Since different preparations contain an unequal amount of iron in different chemical forms, the calculation of the therapeutic dose should be carried out only for elemental iron.

It is better to use parenteral drugs not daily, but with an interval of 1-2 days. With the first 1-3 injections, you can reduce the daily dose of elemental iron by half.

The course dose of elemental iron is calculated by the formula:

Elemental iron (mg) \u003d \u003d MT´ (78 – 0,35 ´ Hb),

where MT - body weight (kg); Hb - hemoglobin (g / l).

The course dose of the iron-containing drug is calculated as follows:

The amount of the drug per course (ml) \u003d \u003d KJ: SZHP,

where KJ - course dose of iron (mg); SGP - iron content (mg) in 1 ml of the preparation.

The course number of injections is calculated by the formula:

Number of injections \u003d KDP: SDP,

where KDP - course dose of the drug (ml); SDP - daily dose of the drug (ml).

Parenteral administration should not exceed 100 mg of iron per day, giving full transferrin saturation. In children under 2 years of age, the daily dose of parenterally administered iron is 25-50 mg, in children over 2 years of age - 50-100 mg.

Single dose of drugs:

Children weighing up to 5 kg - 0.5 ml;

6 to 10 kg - 1 ml;

Children over one year old - 1.5-2 ml;

Teenagers - 4 ml.

Dispensary observation of children with iron deficiency anemia

Dispensary supervision by a pediatrician in the acute period 1-2 times per month

monday, during the period of remission, once every 3 months. Hematologist according to indications. Handling

pay attention to the general condition, the condition of the liver, spleen, gastrointestinal tract, ser-

cardiovascular systems. A blood test once every 2 weeks, during remission -

1 time in 3 months, determination of serum iron. Deregistered through

year with normal hemogram indicators. Preventive vaccinations

after 6 months with normalization of blood counts.

Clinical examination of children with hemolytic anemias (D 55 -D 59)

Dispensary observation: pediatrician 1 time per month, hematologist 2 times a year,

other specialists according to indications. Blood test with reticulocyte count

tov, microspheres once a month; bilirubin, transaminases - 1 time in 3 months.

Physical education at school is contraindicated. Disability

issued in case of anemic crises more often than once a year with a decrease

Нb less than 100g / l. With Minkowski-Shoffard anemia, children can be removed

from dispensary registration 4 years after splenectomy in the absence of re-

cidives. Preventive vaccinations according to the situation.

654.7.6. Clinical examination of children with aplastic anemia (D60 -D 64)

Dispensary supervision: pediatrician and hematologist once a month, others

experts on indications. Pay attention to: pallor, hemorrhages

ic syndrome, liver, spleen condition, of cardio-vascular system,

violation of the gastrointestinal tract. Blood test with platelet count 1 time per

month. Physical education at school is contraindicated. Disability

issued for congenital and acquired aplastic anemias and hy-

in plastic conditions against the background of changes in peripheral blood (Нb

below 100 g / l, platelets below 100x109

/ l, leukocytes less than 4x109

/ l) for a period

before reaching 18 years of age. Preventive vaccinations individually, taking into account

volume of the epidemiological situation. Observation before transfer to adult

(LGD) – anomaly of the constitution, accompanied by diffuse hyperplasia of lymphoid tissue (generalized increase lymph nodes and thymus), dysfunction endocrine system, a sharp change in the reactivity of the body.

The most characteristic feature of PHD is a tendency to significant persistent enlargement of the lymph nodes and thymus. Lymph nodes are multiple, but soft, mobile, and painless. Characterized by an increase in almost all groups, as well as mesenteric and mediastinal, lymphatic follicles of the posterior pharyngeal wall, tongue, an increase in the palatine and nasopharyngeal tonsils. Adenoid vegetation leads to impaired nasal breathing, lingering rhinitis, the formation of an adenoid type of face, impairs the blood supply to the brain, which is associated with some emotional lethargy, immobility, and physical inactivity in children with PHD. With severe thymic hyperplasia, signs of compression develop respiratory tract: low timbre and hoarseness of the voice, throwing the head back during sleep, noisy breathing, mixed shortness of breath, aggravated in sleep and in a horizontal position, "cock's cry" when crying, "causeless" cough. In peripheral blood, lymphocytosis and monocytosis are detected.

In the practice of a family doctor, the prevention of genotypically determined diseases in the observed family is of great importance. Multifactorially inherited pathology at the first stage has nonspecific clinical manifestations that are classified as diathesis or constitutional anomaly. With age, with the proper organization of care, regimen, nutrition, the manifestations of diathesis in most children disappear and only in a part they are transformed into one or another chronic disease. It is generally accepted to distinguish exudative-catarrhal, lymphatic-hypoplastic and neuro-arthritic anomalies of the constitution. The diagnosis of diathesis is established taking into account the pedigree of the child, the nature of the course of pregnancy, clinical manifestations and laboratory tests.

Exudative-catarrhal diathesis the most common anomaly of the constitution. About 28% of children in the first year of life have some kind of clinical manifestations of diathesis. Their development is associated with hereditary shifts in some enzymatic systems. At the same time, there is a reduced histamine-peptic capacity of the blood, a low activity of carboxy-peptidase, acetylcholinesterase, monoamine oxidase, which contributes to an increase in the permeability of the gastrointestinal tract for proteins. In children with exudative-catarrhal diathesis, a delay in the body of sodium, chlorine, water and biogenic amines is found, which is due to an imbalance in the activity of the adrenal glands with an increase in mineralocorticoid function. Among the relatives of children with exudative-catarrhal diathesis, there are patients with allergic diseases: bronchial asthma, hay fever, food allergy, atopic dermatitis, etc.

Exudative-catarrhal diathesis is characterized mainly by catarrhal lesions of the epithelial tracts and skin of an allergic nature with a tendency to secondary microbial infection. Signs of exudative-catarrhal diathesis in many children are noted already in the first months of life. On the scalp, gray oily scales (gneiss), scaly peeling and redness of the skin on the face ("milk crust"), diaper rash in the folds of the neck, palms, armpits and groins are found. In children of the second half of life and after a year, erythematous-vesicular rashes, manifested by dermatitis, eczema, are often noted.

From the mucous membranes in children with exudative-catarrhal diathesis, blepharitis, conjunctivitis, catarrh of the upper respiratory tract, vulvovaginitis, balanitis, infections are often noted urinary tract... Children have a tendency to unstable stools or persistent constipation. Children with clinical manifestations of diathesis upon admission to the children's collective, as a rule, replenish the group of people who often suffer from respiratory diseases.

Laboratory examination often reveals moderate leukocytosis, eosinophilia, lymph and monocytosis, a slight increase in ESR. The second granulo-agranulocytic crossover in children with exudative-catarrhal diathesis is noted later, at about 6-7 years of age. Among the pathogenetic markers, an increase in immunoglobulin E in the blood, a decrease or absence of the secretory component of immunoglobulin A in the secretions of the mucous membranes, and low activity of T-suppressor lymphocytes are important.

Prevention of clinical manifestations of exudative-catarrhal diathesis begins long before the birth of a child and is based on the creation of a hypoallergenic life of a pregnant woman. Children with this constitutional anomaly should stay on breastfeeding... Obligatory and causal allergens are excluded from the diet of a nursing mother. When complementary foods are introduced, the child's reaction to the new food is recorded in the food diary. Thus, it is possible to exclude products for which there is an individual sensitivity. With mixed and artificial feeding, it is necessary, if possible, to reduce the amount of cow's milk and animal fat, which is replaced by 30% with vegetable oil.

Treatment: subject to allergic manifestations, the child is prescribed antihistamines (suprastin, tavegil, ketotifen). At the heart of the pathogenetic treatment of manifestations of exudative-catarrhal diathesis is an increase in the threshold of permeability of the epithelium of the gastrointestinal tract for proteins. In this regard, such children are shown the use of membranoprotective drugs (vitamins A, E, B 6) in age-specific dosages together with mineral preparations (panangin, asparkam). If it is not possible to maintain the satisfactory condition of the child using the above methods. If it is not possible to maintain the satisfactory condition of the child with the above methods, treatment with intal, oral nalcrome is recommended. Taking into account the existing digestive dysfermentopathy, it is possible to use enzymes (pancreatin, mezim-forte, etc.), provided there is no allergic reaction to them. Otherwise, hydrochloric acid with pepsin can be prescribed for a short time until the stool character improves. Intestinal syndrome with exudative-catarrhal diathesis, as a rule, leads to the development of intestinal dysbiosis. In this regard, the use of bacterial preparations (bifidum-bacterin, lacto-bacterin, at an older age - coli-bacterin), as well as feeding with fermented milk mixtures prepared with special bacterial starters (biobacton, "Narine").

In the treatment of cutaneous and gastrointestinal manifestations of exudative-catarrhal diathesis is widely used phytotherapy(baths of herbs of camel thorn, lava leaf, calamus rhizome, oak bark, oregano, St. John's wort, oat bran), starch bath. Inside, the so-called "aerin tea" is used: For severe itching, apply sedativescontaining bromine, valerian, motherwort.

Apply dermally ointmentscontaining zinc or papaverine, Unna cream. During the period of remission, for the prevention of exacerbation, they are used adaptogenic drugs.

Lymphatic-hypoplastic diathesis it is associated with hypofunction of the sympathetic-adrenal system, a decrease in the glucocorticoid function of the adrenal cortex, insufficiency of the immunocompetent function of the adrenal cortex, insufficient immunocompetent function of the lymphoid tissue. Among the relatives of children with this constitutional anomaly, there are patients with chronic diseases of the nasopharynx and respiratory tract.

In such children, hyperplasia of lymphoid tissue is noted with simultaneous hypoplasia of some endocrine glands and internal organs. They often have an anomaly in the development of the thymus gland and deviations in the formation of cellular and humoral immunities. Diathesis often manifests itself in early and preschool age.

Outwardly, children look lethargic, pasty, their body weight exceeds the average standard. The subcutaneous fat is excessively developed, the muscular system is poorly expressed. The body is relatively short, the limbs are elongated, the chest is narrowed. The tonsils are hypertrophied, loose. Significant adenoid growths are often found. Numerous swollen subcutaneous lymph nodes are felt. The thymus gland is enlarged.

Children with lymphatic-hypoplastic diathesis are prone to frequent respiratory diseases of various origins. They often develop broncho-obstructive syndrome. Inflammatory diseases the nasopharynx often occurs with manifestations of lymphadenitis. When stressful situations sudden death syndrome may occur. Often, with this anomaly of the constitution, skin and respiratory allergic reactions occur, which determines the similarity of lymphatic-hypoplastic and exudative-catarrhal diathesis.

In blood such children have a slight leukocytosis, relative or absolute lymphocytosis, sometimes monocytosis, neutropenia.

