Malignant neoplasms of the breast. Mammary cancer. L50.0 Allergic urticaria Diagnosis 50.0 explanation

Lecture on anemia in children for doctors

Definition.

Iron-deficiency anemia is a chronic microcytic hypochromic anemia, which is based on impaired hemoglobin formation due to iron deficiency.

ICD code.

D50 Iron deficiency anemia

Included: anemia:

- hypochromic

- sideropenic

D50.0 Iron deficiency anemia secondary to blood loss (chronic)

Excluded:

- congenital anemia due to fetal blood loss (P61.3)

- spicy posthemorrhagic anemia(D62)

D50.1 Sideropenic dysphagia

D50.8 Other iron deficiency anemias

D50.9 Iron deficiency anemia, unspecified

Epidemiology.

Iron deficiency is the most common cause of anemia in the world. According to calculations published in 1989 (DeMaeyer), 700 million people worldwide suffered from IDA. Even in highly developed countries, 20% of women of childbearing age had iron deficiency before pregnancy, and 2-3% were diagnosed with IDA.

Etiology and pathogenesis

Based on the importance of the etiological factors of IDA, they can be divided into two groups:

1. Anemia from blood loss, more often long-term or repeated, less often acute, but abundant.

2. Anemia caused primarily congenital iron deficiency, if the child was born to women with IDA. This reason is becoming increasingly rare because... Methods for the prevention and treatment of IDA in pregnant women have been developed. If they do not avoid visiting in a timely manner antenatal clinic, there are no problems.

Blood loss. IDA is most often observed in women with increased monthly blood loss. Iron loss and its replacement with food should be equal. The absorption of iron from a complete diet is limited to two milligrams (Fig. 01). An increase in losses, even slightly exceeding intake, will sooner or later lead to iron deficiency, and later to anemia.

For example, with a menstrual volume of about 90 ml, the loss is 45 mg, i.e. average 1.5 mg/day. Taking into account other natural losses of iron equal to 1 mg/day, the total average daily loss reaches 2.5 mg with a maximum absorption capacity of no more than 2 mg. Iron deficiency will be 0.5 mg per day, 15 mg per month, 180 mg per year, 900 mg in 5 years, 1.8 g in 10 years, i.e. almost half of the body’s total iron. Naturally, such a woman will definitely develop IDA by the age of 30, although iron losses will be less than calculated, since the hemoglobin content in the lost blood will decrease as anemia progresses.

Fig.01. Diagram of iron metabolism in the body.

Other possible blood loss:

• nosebleeds,
• hemoptysis and pulmonary hemorrhage (tumor, telangiectasis, primary pulmonary hemosiderosis),
• gastrointestinal bleeding (hiatal hernia, varicose veins veins of the esophagus, peptic ulcer, ulcerative bleeding when taking aspirin and other non-steroidal anti-inflammatory drugs, hookworm, tumors, ulcerative colitis, telangiectasis, vascular dysplasia, diverticulosis, hemorrhoids;
• abortion and childbirth, endometriosis;
• injuries and operations,
• urinary blood loss - hematuria for various reasons,
• hemoglobinuria and hemosiderinuria - intravascular hemolysis, artificial valves hearts,
• bloodletting, donation and chronic hemodialysis;

The causes of IDA may be:

• insufficient absorption (after resection small intestine, malabsorption syndrome);
• increased need (rapid growth, including during puberty, pregnancy and lactation, prolonged profuse sweating);
• transferrin deficiency,
• congenital iron deficiency.

To prevent a child from developing IDA, he must be born with an iron depot of 300 mg. If this reserve is not there (in premature babies the depot is always absent), anemia will manifest itself already in the infant period. If it is a girl, and the iron deficiency is not corrected in a timely manner, it may persist indefinitely.

The appearance of menstruation will aggravate it and lead to IDA. Untreated anemia or remaining iron deficiency, even with normal hemoglobin in a woman of childbearing age who is not observed during pregnancy, leads to the birth of a child without iron reserves and everything will repeat itself in subsequent generations. Is not hereditary pathology, but its social continuity.

Syndrology of IDA. In addition to anemia, patients are diagnosed with sideropenic syndrome, which includes both clinical and laboratory symptoms.

Clinical symptoms:

1) Muscular (general and sphincter weakness, the latter can manifest itself as bedwetting (in children) or urinary incontinence).

2) Symptoms caused by dystrophic changes in the epithelium:

• dryness and flaking of the skin,
• delamination, brittleness, flattening of nails, koilonychia, transverse waviness of nails and other deformations after repeated manicures (Fig. 02),
• fragility and increased hair loss,
• dry mouth,
• dysphagia (the need to drink dry food), less commonly Paterson-Kelli syndrome (Plummer-Vinson) (Fig. 03), which requires differentiation from a tumor,
• smoothness of the papillae of the tongue, sometimes “geographic tongue”,
• angular stomatitis (jams), cheilitis,
• tooth decay,
• dry nose, cracks in the mucous membrane, bloody crusts.

