• large children with high rates of weight gain and height;
• children with constitutional anomalies;
• suffering from atopic diseases;
• those who are artificially fed with unadapted formulas;
• with chronic diseases;
• after blood loss and surgical interventions;
• with malabsorption syndrome.

The dose of iron prescribed for preventive purposes depends on the degree of prematurity of the child:

• for children with birth weight less than 1000 g - 4 mg Fe / kg / day;
• for children with birth weight from 1000 to 1500 g - 3 mg Fe/kg/day;
• for children with birth weight from 1500 to 3000 g - 2 mg Fe/kg/day.

The significance of the problem of IDA in young children is due to its high prevalence in the population and its frequent development in various diseases, which requires constant vigilance among doctors of all specialties. Nevertheless, at the present stage, the doctor’s arsenal has enough diagnostic and therapeutic capabilities for early detection and timely correction of sideropenic conditions.

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L. A. Anastasevich , Candidate of Medical Sciences A. V. Malkoch , Candidate of Medical Sciences, Russian State Medical University, Moscow