Treatment: early tempering, regular massage and gymnastics courses are recommended. Of diets the excess amount of fats, easily digestible carbohydrates, salt and liquid is excluded. In the cold season and in spring, such children are recommended to prescribe complex vitamin preparations ("Aevit", "Undevit", "Alphabet", etc.), containing vitamins of groups A, E, C, B. The effectiveness of courses has been proven adaptogenic drugs. Timely sanitation of the nasopharynx (conservative or operative) in both the child and family members.

In children with lymphatic-hypoplastic diathesis, due to late formation immune system, the issue of preventive vaccinations is decided individually, taking into account the advice of an immunologist. It is desirable to later vaccinate such children in accordance with the immunogram.

Neuro-arthritic diathesis (uric acid) It is based on a genetically determined violation of the activity of a number of enzymes involved in the synthesis of uric acid. In the pedigree of such children, gout, urolithiasis, cholelithiasis, osteochondrosis, hypertension, coronary heart disease, migraine, "spurs", "thorns" are noted.

In children with neuro-arthritic diathesis, weight is often reduced, but it can also be increased due to excess fat deposition. Disturbances from the nervous system are noted in the form of night fears, ticoid hyperkinesis, logoneuroses, less often effective seizures, anorexia, and enuresis. Periodic attacks of acetone vomiting are characteristic. One of the leading symptoms is arthralgia, which is of a meteorological nature. Sometimes there is an abdominal syndrome associated with dyskinesias of the gastrointestinal tract.

Children with this constitutional anomaly have an accelerated mental development, often with one-sided talent.

Allergic manifestations with this diathesis are rare. More often they are noted with a combination of neuro-arthritic and exudative-catarrhal diathesis and have the character of dry eczema. In the blood of such children, the content of uric acid is increased; uraturia, acetonuria, glucosuria, oxaluria are frequent in the urine.

Treatment: it is based on nutrition correction... By-products are excluded from the diet: liver, kidneys, brains, tongue, as well as canned food, cocoa, chocolate, meat broths, sprats, nuts, beans, peas, beans. A dairy-vegetable diet is recommended: fruits, vegetables, eggs, cereals, fruit and berry juices, boiled meat (in the first half of the day), vegetable oil... Fruit and potato days are shown as fasting days. Increase fluid intake, especially in the evening, for which slightly alkaline waters (Smirnovskaya, Slavyanovskaya), citrate mixtures are recommended.

With an exacerbation of neuro-arthritic diathesis, magnesium oxide, vitamin B 6, ATP, cocarboxylase, and in severe cases allopurinol are prescribed. Children with attacks of acetone vomiting are hospitalized in a hospital.

Allergic diathesis means readiness for sensitization, allergic reactions and diseases due to hereditary. Congenital features of immunity, metabolism, neurovegetative system.

It has no characteristic constitutional features. Children are more often hypersthenic, in the first year they have signs of atopic dermatitis. Often these are children with increased nervous excitability and irritability, sleep disorders, decreased appetite, capricious. As a rule, they have an enlarged liver, there are signs of dyskinesia biliary tract or cholecystitis, dysbiosis. Often, chronic foci of infection, hyperplasia of peripheral lymph nodes, spleen, and prolonged subfebrile conditions develop. There is a protracted course infectious diseases, especially respiratory, flowing with an obstructive component. Children do not tolerate large physical exercise... The manifestation of atopic diathesis into an allergic disease in the first year of life occurs more often in the form of atopic dermatitis, at preschool age - in the form of respiratory allergies, incl. bronchial asthma, in school - eczema, neurodermatitis, dermatorespiratory allergies.

The following variants of allergic diathesis are distinguished: atopic, autoimmune, infectious-allergic.

Atopic diathesis: positive family history of allergy. Both on the paternal and maternal lines (especially with a bilateral character). It is characterized by a high synthesis of Ig E, an increase in the number of Th 2 -helpers, an imbalance in the production of interleukins (IL) (an increase in the synthesis of IL-4 with a reduced synthesis of γ-interferon), a deficiency of total and secretory Ig A, and a deficiency in the phagocytic activity of neutrophils and macrophages.

Autoimmune diathesis – hypersensitivity skin to UV radiation. Significant increase in the level of γ-globulins in the blood, frequent detection of LE-cells of antinuclear factors in a state of complete clinical well-being, polyclonal activity of B-lymphocytes, as well as T-helpers with a decrease in the activity of T-suppressors, increased blast transformation of lymphocytes, elevated level Ig M in the blood, C3 complement deficiency. A congenital tendency to autoimmune diseases in women is 2 times more common than in men.

Infectious-allergic diathesis - long periods of increased ESR and subfebrile temperature after acute respiratory viral infections and diseases of the nasopharynx, the appearance after these diseases of symptoms such as arthralgia and cardialgia. With this variant of allergic diathesis, children are prone to vascular lesions (vasculitis).

TREATMENT DYSTROPHY
When fetal malnutrition is detected, the pregnant woman's nutrition is corrected, vitamins, methionine, as well as vasodilators and antispasmodics that improve placental blood circulation are prescribed. After birth, with a weakened sucking or swallowing reflex, the baby is fed through a tube. The frequency of feeding is 7-8 times a day. The calculation of the volume and daily calorie content is carried out in the same way as in postnatal malnutrition. In the first 7 days of life, they give only breast milk, then, when the condition improves, 5-7 g of cottage cheese is introduced per day. The principles of care are the same as for premature babies. During the first week, especially with hypotrophy II and III degree, shows plasma transfusion, vitamin therapy (vitamins B1, B6, B12 in age-specific dosages). By the end of the first month, against the background of an improvement in the condition, anabolic steroids and apilak are prescribed.

With postnatal malnutrition of the 1st degree, treatment is carried out on an outpatient basis, with malnutrition of the II and III degrees - in a hospital (preferably in boxed wards). The main principles of treatment are elimination of the cause of malnutrition, diet therapy, organization proper care for the child, elimination of metabolic disorders and vitamin deficiency, stimulating therapy, sanitation of foci of infection in the body. The nature of therapeutic measures is determined individually, depending on the causes and severity of malnutrition. When it is established during the control calculation that nutrition does not cover the body's needs for nutrients and energy, the necessary correction is carried out. So, if the child of the first months of life due to hypogalactia from the mother receives an insufficient amount of breast milk, supplementary feeding with donor milk or milk mixtures is prescribed. If a deficiency of any nutrient in the diet is detected with mixed and artificial feeding, this substance is added additionally (for example, with a lack of proteins, kefir, cottage cheese, protein milk, protein and fatty enpits are usually prescribed); deficiency of carbohydrates is eliminated with the help of sugar syrup, which is added to food and water for drinking; to replenish the missing amount of fat, 10-20% cream is used. They also use special milk mixtures with increased content a particular substance, and in severe cases resort to intravenous administration glucose solutions, protein hydrolysates.

When carrying out diet therapy, a two-phase method of nutrition is used: in the first phase, food tolerance is specified, in the second, enhanced nutrition is prescribed to cover the needs for nutrients and restore exhausted reserves. With I degree hypotrophy, the first phase usually lasts 1-3 days; calorie content and volume of food may be slightly reduced compared to the norm, depending on the appetite and food tolerance. In the second phase, the child should receive proteins, carbohydrates and calories per 1 kg of the required body weight, and fats per 1 kg of actual body weight.

With hypotrophy of II and III degrees, the first phase lasts at least 5-7 days, at this time 2/3, 1/2 or 1/3 of the required daily caloric intake are prescribed. Calculation of proteins and carbohydrates in case of hypotrophy of the II degree is carried out for the required body weight, with hypotrophy of the III degree for approximately the required body weight (actual weight + 20% of it). Calculation of fat is based on actual body weight. The amount of food missing in volume is replenished with fruit and vegetable broths, 5% glucose solution, juices. The number of feedings is increased from 7-8 (with grade II malnutrition) to 10 times (with grade III malnutrition) per day, the volume of portions is reduced accordingly. It is recommended to feed a baby in the first year of life in the first days with breast milk.

In the phase of enhanced nutrition, the amount of food is gradually increased, milk mixtures are introduced, then complementary foods in order to provide a normal daily calorie intake. During this period, with natural feeding, the daily amount of protein is calculated on the basis of 2-2.5 g / kg (at the age of 1 month) or 2.5-3 g / kg (at the age of over 1 month). With artificial feeding with adapted milk formulas such as "Baby", "Baby", "Detolakt", "Vitalakt", the amount of protein should be 3.5 g / kg per day, and unadapted - 4 g / kg per day. The amount of fats and carbohydrates is gradually brought to the age norm.

Treatment of critically ill patients with grade III malnutrition begins with total parenteral nutrition or tube feeding. With parenteral nutrition on the 1st day, the daily calorie content of the injected solutions should be 60 kcal / kg (this prevents the disintegration of the body's own proteins), then it gradually increases to the age requirement, and if necessary, it is increased by another 10-15%. The need for protein is replenished with amino acid solutions (on the 1st day they are administered at the rate of 0.6-0.7 g / kg, gradually increasing the dose to 2.0-2.5 g / kg per day). The need for fat is covered by fat emulsions, the daily dose of which is initially 0.5 g / kg, then slowly rises to 3-4 g / kg. The need for carbohydrates is calculated for the missing amount of calories, a 10 or 20% glucose solution is used so that the patient receives 15 g / kg of carbohydrates per day. Solutions of glucose and amino acids are distributed evenly throughout the day, and fat emulsions are injected fractionally (every 6 hours), sometimes simultaneously with heparin (50 U / h). From the 3-4th day, it is necessary to apply cocarboxylase, vitamins C, B6, to carry out measures aimed at eliminating hypokalemia, hypocalcemia, hypermagnesemia. Total parenteral nutrition should not be given for a long time. As the general condition of the child improves, they switch to mixed parenteral-enteral nutrition. First, food is introduced into the gastrointestinal tract using a tube, reducing the amount of parenterally administered solutions. Young children are given breast milk inside, and in its absence - adapted milk formulas (in case of lactase deficiency, milk formulas that do not contain lactose). Children over 6 months. you can assign enpits (protein, fat). As soon as the patient's condition allows, they switch completely to enteral nutrition through the mouth. Gradually, the diet is expanded, bringing it closer to physiological.

In the case of hypotrophy due to fermentopathies, special therapeutic nutrition is prescribed, depending on the nature of the pathology identified. So, with lactose intolerance, the use of low-lactose mixtures is shown, in which lactose is significantly less than in milk. With malnutrition, which has arisen against the background of malformations digestive system, endocrine pathology, lesions of c.ns. treat the underlying disease.

All children with malnutrition, regardless of its cause, are prescribed vitamins, enzyme preparations (for example, pepsin, abomin, pancreatin, panzinorm, festal), stimulants (apilak, dibazol, in severe cases - anabolic hormones, immunoglobulin, plasma), massage, exercise therapy, UV irradiation.

The child should be kept in a bright, regularly ventilated room irradiated with a bactericidal lamp, at a temperature of 24-27 °. In the absence of foci of infection, they organize walks in the open air or on a veranda (at an air temperature below -5 °). Warm baths (38 °) are recommended daily (in the absence of contraindications).

Children with malnutrition are under dispensary supervision pediatrician, are examined by a doctor at least 1 time in 2 weeks. During each examination, anthropometry, calculation and correction of nutrition are carried out. Enzyme preparations, vitamins, stimulants, massage, exercise therapy are periodically prescribed.

The prognosis for hypotrophy of I and II degrees in the case of timely and adequate treatment, as a rule, is favorable. With III degree malnutrition, mortality can reach 30-50%.

Prevention of intrauterine malnutrition includes adherence to the daily regimen and a balanced diet of a woman during pregnancy; exclusion of industrial hazards and other factors that have an adverse effect on the fetus (see Antenatal fetal protection); systematic monitoring of the condition of the pregnant woman and the fetus, timely treatment of pathological conditions of the pregnant woman (for example, toxicosis of pregnant women) and fetal hypoxia.

In the postnatal period, it is necessary to monitor the nutrition of the nursing mother. Early diagnosis and treatment of hypogalactia is important. It is necessary to transfer the child to mixed or artificial feeding in a timely manner, to introduce complementary foods by age (see Feeding children), to monitor the dynamics of the growth of the child's body weight, to observe the rules of caring for him.

Hypostatura - malnutrition in children of the first year of life, manifested mainly by growth retardation; body weight for a given height is close to normal. The rest of the clinical symptoms correspond, as a rule, to grade I hypotrophy. Treatment is the same as for grade I hypotrophy, it is necessary to prescribe anabolic steroids earlier. The forecast is favorable.

Paratrophy (flour disease, meal disorder, pseudo-nutritional status) is a chronic nutritional disorder in young children that occurs when eating predominantly carbohydrate-rich foods with a low protein content and is characterized by a slight excess in body weight compared to the norm due to tissue hydrolability. For the first time, A. Czerny was described in children who, due to a lack of milk, were transferred to a one-sided diet with flour products (flour broths or soups without the addition of butter and milk), as a result of which the intake of proteins and fats into the child's body was noticeably reduced. If the intake of protein did not decrease sharply, then at first the "flour" children even gained weight against the background of increasing pallor and pastiness. IN modern conditions the development of paratrophy is possible in children who are bottle-fed, when feeding mainly carbohydrate foods with a low protein content (for example, semolina) and an insufficient amount of dairy products in the diet.

With paratrophy, all types of metabolism are disturbed, tissue hydrolability develops, hypovitaminosis, rickets, anemia occur, and the body's resistance to infection decreases. The thickness of the subcutaneous tissue in a child is usually increased, especially on the abdomen and in the thighs, but palpation reveals looseness, pastiness. There may be swelling of the eyelids, dorsum of the hands and feet. The height of the child is usually in line with the age. The skin is pale, dry. Tissue turgor and muscle tone are reduced. Psychomotor development is somewhat delayed. In some cases, emotional lability, sleep disturbances, and decreased appetite are observed. The stool is unstable, often quickened, the stool is liquid with an admixture of greenery and mucus, sometimes frothy. The child often suffers from acute respiratory viral diseases, which take a protracted course and are often complicated by otitis media, pneumonia. With intercurrent diseases, loss of appetite, dehydration easily develops, the child's body weight decreases rapidly.

Paratrophy is often mistakenly identified with obesity (more often I degree), which develops as a result of excessive consumption of foods rich in carbohydrates, with a sufficient intake of proteins and fats. Obese children are active, their skin is velvety, pallor and pasty are absent; excess body weight is due to excessive, generalized development of subcutaneous tissue.

Treatment of paratrophy consists in the organization of the correct, age-appropriate diet. You should limit food containing a large amount of carbohydrates (for example, replace porridge with vegetable dishes). The diet is enriched with proteins - fermented milk mixtures (for example, "Biolact"), cottage cheese, protein enpit are shown. Prescribe vitamins B1, B2, B6, B12, A, stimulants (pentoxil, methyluracil, dibazol), massage, exercise therapy. The prognosis is generally good. Prevention consists in monitoring the nutrition of children who are mixed and formula fed.

Catad_tema Iron deficiency anemia - articles

Factors determining the correctness and effectiveness of treatment of children with iron deficiency anemia

I.S.Tarasova, V.M. Chernov / Questions of practical pediatrics, 2011, vol. 6, No. 3

I. S. Tarasova, V. M. Chernov
Federal Scientific and Clinical Center of Pediatric Hematology, Oncology and Immunology of the Ministry of Health and Social Development of Russia, Moscow

The lecture is dedicated to treatment iron deficiency anemia in children. Considered in detail: calculation of the optimal dose of oral iron preparations; choice modern drug gland; applying the most effective therapeutic plan; control of the effectiveness of treatment and its cost. The advantages and disadvantages of basic iron preparations are discussed. The high efficiency of a new therapeutic plan for the treatment of iron deficiency anemia with the use of a 100% dose of iron during the entire course has been proven. Calculations that take into account the amount of elemental iron in one tablet, the number of tablets in a package and the need for a drug for a course of treatment showed that the cost of a course of treatment for iron deficiency anemia using ferric iron preparations based on a hydroxide-polymaltose complex is higher than when using salt iron preparations. However, this difference is not as great as it might seem when comparing the cost of one package of drugs. The higher cost should not serve as a reason to abandon the use of ferric iron preparations based on the hydroxide-polymaltose complex, since their good tolerance and the absence of undesirable effects determine the patient's high adherence to therapy, which ultimately determines its success.

Key words: children, iron deficiency anemia, iron supplements, doses, therapeutic plan, efficacy, cost of treatment, Maltofer

Factors determining correctness and effectiveness of treating children with iron-deficiency anemia
I.S.Tarasova, V.M. Chernov
Federal Scientific and Clinical Center of Pediatric Hematology, Oncology and Immunology, Ministry of Public Health and Social Development of the Russian Federation, Moscow;

The lecture deals with treatment of iron deficiency anemia in children. A detailed account is given of calculating optimal doses of peroral iron drugs; choice of a modern iron drug; use of the most effective therapeutic treatment plan; control of effectiveness of treatment and its cost. Shortcomings and benefits of the main iron drugs are discussed. High effectiveness of a new therapeutic treatment plan for iron deficiency anemia with using a 100% dose of iron medication during the whole course has been proven. Calculations taking into account the amount of elemental iron in a tablet, the number of tablets in a package and drug requirements for a course of treatment showed that the cost of the course of treatment of iron deficiency anemia with using ferric (III) hydroxide polymaltose complexes is higher than in using iron salt drugs. However, this difference is not so great as it might seem as compared to the cost of one drug package. A higher cost should not be the reason to reject the use of ferric iron drugs based on hydroxide-polymaltose complex, since their good tolerance and absence of adverse effects ensure high adherence of a patient to therapy, which, in the long run, conditions its success. Key words: iron-deficiency anemia, iron drugs, doses, therapeutic plan, effectiveness, cost of treatment, Maltofer

When starting the treatment of iron deficiency anemia (IDA), it is necessary to check once again whether the diagnosis is correct. In pediatric practice, 90% of all anemias are iron deficient. The remaining 10% are anemias accompanying chronic diseases, early anemia of prematurity, hereditary and acquired hemolytic and aplastic anemias. With these anemias, iron preparations are not only ineffective, but in some of them they are contraindicated.

Calculation of the dose of the iron preparation

In Russia, the treatment of IDA is determined by the protocol approved by the Ministry of Health and Social Development of Russia on October 22, 2004 - “Patient Management Protocol. Iron-deficiency anemia" . The creation of this protocol by a group of leading specialists of our country was a significant movement forward, since it "armed" doctors with a unified understanding of the problem of iron deficiency, criteria for its diagnosis, principles of treatment, management of patients with IDA, and assessment of their quality of life.

From the point of view of a pediatrician, the treatment of IDA in children has some features that should be taken into account in the treatment protocol. First of all, the use of ferrous salt preparations in children under 3 years of age at a dose of 5-8 mg / kg of body weight per day, as recommended in the "Protocol", causes toxicity in many patients and is not justified from a therapeutic point of view.

When calculating the doses of iron salt preparations, we use the recommendations of the World Health Organization (WHO) (Table 1). A similar dose of iron salt preparations (3 mg / kg of body weight per day) for children under the age of 3 is also indicated in the manual for doctors approved by the Moscow Department of Health in 2004.

The different ages of children (from the neonatal period to the older adolescence) and, accordingly, different body weights (3.2-70 kg and more) make it necessary to individually calculate the dose of iron preparation for each child.

The "Protocol" recommends calculating the dose of the drug based on the hydroxide-polymaltose complex (HPA) of trivalent iron, focusing on the age of the children, and not on their body weight. We believe that in pediatric practice, the dose of iron (III) preparations based on HPA should be 5 mg / kg of body weight per day, regardless of age; this is the dose recommended by the above-mentioned physician's manual.

Choosing an iron supplement

The choice of an iron preparation for the treatment of IDA is the task of the attending physician. The doctor prescribes the drug taking into account his own experience, information about new drugs received at exhibitions, from medical journals or the Internet, the financial capabilities of the parents of a sick child (purchasing the drug for the entire course of treatment). At the same time, one cannot ignore the fact that in world practice there has been a tendency to replace salt preparations of bivalent iron with less toxic preparations of iron (III) based on CHP.

For many years in the treatment of IDA in children and adults, salt preparations of iron were used, and the appointment of iron sulfate was considered the "gold standard" of therapy, therefore it is no coincidence that most of the salt preparations of iron are represented by this very compound (Table 2). In addition, ferrous sulfate has the highest absorbability, followed by ferrous gluconate, chloride and fumarate as this quality decreases.

However, the use of iron salt preparations is associated with many problems and undesirable phenomena:

The possibility of overdose and even poisoning due to uncontrolled absorption in the gastrointestinal tract (GIT);
interaction with others medicines and food;
expressed metallic taste drugs;
staining of the enamel of teeth and gums, sometimes persistent;
frequent refusal of patients from treatment (up to 30-35% of those who started treatment), that is, low compliance.

The situation changed fundamentally with the development of iron (III) preparations based on HPA. The structural features of this complex: high molecular weight, the presence of a ferric hydroxide core, consisting of 260 atoms, a high iron content in the core (about 27%), a polymaltose shell. In terms of structure and valence, the molecule of an iron (III) preparation based on HPA is similar to a ferritin molecule.

Iron (III) preparations based on HPA have the following main properties and advantages:

High efficiency;
high safety, no risk of overdose, intoxication and poisoning;
no darkening of the gums and teeth;
pleasant taste;
excellent tolerance, which determines high compliance;
lack of interaction with other drugs and food;
the presence of antioxidant properties.

Reasons for the ineffectiveness of treatment with iron preparations:

The use of low doses;
reduction in the duration of the course of treatment due to the fault of the patient or the doctor;
violation of absorption;
treatment of chronic posthemorrhagic anemia without identifying and / or without eliminating the source of blood loss.

It is extremely rare to achieve a cure for IDA with standard iron therapy. Recently, American scientists have found that the chronic course

diseases and lack of response to iron therapy in IDA are due to the presence of various mutations in the TMPRSS6 gene. It is assumed that the detected mutations lead to excessive synthesis of hepcidin, a protein that regulates two important processes in the body: the absorption of iron in the intestine and its release from macrophages during the process of reutilization.

Therapeutic plan for the treatment of IDA

In Russian pediatric practice, the so-called "trapezoidal" therapeutic plan for the treatment of IDA in children has been adopted for many years (Figure). This plan was based on iron salt preparations, since others simply did not exist then. In accordance with this plan, in the first 3-5 days, the dose of iron salt preparations was gradually increased so as not to irritate the patient's gastrointestinal mucosa. The full (100%) dose of the iron salt preparation was used for 1.5-3 months, depending on the severity of the anemia, with its subsequent decrease to 50% by the end of treatment. This plan, like most others, was developed empirically, and its effectiveness has never been confirmed by randomized trials.

The advent of iron (III) preparations based on CHP forced a revision of the IDA treatment plan.

Under the guidance of the staff of the Federal Scientific and Clinical Center of Pediatric Hematology, Oncology and Immunology of the Ministry of Health and Social Development of Russia, a randomized study was carried out comparing the effectiveness of two treatment plans for IDA of varying severity in children and adolescents: the traditional "trapezoidal" and the new one, which provides for a 100% dose of iron ( III) based on HPA during the entire treatment period. During the study, the tolerability of the drug Maltofer (Vifor International, Switzerland) and the effectiveness of therapy in the early (reticulocytic reaction, increase in hemoglobin concentration - Hb) and late periods (normalization of the concentration of Hb, serum iron and serum ferritin) were assessed. Proven to be effective substitution therapy in children and adolescents with IDA, an iron (III) preparation based on CHP. After completion of the course of treatment, normalization of Hb concentration was achieved in 96.9%, serum iron - in 73.4%, serum ferritin - in 60.9% of patients. A small number (6.3%) of adverse events (constipation within 1 month of treatment) and 100% adherence of patients to treatment allowed us to conclude that iron (III) preparation based on HPA is optimal drug for the therapy of IDA in children and adolescents.

Drawing.Therapeutic "trapezoidal" treatment plan for IDA used in Russia.

The advantage of using a 100% dose of an iron (III) preparation based on HPA during the entire course of treatment was also proven: normalization of the concentration of serum iron was recorded in 90.6%, serum ferritin - in 75% of children and adolescents. When using the traditional "trapezoidal" treatment plan, these figures were 56.3 and 46.9%, respectively.

The doctor can judge the effectiveness of IDA treatment by a number of criteria. The earliest criterion of response, indicating the correctness of the diagnosis and the effectiveness of treatment, is the reticulocytic reaction. After 7-10 days from the beginning of the use of iron preparations, the number of reticulocytes increases, usually by 1-2% (10-20 %about)compared to the original. The criteria developed by the Centers for Disease Control (CDC) can also be used to assess the effectiveness of iron treatment for IDA. According to these criteria, by the end of the 4th week of IDA treatment, the Hb concentration should increase by 10 g / l, and the hematocrit - by 3% compared to the initial values.

The late criteria for the effectiveness of IDA treatment include the normalization of the concentration of Hb and serum ferritin.

The cure for IDA is considered to be overcoming tissue sideropenia and restoring iron stores in the body. Today, the internationally recognized marker of iron stores in the body is serum ferritin, despite some existing limitations (a protein of the acute phase of inflammation), the need for blood sampling from a vein and the relatively high cost of its determination.

The cost of treating IDA in children

According to some doctors, the only limiting factor for the widespread and widespread introduction of iron (III) preparations based on CHP is their higher cost (2-3 times) compared to salt preparations. We calculated the real cost of the course of IDA treatment with the use of iron salt preparations and iron (III) preparations based on CHP (Table 3). retail prices for iron preparations in Moscow pharmacies as of 01/30/2011. It turned out that taking into account the amount of elemental iron contained in one tablet, the number of tablets in the package and the need for the drug for the course of IDA treatment, the cost of the latter when using the iron (III) drug based on CHP is higher, but not as much as it might seem when comparing the cost of one package of drugs. We called the lower cost of one package of a salt preparation of iron and the purchase of a medicine only on this basis "the syndrome of the pharmacy counter." It should be emphasized that the higher cost should not serve as a reason to abandon the use of iron (III) preparations based on CHP. Their previously mentioned advantages, first of all, good tolerance and the absence of undesirable phenomena, determine the patient's high adherence to therapy (compliance), which ultimately determines the success of treatment.

Table 3. Main characteristics of various iron preparations for the treatment of iron deficiency anemia in children
Characteristic	A drug
	Aktiferrin	Tardiferon	Ferroplex	Maltofer
Release form		Pills,		Chewable tablets;
	in a blister of 10 capsules; 2 blisters per pack	coated; 10 tablets in a blister; 3 blisters per pack	100 pieces per pack	in a blister of 10 tablets; 3 blisters per pack
Iron compound	Ferrous sulfate Fe 2 +	Ferrous sulfate Fe 2 +	Ferrous sulfate Fe 2 +	Hydroxide-polymaltose complex Fe 3 +
iron in a package, mg
Average retail price
packaging in pharmacies in Moscow
as of 01/30/2011, rub.
Cost of 1 mg elemental
iron, rub.
Dose, mg / kg body weight
Treatment course cost *, rub.
"The cost of a course of treatment for iron deficiency anemia lasting 90 days is calculated for a child weighing 30 kg.

We believe that practitioners should be fully oriented in the economic part of the issue and explain to parents the benefits of treating IDA with iron (III) HPA-based preparations.

Literature

1. Hurtle M. Differential diagnosis in pediatrics. M .: Medicine, 1990; 2: 512.
2. Patient management protocol. Iron-deficiency anemia. M .: Newdiamed, 2005; 76.
3. WHO, UNICEF, UNU. IDA: prevention, assessment and control: report of joint WHO / UNICEF / UNU consultation. Geneva, WHO; 1998.
4. World Health Organization. Iron deficiency anemia: assessment, prevention and control. A guide for program managers. Geneva, 2001 (WHO / NHD / 01.3): 132.
5. Rumyantsev A.G., Korovina N.A., Chernov V.M. and other Diagnosis and treatment of iron deficiency anemia in children. Methodological guide for doctors. M., 2004; 45.
6. Samsygina G.A. Iron deficiency anemia in children. Pharmacology and pharmacokinetics of modern ferro-preparations. In the book: Iron deficiency and iron deficiency anemia / ed. NS Kislyak et al. M .: Slavic dialogue, 2001; 108-13.
7. Butler L.I., Zaspa E.A. Iron deficiency anemia in the practice of an obstetrician-gynecologist. Russian medical journal 2008; 16(29): 1898-906.
8. Maltofer. Monograph on the preparation. 3rd ed. M .: Mega Pro, 2001; 96.
9. Finberg K, Heeney M, Campagna D, et al. Mutations in TMPRSS6 cause iron-refractory iron deficiency anemia (IRIDA). Nat Genet 2008; 40 (5): 569-71.
10. Mayansky N.A., Semikina E.L. Hepcidin: the main regulator of iron metabolism and a new diagnostic marker. Diagnostic Issues in Pediatrics 2009; 1 (1): 18-23.
11. Ozhegov E.A., Tarasova I.S., Ozhegov A.M. et al. Comparative effectiveness of two therapeutic plans for the treatment of iron deficiency anemia in children and adolescents. Issues of Hematology / Oncology and Immunopathology in Pediatrics 2005; 4 (1): 14-9.
12. Ozhegov E.A. Optimization of treatment of iron deficiency anemia in children and adolescents. Author's abstract. diss. ... Cand. honey. sciences. M., 2005; 23.
13. Recommendations to prevent and control iron deficiency in the United States. Centers for Disease Control and Prevention. MMWR Recomm Rep 1998; 47 (RR-3): 1-29.

Holders of the patent RU 2478964:

The invention relates to the field of medicine. The individual course dose (A) of elemental iron (mg) is calculated according to the formula: A \u003d 0.34M (HbN-HbB) + DFe, where A is the course dose, mg; , M is the patient's body weight, kg, HbN is the target hemoglobin value in g / l for men, taken as 160 g / l, HbB is the hemoglobin content in the patient's blood, the actual hemoglobin level in g / l, DFe is the deposited iron content in mg is normal. The method allows you to quickly and accurately calculate the individual course dose of elemental iron for patients ischemic disease heart with concomitant iron deficiency. 3 tbl, 2 ex

The invention relates to medicine, cardiology and can be used to determine the course dose of elemental iron in men with ischemic heart disease (IHD) and concomitant iron deficiency.

Anemic syndrome in coronary artery disease enhances the clinical symptoms of coronary insufficiency. Clinical observations indicate that with a limited coronary reserve, ischemic, chronic myocardial dysfunction (systolic-diastolic) can form even against the background of a normal volume of coronary blood flow at rest.

Patients with ischemic heart disease and iron deficiency anemia (IDA) have less compensatory capabilities of the erythrocyte link aimed at eliminating myocardial ischemia, which is clinically manifested by a greater frequency and duration of ischemic attacks. It is impossible to use iron preparations without making sure that its content in the blood serum is reduced, and iron deficiency anemia. Iron overload is thought to be a significant contributor to the progression of atherosclerosis and an increased risk of myocardial infarction. The calculation of the daily and course dose of the drug must be made taking into account the severity of the anemic syndrome, visceral lesions, and the level of serum iron.

In patients with coronary artery disease with anemia, normalization of iron metabolism and erythron parameters has a bradycardic, cardioprotective, anti-ischemic effect. The heart rate decreases (R \u003d 0.23; p \u003d 0.0001). Therapeutic effect when taken orally, iron appears gradually. Patients have minimal side effects at individually calculated doses. Complaints do not require discontinuation of iron supplementation, and patients receive a full course of therapy. Patients receive 1 tablet a day, which reduces polyprogasia and toxic effects. Initially, clinical improvement is noted, and only after a while does the hemoglobin level normalize. First positive clinical sign, appearing in the treatment with iron preparations, is the disappearance or reduction of muscle weakness. The latter is due to the fact that iron is part of the enzymes involved in the contraction of myofibrils. From day 4, the hemoglobin content increases, reaching normal values \u200b\u200bby day 21. All patients showed a decrease in the general symptoms of anemia, the number of episodes of myocardial ischemia, and a decrease in the average value of ST segment depression. After normalization of red blood counts and iron metabolism, the duration of ischemic episodes significantly decreased. Pathogenetically grounded treatment is the appointment of iron preparations. The total amount of blood in the body of an adult is on average 6-8% of the body weight, which corresponds to 5 to 6 liters of blood, and in men - from 7 to 10. Every day this amount of blood passes through the heart more than 1000 times. A normal red blood cell contains approximately 30 pg of hemoglobin, which contains 0.34% iron. Normally, about 7-10% of the iron administered inside is absorbed, with the depletion of its reserves (prelate and latent iron deficiency state) - up to 17%, and with iron deficiency anemia - up to 25%. The maximum amount of iron included in erythroblasts and used for the synthesis of hemoglobin is about 25-30 mg per day. An increase in the daily dose over 200 mg (in terms of elemental iron) significantly increases the frequency and severity adverse reactions... The iron toxicity threshold for humans is 200 mg / day. In this regard, it is most advisable to prescribe 100-200 mg of iron per day. Such daily doses fully satisfy the body's need for iron to restore the amount of hemoglobin. WHO (1990) recommends prescribing iron preparations for administration at the rate of 3 mg / kg per day until the hemoglobin parameters are restored, and then iron preparations should be used for at least 2 months at 1-2 mg kg / day to replenish iron stores in the body. Known methods for determining course doses for parenteral administration of elemental iron, methods for determining course non-toxic doses for oral administration are not described in the known literature. The introduction of parenteral forms of elemental iron has strict indications and cannot be used in patients with mild forms, and even more so with iron deficiency. In many works, examples of iron deficiency correction are given according to an individual formula without taking into account the patient's sex, the average values \u200b\u200bof the standards for patients are taken instead of the target values. So, in the works of A.M. Shilov, it was suggested that intravenous administration of iron preparations with a mild degree of anemia was proposed, which is a contraindication. Determination of the dose in mg of the drug ferofolgamma was 375.2 mg, and 1 capsule contains 35 mg of ferrous sulfate, i.e. the patient had to take 10 tablets a day. There are also recommended average doses for anemia without indicating the severity and concomitant pathology, the sex of the patient. For patients with coronary artery disease, this is essential, since an excess of iron in the body is toxic to the myocardium. All these effects are realized when determining the individual course dose of elemental iron for oral administration and the use of average therapeutic doses with minimal side effects with mild anemias for the correction and prevention of latent iron deficiency. Individually determined course doses do not cause toxic effects on the myocardium and lead to the normalization of erythron, serum iron and ferritin.

In the known sources of information, there are no ways to determine the course individual doses, in particular for men.

A new technical problem is to expand the arsenal of methods for determining the course individual dose for men with coronary heart disease in combination with mild iron deficiency anemia or latent iron deficiency, to reduce the number of complications by increasing the accuracy of the method.

To solve this problem, in the method for determining the course dose of elemental iron in men with coronary heart disease (IHD) and concomitant iron deficiency, capillary hemoglobin, body weight and serum iron are determined, and in the presence of a decrease in serum iron from the norm for men, an individual course dose (A) of elemental iron (mg) according to the formula:

A \u003d 0.34M (HbN-HbB) + DFe,

A - course dose, mg;

Coefficient 0.34 \u003d 0.0034 * 0.1 * 1000,

where 0.0034 is the iron content in hemoglobin,

0.1 - total blood volume as a percentage of body weight in men,

1000 \u003d conversion factor from grams to milligrams

M is the patient's body weight, kg,

HbN is the target hemoglobin value in g / l for men, taken as 160 g / l,

The method is carried out as follows in men with coronary artery disease (CHD) and concomitant iron deficiency, capillary blood hemoglobin is determined, body weight, and in the case of an unstable course of CHD, serum iron is determined, and in the presence of a decrease in serum iron from the norm for men, the individual course dose is calculated (A ) elemental iron (mg) according to the formula:

A \u003d 0.34M (HbN-HbB) + DFe,

A - course dose, mg;

Coefficient 0.34 \u003d 0.0034 * 0.1 * 1000,

where 0.0034 is the iron content in hemoglobin,

0.1 - total blood volume as a percentage of body weight in men,

1000 \u003d conversion factor from grams to milligrams

M is the patient's body weight, kg,

HbN is the target hemoglobin value in g / l for men, taken as 160 g / l,

The proposed method is based on the results of the analysis of clinical observations.

The study involved 98 male miners working in coal mining, located on inpatient treatment... The average age was 51 ± 7.9 years. Depending on the initial level of hemoglobin and iron, the patients were divided into 4 groups: the 1st group (control) consisted of 18 patients with coronary artery disease without anemia, the average age of the examined patients was 46.09 ± 7.06 years, the percentiles were 25% - 37, 0 years old; 75% - 59 years old; Group 2 included 28 patients with coronary artery disease without myocardial infarction in combination with IDA, the average age of the examined was 51.0 ± 6.1 years, percentiles - 25% - 48.0 years; 75% - 53.5 years; Group 3 - patients with coronary artery disease with myocardial infarction in combination with IDA - 23 examined, average age 50.0 ± 6.4 years, percentiles - 25% - 47.0 years, 75% - 55.0 years; Group 4 consisted of 29 patients with ischemic heart disease and sideropenia (latent form of iron deficiency anemia), the average age of the examined was 52.0 ± 4.6 years, percentiles - 25% - 49.0 years; 75% - 55.0 years. The composition of the patients in the groups is identical in gender and age. Clinical, morphological and functional manifestations, changes in laboratory parameters and tolerability of therapy were compared in patients with coronary artery disease with concomitant IDA of mild severity before and after correction of the anemic syndrome, who were treated in the therapeutic department of the MUSH Central City Hospital of Anzhero-Sudzhensk. Diagnosis of ischemic heart disease was carried out in accordance with the recommendations of the All-Russian Society of Education and Science. Anemia was diagnosed, according to the WHO classification, with the hemoglobin level in men below 130 g / l and erythrocytes less than 4.5 × 10 12 / l. Iron deficiency has been associated with nutritional factors. The study excluded patients with severe concomitant diseases and operations, bleeding, anemia of non-ferrous deficiency genesis, patients with angina pectoris of functional class VI. All patients underwent clinical analysis capillary blood with the determination of the number of erythrocytes, hemoglobin (Hb) concentration, hematocrit, erythrocyte indices: an indicator of the average erythrocyte volume (MCV), the average hemoglobin content in the erythrocyte (MCH), the average concentration of hemoglobin in the erythrocyte (MCHC) on the hematological analyzer 19 HEMOLUX »Using original consumables. The quantitative determination of serum iron (SG), total iron-binding capacity of serum (TIBC), saturation of transferrin with iron (CST) in blood serum was carried out on a Stat Fax 3300 biochemical analyzer (USA) using reagent kits for clinical biochemistry manufactured by Vital Diagnostics ... Determination of ferritin was carried out on an enzyme immunoassay analyzer “Stat Fax 2100” (USA) using a diagnostic test system “Ferritin-IFA-Best” manufactured by ZAO “Vector-Best”. ECG registration for calculating the values \u200b\u200bwas carried out synchronously at 12 standard leads (V \u003d 50 mm / s), in the supine position, after a 10-minute rest on a digital 3-channel apparatus "Fukuda" (Japan). Left ventricular myocardial hypertrophy was determined using the Socolowa-Lyon criteria. Daily Holter ECG monitoring (SM ECG) was carried out in a hospital setting using the Ar MaSoft N. Novgorod 2000-2004 Safe Haert System 24h version 2.02. Signal recording and processing was carried out in accordance with the recommendations of the Working Group of the European Heart Society and the North American Society of Stimulation and Electrophysiology (1996). The work uses a gradation system modified by M. Ryan (1975) ventricular premature beats according to B.Lown and M. Wolf (1971), based on the data of daily monitoring of the ECG. The structural and functional state of the heart was investigated on an Aloka-2000 echo chamber with a 3.5 MHz phase-electronic transducer. Ultrasound procedure in B- and Doppler modes were performed in the supine position on the left side according to the generally accepted technique proposed in 1980 by the American Association for Echocardiography (ASE). Treatment of anemia was carried out by ingestion of iron sulfate (Sorbifer-Durules, company "Egis", Hungary), with a tablet containing 100 mg of elemental iron and 60 mg ascorbic acid 1 tablet 1 time per day 30 minutes before meals in compliance with dietary recommendations. The study is prospective. Statistical data processing was carried out using the STATISTICA 6.1 software package (Stat Software, USA), license agreement BXXROO6BO92218FAN11. Parameters by group are represented by median (Me) and percentile interval 25% -75% (Q1: Q2), mean (M) and mean error (m). To compare groups and study relationships, nonparametric methods were used (Mann-Whitney, Wilcoxon tests, Spearman's correlations). The threshold level of statistical significance was taken at the value of the criterion p<0,05.

The patients included in the studies had more often angina pectoris of the second grade of the functional class (FC), which amounted to 69 (70%) patients. In 23 (23.5%) patients, stable angina pectoris of the III functional class was observed, and in 6 (6.1%) patients of the I class. When assessing the severity of FC of stable angina pectoris, it turned out that in the group of patients with anemic syndrome, they had a more severe course of the disease and FC III angina was recorded 2 times more often in them (p \u003d 0.00001). 19.6% of patients had more than seven angina attacks per week - they experienced angina episodes daily. No significant differences were observed with regard to glycemia. Of the concomitant diseases, 16 (17.8%) were diagnosed with chronic obstructive pulmonary disease (stages 1-II), 48 (42.8%) miners were diagnosed with mild vibration disease. The occurrence of angina attacks and their frequency in groups 1 (control) and 2, 3 were the same. Statistically significant changes consisted in a longer duration of angina attacks in patients with anemia and with predominant physical activity (p \u003d 0.001 and p \u003d 0.003, respectively). The nitroglycerin intake was the same in all groups, where the differences were not statistically significant. The 6 min walking test (TSH) also did not differ in the comparison groups. Anemia in groups 2 and 3 was mild iron deficiency, group 4 was characterized by a decrease in the level of ferritin and iron in plasma. In the studied groups, no connection was found between the indicators of red blood, iron metabolism and the age of patients. In all patients with anemia, compared with the control group, dystrophic changes in the myocardium were noted, characterized by a decrease in the voltage of the QRS complex, mainly in standard leads, and changes in the terminal part of the ventricular ST-T complex in the form of a horizontal decrease in ST in standard leads, V1-3, V5 -6 to 2.4 ± 1.2 mm (p \u003d 0.000002) in group 2, 2.5 ± 0.61 (p<0,0001) в 3-й группе и 1,8±0,4 (р=0,001) в 4-й группе. Гипертрофия левого желудочка (ГЛЖ) была у 50 больных с анемией. При CM-ЭКГ нарушения ритма сердца выявлялись во всех группах. Оценка связи эктопической активности миокарда с изучаемыми показателями выявила, что снижение гемоглобина и ферритина крови сопровождается увеличением желудочковой эктопической активности. У 40,2% пациентов отмечались нарушения ритма: неспецифические внутрижелудочковые блокады, атриовентрикулярная блокада 1 степени, предсердные и желудочковые экстрасистолы. У больных 3-й группы наблюдалось более значимое увеличение количества желудочковых экстрасистол. ИММЛЖ был больше у больных 2-й, 3-й и 4-й групп по сравнению с контрольной группой (р=0,00001) табл.1. Обнаружена прямая слабая корреляция ММЛЖ с концентрацией железа в плазме крови (R=0,21; р=0,005), и обратная слабая корреляционная связь с ферритином крови (R=-0,19; р=0,05) в группах по сравнению с контрольной. Отношение Е/А у пациентов 2-й, 3-й и 4-й групп ниже, чем в группе контроля (р=0,0035). В результате приема препарата железа в течение трех недель и соблюдения пищевого регламента у всех пациентов нормализовались показатели эритрона и обмена железа (табл.1).

With this circumstance, we associate regression and clinical manifestations of ischemic heart disease. The clinical dynamics of the course of ischemic heart disease was positive both in relation to the symptoms characteristic of ischemic heart disease and for anemic syndrome. The heart rate has dropped. Undoubtedly, the anemic syndrome in ischemic heart disease enhances the clinical symptoms of coronary insufficiency. Probably, patients with ischemic heart disease and IDA have less compensatory capabilities of the erythrocyte link, aimed at eliminating myocardial ischemia, which is clinically manifested by a higher frequency of ischemic attacks. So, after normalization of red blood counts and iron metabolism, the number of angina attacks decreased by 10-15 times compared with the 1st group. The nature of angina pectoris has changed - the attacks that occurred earlier at rest have disappeared, the number of attacks during physical exertion has decreased by a factor. The need for patients to use short-acting nitrates (nitroglycerin), used to relieve seizures, has decreased approximately 30 times. The duration of angina excesses in the 2nd, 3rd and 4th groups decreased tenfold. The patients had an increase in the distance covered in the TShH (p \u003d 0.00004) in Table 1. The positive dynamics of this indicator reflects both effective therapy of anemic syndrome and manifestations of coronary artery disease (before the relief of anemia, 36% of patients stopped the test due to an attack of angina pectoris). After correcting anemia, this reason for the decrease in the covered distance was not recorded. The therapeutic effect of oral iron supplementation appeared gradually. Patients had minimal side effects at individually calculated doses (Table 2).

These complaints did not require discontinuation of iron supplementation, and the patients received a full course of therapy. Initially, clinical improvement was noted, and only after some time did the hemoglobin level normalize. The first positive clinical sign appearing in the treatment with iron preparations was the disappearance or reduction of muscle weakness. The latter is due to the fact that iron is part of the enzymes involved in the contraction of myofibrils. On the 3rd day, the first signs of reticulocytosis appeared, reaching a peak by the 5-10th day from the start of ferrotherapy. From day 4, the hemoglobin content increased, reaching normal values \u200b\u200bby day 21. The results of the study show that after the course of treatment with iron preparations, all patients show a decrease in the general symptoms of anemia, the number of episodes of myocardial ischemia, and a decrease in the average value of ST segment depression. After normalization of red blood counts and iron metabolism, the duration of ischemic episodes significantly decreased. Against the background of normalization of erythron and serum iron parameters, there was a significant increase in LV ejection fraction in the groups of patients with anemia.

Example 1. Sick male Z., 34 years old, working, suffering from ischemic heart disease and concomitant mild iron deficiency anemia

Made the definition of the course dose according to the proposed method. The examination revealed a body weight of 83 kg, in the general analysis of blood hemoglobin - 110 g / l, serum iron was 7.2 mmol / l.

We compose the formula: A \u003d 0.34 * 83 (160-110) +500; A \u003d 1911 mg - elemental iron. Each annotation to the iron-containing preparation indicates the amount of active iron in the tablet and the recommended average therapeutic dose. We use table 3 indicating the amount of elemental iron, according to which you can choose a drug and calculate the number of tablets and doses per day.

The number of days (N) of taking the course dose was calculated using the formula: N \u003d A / D, where A is the course dose, mg; D is the amount of elemental iron in the iron-containing preparation, mg.

For example, to determine the course dose of the drug "Sorbifer-durulis", where 1 tablet contains 100 mg of active iron sulfate, calculate the number of days of taking 100 mg per day (average non-toxic dose) \u003d 1911 mg / 100 mg \u003d 19 days

Patient I., 56 years old, working, suffers from coronary artery disease and concomitant latent iron deficiency.

The calculation of the course dose of the drug "Ferrum-Lek" was carried out.

The examination revealed a body weight of 93 kg, in a general blood test, hemoglobin was 135 g / l, serum iron was 8.2 mmol / l.

According to the formula: A \u003d 0.34 * 93 (160-135) +500; A \u003d 1291 mg determine the dose of elemental iron. 1 tablet of the drug "Ferrum-Lek" contains 100 mg of active iron, we get N \u003d 1291 mg / 100 mg \u003d 13 days.

The proposed method for determining the course dose of iron-containing drugs in the treatment of men with coronary artery disease with mild IDA or latent iron deficiency is advisable to use in the work of cardiological, therapeutic and cardiac surgery departments. Thus, correction of iron deficiency states in patients is carried out, taking into account the directed effect of energy-supplying and other anti-ischemic agents on oxygen transport to the ischemic myocardium due to the effect on the affinity of hemoglobin for oxygen.

List of references

1. De Valk B., Marx J.J. Iron, Atherosclerosis, and ischemic heart disease // Arch Intern Med. - 1999. - Vol. 159. - P. 1542.

2. O "Meara E, Murph C, Mcmurray JJ. Anemia and heart failuare. / Curr Heart Fail Rep 2004; 10: 40-43.

3. Salonen J., Nyyssonen K., Korpela H. High stored iron levels are associated with excess risk of myocardial infarction ineastern Finnish men // Circulation. - 1992. - Vol.86. - P.803-811.

4. Butler A.I. Hypochromic anemia / A.I. Dvoretsky // Consilium Med. - 2001. - No. 9. - C.443.

5. Kazyukova T.V. New possibilities of ferrotherapy for iron deficiency anemias / T.V. Kazyukova, N.V. Kalashnikova, A.Fallukh // Clinical. Pharmacology and therapy. - 2000. - No. 9 (2). - p.88.

6. Crichton, Robert; Danielson, Bo J., Geiser, Peter. Treatment with iron preparations: a special emphasis on intravenous therapy // Publishing house "Triada" LLC. - 2007. - P.9-13.

7. Sokolova R.I., Zhdanov B.C. Mechanisms of development and manifestations of "hibernation" and "staning" of the myocardium. // Cardiology. No. 9. - 2005. - P.71-78.

8. Shilov A.M., M.V. Melnik, O. N. Retivykh, I. R. Kim. Correction of iron deficiency anemia in chronic heart failure // Russian medical journal. Cardiology. - 2005. - Volume 13. - №19. - S. 1254-1257.

9. Shilov A.M., Melnik M.V., Sarycheva A.A. Anemia with heart failure. // Russian medical journal. Cardiology - 2003. - Volume 11. - №9. - S. 545-547.

application

1) Table 1. Influence of anemia correction on various parameters (M ± m)

2) Table 2. Course doses of elemental iron and side effects

3) Table 3. The amount of elemental iron in the preparation

table 2
index	Ischemic heart disease (angina pectoris) in combination with anemia (n \u003d 28)	Ischemic heart disease (myocardial infarction) in combination with anemia (n \u003d 23)	Ischemic heart disease and sideropenia (n \u003d 29)
Heading dose of elemental iron (mg) M ± SD	1247.7 ± 186.5	1501.7 ± 0.5	1000 ± 0.38
Treatment duration (days) M ± SD	12.8 ± 2.1	15.5 ± 2.5	10.0 ± 0.1
Fever (n,%)	-	-	-
Itching (n,%)	-	1 (4,3)	-
Flushing of the skin (n,%)	1 (3,6)	-	-
Arrhythmias (n,%)	-	-	-
Arthralgia (n,%)	-	-	-
Hematuria (n,%)	-	-	-
Allergic dermatitis (n,%)	-	-	-
Anaphylactic shock (n,%)	-	-	-
Metallic taste in the mouth (n,%)	2 (7,2)	2 (8,6)	3 (10,3)
Darkening of teeth, gums (n,%)	-	-	-
Nausea, vomiting (n,%)	1 (3,6)	-	-
Decreased appetite (n,%)	1 (3,6)	-	-
Diarrhea (n,%)	-	-	-
Lumbar pain (n,%)	-	-	-
Hemosiderosis (n,%)	-	-	-

Instructions for medical use

drug

MonoFer Ò

Tradename

MonoFer Ò

International non-proprietary name

Dosage form

Solution for injection / infusion 100 mg / ml

Composition

One milliliter of solution contains

active substance - iron isomaltoside 100 mg,

excipient: water for injection

Description

Dark brown solution

Pharmacotherapeutic group

Iron (III) preparations for parenteral administration

ATX code B03AS

Pharmacological properties

Farmakokinetics

The drug MonoFer Ò is a colloidal solution of spherical particles of iron-carbohydrate isomaltoside complex. In the isomaltoside iron-carbohydrate complex, the iron is tightly bound to isomaltoside carbohydrate, which allows the slow release of bioavailable iron in the form of iron bound to proteins to be controlled, with minimal risk of free iron formation.

After a single intravenous injection of MonoFer Ò, iron isomaltoside is rapidly captured by the cells of the reticuloendothelial system (RES) in the cells of the liver and spleen, in which iron is gradually released into the blood.

The half-life (T ½) of iron is 5 hours for iron in the systemic circulation and 20 hours for total iron (iron bound and located in the systemic circulation).

Iron is removed from blood plasma with the participation of RES cells, which break down the complex into its constituent parts - iron and isomaltoside. Iron immediately binds to the available protein fragments to form hemosiderin and ferritin, which are physiological forms of iron deposition, or, to a lesser extent, enters into a bond with the transferrin transport molecule.

Thus, the iron concentration is physiologically controlled, increasing the concentration of hemoglobin in the blood plasma and increasing the iron content in the depleted depot organs.

Pharmacodynamics

In the MonoFer Ò preparation, spherical particles of iron (III) carbohydrate isomaltoside complex consist of a core - iron (III), and a shell - isomaltoside carbohydrate, which surrounds and stabilizes the core. Iron (III), protected by a shell of isomaltoside carbohydrate, forms a structure similar to natural ferritin, which represents protection against toxicity of unbound inorganic iron (III). The clinical efficacy of the drug is noted after a few days of administration of MonoFer Ò and is confirmed by an increase in the number of reticulocytes in the general blood test.

The maximum concentration of ferritin in the blood plasma is reached approximately on the 7 - 9th day of intravenous administration of the drug, then slowly returns to the initial concentration after 3 weeks.

Indications for use

Treatment of iron deficiency conditions in the following cases:

In the absence of effectiveness or inability to use oral iron preparations

If you need to quickly replenish iron.

Iron deficiency should be confirmed by appropriate laboratory tests (serum ferritin, serum iron, transferrin saturation, hemoglobin and hematocrit levels, red blood cell count, average red blood cell volume, average red blood cell hemoglobin).

Method of administration and dosage

Calculation of the total dose of iron:

Iron replacement therapy in patients with chronic iron deficiency anemia:

The dose and dosage regimen of the drug MonoFer Ò are selected for each patient individually, taking into account the determination of the total iron deficiency. The optimal target hemoglobin level may differ in different patient groups.

The official guidelines must be followed. The dose of the drug MonoFer Ò is expressed in mg of elemental iron.

The total iron dose is calculated using the Ganzoni formula:

Total iron dose (mg iron) \u003d body weight (A) in kg x (the desired hemoglobin value in g / l - the patient's real hemoglobin value g / l) (B) x 0.24 (C) + deposited iron (D) in mg.

Iron therapy should replenish the iron content in hemoglobin and depot organs. After the general iron deficiency is corrected, patients may need to continue therapy with MonoFer Ò to maintain the target level of hemoglobin in the blood plasma, as well as other indicators indicating the content of iron.

Iron replacement for blood loss:

Iron therapy in patients with blood loss should correspond to the equivalent iron content in blood loss.

If the hemoglobin level is low : use the previous formula, assuming that there is no need to restore the iron depot:

Total iron dose (mg of iron) \u003d body weight in kg x (the desired hemoglobin value in g / l - the patient's real hemoglobin value g / l) x 0.24

If the amount of blood loss is unknown : the use of 200 mg of the drug MonoFer Ò increases hemoglobin equivalent to a transfusion of 1 unit of blood:

Introduction

MonoFer Ò is administered as an intravenous bolus, as well as infusion of the total dose (infusion of the entire dose of the drug), intravenous drip or direct injection into the venous section of the dialysis system.

MonoFer Ò should not be used concomitantly with iron preparations for oral administration, because the absorption of the iron preparation may be reduced.

Intravenous bolus

MonoFer Ò can be administered in a dose of 100-200 mg intravenous bolus over 2 minutes up to 3 times a week. Before administration, the drug is diluted in 10 - 20 ml of sterile 0.9% sodium chloride solution.

Total dose infusion:

The entire dose of MonoFer Ò can be administered as a single infusion. In the form of a single intravenous drip infusion of MonoFer Ò for 15 minutes, you can enter a single dose of up to 20 mg / kg of body weight.

If the total dose of iron exceeds 20 mg iron / kg body weight, the dose should be divided into two doses with an interval between doses of at least 1 week. MonoFer Ò is diluted in 100 - 500 ml of sterile 0.9% sodium chloride solution.

Intravenous drip:

MonoFer Ò should be injected intravenously in doses of 200 - 1000 mg once a week until the entire required dose of iron has been injected.

A dose of 0-5 mg iron / kg of body weight is administered for at least 15 minutes.

A dose of 6-10 iron / kg of body weight is administered for at least 30 minutes.

The dose of the drug 11 - 20 iron / kg of body weight is administered for at least 60 minutes.

MonoFer Ò is diluted in 100 - 500 ml of sterile 0.9% sodium chloride solution.

Dialysis administration:

MonoFer Ò can be injected directly into the venous section of the dialysis system, strictly following the intravenous injection technique.

Side effects

More than 1% of patients can expect the development of adverse reactions.

Parenteral administration of iron-containing drugs may be accompanied by hypersensitivity reactions.

Although rare, acute, severe anaphylactoid reactions may occur with parenteral iron supplementation. They usually develop within the first few minutes of drug administration and are usually characterized by sudden onset of breathing difficulties and / or cardiovascular failure; no deaths were reported. Other less severe manifestations of an immediate hypersensitivity reaction are also rare and include hives, rash, pruritus, nausea, and chills. The administration of the drug should be stopped immediately if signs of anaphylactoid reaction are observed.

With the use of parenteral iron preparations, delayed adverse reactions can develop, which can be serious. They are characterized by arthralgias, myalgias, and sometimes fever. The onset of their development ranges from several hours to four days after drug administration. Symptoms usually last two to four days and resolve on their own or with analgesics. In addition, exacerbation of joint pain in rheumatoid arthritis may develop, local reactions can also cause pain and inflammation at or around the injection site, local phlebitis.

On the part of the cardiovascular system

- rarely:heart rhythm disturbance, tachycardia, hypotension

- very rarely:fetal bradycardia, palpitations, hypertension

Disorders in the blood and lymphatic system

- very rarely:hemolysis

From the nervous system

- infrequently:blurred vision, numbness, dysphonia

- rarely:loss of consciousness, convulsions, dizziness, agitation, tremors, fatigue, decreased thinking ability

- very rarely:headache, paresthesia

Hearing and labyrinth disorders

- very rarely:temporary deafness

Respiratory, thoracic and mediastinal disorders

- infrequently:difficulty breathing

- rarely:chest pain

Disorders of the gastrointestinal tract

- infrequently: nausea, vomiting, abdominal pain, constipation

- rarely:diarrhea

Disorders of the skin and subcutaneous tissues

- infrequently:hot flashes, itching, rash

- rarely: angiodema, sweating

From the musculoskeletal system and connective tissue

- infrequently: convulsions

- rarely: myalgia, atralgia

General reactions and disorders at the injection site

- infrequently:anaphylactoid reactions, fever, fever, inflammation around the injection site, local phlebitis

- rarely: weakness

- very rarely: acute severe anaphylactoid reactions.

Contraindications

Hypersensitivity to drug components

Anemia not associated with iron deficiency (eg, hemolytic anemia)

Excess iron or impaired absorption of iron (eg, hemochromatosis, hemosiderosis)

Decompensated liver cirrhosis and hepatitis

Rheumatoid arthritis with symptoms or signs of intense inflammation

Bacteremia

Children under 18 years of age (insufficient data on efficacy and safety)

Acute and chronic infectious process, asthma, eczema or atopic allergies.

Drug interactions

MonoFer Ò should not be prescribed simultaneously with oral iron dosage forms, since their combined use helps to reduce the absorption of iron from the gastrointestinal tract. Treatment with oral iron preparations can be started no earlier than 5 days after the last injection of MonoFer Ò.

special instructions

The drug MonoFer Ò can be mixed in one syringe only with sterile saline solution.No other intravenous solutions and therapeutic agents are allowed to be added as there is a risk of precipitation and / or other pharmaceutical action. Compatibility with containers made of materials other than glass, polyethylene and polyvinyl chloride has not been studied.

Intravenous iron supplements can cause allergic or anaphylactoid reactions that can be potentially life-threatening.

The rate of administration of the drug MonoFer Ò should be strictly observed (with rapid administration of the drug, blood pressure may decrease). A higher incidence of adverse events (especially a decrease in blood pressure), which can also be severe, is associated with an increase in dose. Thus, the time of administration of the drug, given in the section "Dosage and Administration", must be strictly observed, even if the patient does not receive the drug in the maximum tolerated single dose.

Avoid penetration of the drug into the peri-venous space, because ingestion of the drug outside the vessel leads to tissue necrosis and brown skin coloration. In the event of the development of this complication, to accelerate the excretion of iron and prevent its further penetration into the surrounding tissues, it is recommended to apply heparin-containing preparations to the injection site (the gel or ointment is applied with light movements, without rubbing).

Pregnancy and lactation

The corresponding tests of MonoFer Ò have not been carried out on pregnant women. Therefore, the risk / benefit should be carefully evaluated before taking the drug during pregnancy. You should not prescribe MonoFer® during pregnancy if there is no clear need for parenteral iron supplementation.

Iron deficiency anemia that develops during the first trimester can be treated with oral iron supplements. If the benefits of using MonoFer Ò outweigh the potential risk to the fetus, then treatment should be carried out during the second and third trimesters.

There is no available information on the excretion of MonoFer Ò into human breast milk.

Features of the influence of the drug on the ability to drive a vehicle and potentially dangerous mechanisms

Considering the side effects of the drug, care should be taken when driving vehicles and other potentially dangerous machinery.

After the first opening of the container, the drug should be used immediately. MonoFer Ò is intended for single use only. Residual unused solution should be disposed of in accordance with local national regulations.

Overdose

MonoFer Ò has low toxicity. The drug is well tolerated and the risk of overdose is minimal. Overdose can develop due to accumulation of iron or acute iron overload, and manifests itself as symptoms of hemosiderosis. Control of the iron content in the body is carried out by determining the concentration of ferritin. In case of an overdose, symptomatic therapy is recommended, drugs that bind iron.

Release form and packaging

1 ml, 5 ml and 10 ml of the preparation are poured into glass ampoules (1 ml) or vials (5 ml and 10 ml) made of glass. A self-adhesive label is attached to each ampoule (bottle).

5 ampoules (1 ml) or 5 vials (5 ml), or 2 vials (10 ml), together with instructions for medical use in the state and Russian languages, are placed in a cardboard box.

Storage conditions

In a dry, dark place at temperatures from 5 0 C to 30 ° C Keep out of the reach of children!

Storage period

Do not use after the expiration date.

Terms of dispensing from pharmacies

On prescription

Manufacturer

Pharmacosmos A / S, Roervangsvej 30, DK-4300 Holbaek, Denmark

Name and country of the owner of the marketing authorization

Pharmacosmos A / S, Denmark

Name and country of organization of the packer

Pharmacosmos A / S, Denmark

The address of the organization that accepts claims from consumers on the quality of products (goods) on the territory of the Republic of Kazakhstan

11272 0

After stopping bleeding and normalizing hemodynamic parameters, it is necessary, simultaneously with the treatment of the underlying disease, to carry out adequate full-fledged therapy of iron deficiency anemia with the restoration of not only the level of hemoglobin in the blood, but also the creation of the necessary reserves of iron in the body. With some chronic bleeding, for example, in patients with ulcerative colitis, this therapy continues for years.

In the treatment of iron deficiency anemia, attention is paid to the use of foods rich in iron. In food, iron is found in two types, heme and non-heme. Heme iron is found in animal products. It is associated with the porphyrin ring (hemoglobin, myoglobin) or with protein complexes (ferritin, hemosiderin) or is part of specific proteins (milk lactoferrin, protein ovotransferrin and egg yolk phospfovitin).

Non-heme iron is found in plant products in the form of phytoferritin salts and complexes with organic acids. About 40% of iron from meat, fish, birds is heme, the rest is non-heme. The assimilability of heme iron is 5-30 times higher than that of non-heme iron.

In foodstuffs, the largest amount of iron (\u003e 5 mg%) contains the tongue, liver, beans, peas, strawberries, and moderate (1 -5 mg%) - beef, chicken eggs, rye bread, cereals (oat, buckwheat, wheat). Poor iron
(<1мг%) - молочные продукты, рис, картофель, капуста, цитрусовые. Лучше всего всасывается гемовое железо (25-30%) в то время как негемовое усваивается всего на 3-5%. Способствует всасыванию железа в кишечнике соляная, аскорбиновая, яблочная, лимонная и янтарная кислоты, витамины группы В, аминокислоты, препараты цинка и меди, фруктоза, цитрусовые, персики.

On the contrary, they inhibit absorption:
1. Cereals, bran, soy, corn, rice
2. Foods containing phytates, tannins, phosphate, oxalates, pectins, lectins.
3. Products and medicinal products containing:
- Ca, Mg, Bi, Al (form insoluble complexes with iron)
- Mo, Co, Cn, Ca, Se, Mn (possess competence antagonism, i.e. absorbed instead of Fe)
4. Mineral and drinking water containing carbonate, bicarbonate, phosphate;
5. Red wine (contains polyphenols)
6. Milk (calcium)
7. Tea (tannin)
8. Coffee (polyphenols)

Thus, iron supplements are not recommended to be combined with these products, they are prescribed 1 hour before or 1 hour after a meal. However, with massive and moderate bleeding, as well as when chronic iron losses are significant, its content in the body cannot be compensated for only by food rich in iron, since it is absorbed from food no more than 2.5 mg per day. The intake of iron 20 mg or more into the body is possible only through pharmaceutical preparations.

Currently, there is a sufficient number of iron preparations, which can be divided into 6 groups (Table 37)
The earliest preparations containing inorganic iron salts (sulfates, hydroxides) have not lost their importance in the treatment of iron deficiency anemia and at present, they are well absorbed from the intestine, exhibit a sufficiently high clinical efficacy, but they give a high frequency of undesirable side reactions from the gastrointestinal tract, reaching 15+ 20%. This is due to their irritating effect on the mucous membrane, primarily of the stomach, which is manifested by pain in the epigastric region, nausea, vomiting, flatulence, diarrhea or constipation. Moreover, they are mostly deposited in adipose tissue.

Table 37 Clinical classification of iron preparations (Dotsenko N.Ya. et al., 2004)

In order to prevent the side effects of iron preparations, chelated forms have been developed, i.e. its organic salts. They are less toxic, better tolerated by patients, give side effects only in 0.5-1% of patients. Iron in a chelated form is better stored in the body, is well transported by the blood and is included in the composition of hemoglobin.

In case of undesirable side effects in order to minimize the irritating effect of iron on the gastrointestinal tract with a high concentration as a result of its rapid decomposition in the stomach of its tablet or capsule form, it is better to prescribe drugs in which iron is released gradually throughout the entire gastrointestinal tract, without creating high concentrations, for example: sorbifer durules , ranferon-12, tardiferon, etc.

In diseases of the gastrointestinal tract and the need to administer large doses of iron, drugs of the 4th group are used, including additional ingredients to increase the absorption of iron. This allows you to reduce your total iron intake.

The effectiveness of post-hemorrhagic anemia treatment must be monitored according to the algorithm (Fig. 13).

Figure: 13 Algorithm for the treatment of iron deficiency anemia

The initial dose of iron is set depending on the severity of the anemia: from 60 mg / day with mild to 200 mg / day with super-severe iron deficiency anemia. Usually, in the first 2 days, half the dose of the established one is prescribed in order to identify a possible adverse reaction from the gastrointestinal tract.

On the 7-9th day, a detailed general blood test is performed. With an increase in the content of reticulocytes up to 10-12% ("reticular crisis") and an increase in hemoglobin by 1 g / l per day, it is considered that the process of hemoglobin formation and treatment of anemia proceed normally, and the dose of iron is selected correctly. If the increase in reticulocytes does not exceed 2% and the rate of increase in hemoglobin is not less than 1 g / L per day, it is necessary to double the daily dose of iron or replace the iron preparation with another containing additional ingredients that improve the absorption of iron and its participation in metabolic processes. Such treatment continues until the hemoglobin level is reached in men 130 g / l, in women - 125 g / l.

However, the normalization of the hemoglobin level in the blood is not a reason for stopping the treatment of anemia, the dose of iron is reduced to 60 mg / day. Treatment lasts 2-3 months and is monitored by a blood test for iron in the serum. When the serum iron level is 140 mmol / L. further saturation of iron stores in the body continues at a dose of 40-50 mg / day for 2-4 months.

The clinical indicator of the completion of the restoration of iron stores is the disappearance of sideropenic syndrome, as well as an indicator of the level of ferritin in the blood (60-150 μg / l) and an increase in the excretion of iron in the urine, which, according to the dysferal test, should be 0.8-1.3 μg / l.

It should also be borne in mind that the process of assimilation of iron and increasing the efficiency of hematopoiesis depends on the synergistic interaction of iron with other microelements (talb. 38). Therefore, when prescribing a diet, it is necessary to take into account not only the content of Fe in food, but also those trace elements that contribute to its entry into the body and improve its participation in metabolic processes.

Table 38 Trace elements that improve blood formation (Pertseva T.A., Konopkina L.I. Kirova T.A., 2002)

There is also evidence of the benefits of using a combination of iron with trace elements, which, on the one hand, act as synergists and, on the other, antagonists, thus balancing the functions of iron in the body. For example, copper and manganese are involved in the transformation of iron and the formation of hemoglobin, and on the other hand, a lack of copper in the body causes a lack of iron and transformation into iron deficiency anemia, while the body is overloaded with iron. In turn, the intake of excess Mp decreases the tissue concentration of iron, but at the same time increases the concentration of serum ferritin.

Thus, the intake of iron at the same time better reveals the body's need for these elements than the intake of one of them separately. Taking this principle into account, the Totem preparation was created, containing iron, copper and manganese. From this it follows that in the treatment of iron deficiency anemia, along with iron preparations, it is necessary to prescribe complexes consisting of microelements and vitamins in a balanced composition.

With a large blood loss, giving severe and super-severe iron deficiency anemia, as well as with any degree of anemia, if it is combined with malabsorption syndrome or other gastrointestinal lesions, accompanied by impaired absorption of iron or its poor tolerance, iron preparations are administered intravenously. At the same time, recently, attention has been paid to the use of iron with erythropoietin, especially if the blood loss is more than 25% of the BCC.

To calculate the amount of iron administered intravenously, the following formula is used:
Iron deficiency (mg) \u003d patient's body weight (kg) x (150 - patient's hemoglobin level + 500 g (total level of deposited Fe). If, for example, iron deficiency is 1700 mg, it is divided by the iron content in one ampoule of the drug (100 mg ) \u003d receive the total amount of the drug (17 ampoules), which must be administered to the patient.

Apply 1 ampoule daily for 17 days. The daily dose of intravenously administered iron should not exceed 100 mg, because it fully ensures complete saturation of the transferin. To prevent anaphylactic reactions, iron saccharate is used (ferrum Lek, fercoven, ferlecite, ferrolek). It should be borne in mind that even slow intravenous administration does not provide complete iron binding.

Therefore, part of the iron preparation spreads in the blood in an unbound form can have a toxic effect on the liver, pancreas, gonads, etc., and is also partially absorbed by phagocytic macrophages.

Parenteral administration of iron can cause phlebitis, abscesses, allergic reactions (anaphylactic shock, chills, arthralgia, urticaria), angina pectoris, hypotension, and overdose of the drug - hemosiderosis with damage to the liver, myocardium, kidneys, adrenal glands, pancreas, etc. Therefore, parenteral administration of iron, etc. it is performed when it is impossible to carry out full-fledged oral therapy or anemia manifests itself with a hemoglobin level in the blood of 50 g / l and below.

In recent years, in connection with the emergence of erythropoietin preparations, the risk of complications during parenteral administration of iron preparations has been significantly reduced, as well as accelerated the formation of erythrocytes in the bone marrow.

Erythropoietin belongs to the cytokine family. Formed mainly in the kidneys (90%), it acts on erythropoiesis progenitor cells in the bone marrow. The drug has the most pronounced effect on the very initial erythroid progenitor cells, less pronounced on their descendants, i.e. on morphologically identifiable young erythroid elements (proerythroblasts, basophilic erythroblasts and normoblasts), causing their maturation and differentiation. In addition, erythropoietin prevents the apoptosis of erythroid progenitor cells at late stages of development by inhibiting their phagocytosis by macrophages. Erythropoietin does not affect mature erythrocytes.

Recombinant drugs are used in the treatment: alpha-rh-EPO (precreit, eprex) and beta-rh-EPO (recormon, neocormone). The effect after the first injection of recormon is observed after 3-4 weeks. In case of iron deficiency post-hemorrhagic anemia, the use of Recormon is recommended at the level of hemoglobin in the blood<100г/л или гематокрита ниже 30% в дозе 125 МЕ подкожно 1 раз в неделю в течении 4 недель.

In post-hemorrhagic anemia in patients with chronic renal failure, the initial dose of Recormon is 20 IU 3 times a week or 60 IU / kg 1 time per week; in the absence of an effect, the dose is gradually increased until an effect is obtained (Fig. 14), but not more than 720 IU / kg per week [European recommendations, 1999].

Fig. 14 European recommendations for dosing of Recormon for subcutaneous administration (1999)

The inclusion of erythropoietin in the therapy of anemia makes it possible to increase the production of hemoglobin up to 2 g / l or more daily, which leads to a correspondingly higher consumption of iron, a deficiency of folic acid, and vitamin B12. This is reflected in serum ferritin levels and decreases transferrin saturation. Therefore, treatment should be monitored by measuring serum ferritin and iron transferrin saturation. With a decrease in ferritin less than 100 μg / ml, and transferrin less than 20%, it is necessary to increase the oral intake of iron in a dose of up to 200-300 mg / day or to be administered intravenously at 100 mg / day.

The criteria for the effectiveness of the treatment of anemia are: the disappearance of the sideropenic syndrome, the achievement of the blood hemoglobin level in men\u003e 130 g / l, in women\u003e 120 g / l, the iron content in the blood serum\u003e 140 mmol / l, ferritin\u003e 60 μg / l, discharge with urine 0.8-1.3 mcg / l.

Thus, the treatment of posthemorrhagic anemia should be comprehensive, complete, taking into account not only the severity of anemia, but also the state of the hematopoietic organs, with appropriate correction.

Stepanov Yu.V., Zalevsky V.I., Kosinsky A.V.