Fig.02. Typical nail deformation in severe iron deficiency anemia.

Fig.03. Paterson-Kelli (Plummer-Vinson) syndrome. The formation of a fold of mucous membrane at the border of the pharynx and esophagus, which makes it difficult to swallow food. X-ray contrast study.

Figure from: Hoffbrand A.V., Pettit Y.E., Hoelzer.D. Roche Grundkurs Hamatologie. – Berlin-Wien: Blackwell Wissenschafts-Verlag, 1997 – 476 S.

3) Gustatory whims (pica chlorotica) and (or) olfactory, including during pregnancy.

Options for whims.

Taste whims.

Food: raw or well-fried potatoes, starch, dry cereals (various), dry pasta, raw carrots, raw meat, incl. minced meat, raw liver, various burnt foods, powdered food (optional), egg powder, raw fish, roasted and overcooked sunflower seeds, alcohol, raw dough, etc.

Inedible products: barium sulfate, toilet paper, clay (various of choice), earth (various of choice), ash, tooth powder, slaked lime, bleached plaster, painted plaster, crushed brick, pieces of ice, ice icicles, plantain leaves, chalk, cigarette butts, sand , matches, cinders, rubber (laboratory tubes), eraser, various green grass, coal.

Olfactory whims: acetone, gasoline, polish, car exhaust, freshly planed or sawn wood, soil after rain, fresh lime whitewash, kerosene, oilcloth, leather, shoe polish, varnishes, linoleum, soap of choice, fuel oil, menstrual fluid, mothballs, mold, freshly washed (cement, wood) floor, wormwood, sweat, rubber, ethanol, a flashing match, toilet odors (urine, etc.).

The cause of these perversions is not clear; they disappear after the administration of iron supplements and often recur with exacerbation of IDA. It should be remembered that patients are reluctant to talk about their taste and olfactory perversions, which requires careful additional questioning.

Laboratory symptoms:

• low color index, hypochromia of red blood cells in a stained smear,
• decrease in the average hemoglobin content in a red blood cell (MCH, mean corpuscular hemoglobin),
• decreased serum iron levels with increased total iron-binding capacity (TIBC),
• decrease in serum ferritin,
• decrease in transferrin saturation with iron,
• decreased gastric secretion and acid production (not always),
• lack of iron in the bone marrow (smears bone marrow or sections from trepanates are stained by Perls, while blue granules are absent in both macrophages and erythrokaryocytes).

Diagnosis of IDA, like any anemia and, in general, any other disease, consists of several stages:

Direct examination of the patient (questioning, examination by physical methods).

Routine additional examinations

Formulation of a diagnostic hypothesis

Differential diagnosis, likely return to stages 1 and/or 2, evaluation of results

Making a diagnosis of iron deficiency anemia

At the first stage, it is important to identify the symptoms of anemia, ask about the clinical signs of sideropenia listed above and try to clarify the questions:

• what were the blood losses (frequency, volume), in women - clarification of the volume of monthly losses,
• number of pregnancies, their outcome,
• have you been diagnosed with anemia in the past, including during pregnancy,
• If there was anemia, what was the treatment?
• whether there were any whims in the past, including during pregnancy (often patients do not attach importance to this, sometimes they are embarrassed to talk about it, they may hide it, the conversation should be private, friendly, but persistent; it is important to list the main options for whims and addictions to smells)
• no, and whether the patient’s children had any whims in the past.

It is very important to conduct a detailed examination to identify dystrophic changes skin, hair, nails, mucous membranes, teeth.

Additional studies include: a clinical blood test, necessarily with platelet and reticulocyte counting, serum bilirubin, urine test, including a test for hemosiderin, and chest x-ray. If at the first stage signs of anemic and (or) sideropenic syndromes are identified, additionally - iron and PVSS, and, if possible, the level of serum ferritin.

If sideropenia is detected with normal hemoglobin, latent iron deficiency is diagnosed. If anemic and sideropenic syndromes are present, IDA is diagnosed (Fig. 04).

Fig.04. Diagnosis scheme for iron deficiency anemia and latent iron deficiency.

IDA is not always the underlying disease. It can be a complication of a tumor, most often of the colon, or bleeding intestinal hemangiomas. At the slightest suspicion of these diseases, a number of additional studies are necessary.

Since the main disease is the one that requires priority treatment or directly threatens the patient’s life, in hyperpolymenorrhea IDA is the main one, and in cancer, for example, the cecum, a complication.

Differential diagnosis of IDA with other hypochromic anemias.

Schematically, the development of hypochromic anemia can be represented as the following diagram (Fig. 05). Both iron deficiency (1) and disorders of porphyrin metabolism (2) or globin synthesis (3) lead to hypochromia (Fig. 05). The main laboratory parameters that allow for differential diagnosis are given in Table 1.

Three points in hemoglobin synthesis, disturbances in which lead to hypochromia.

Table 1. Differential diagnosis of hypochromic anemia

Treatment of iron deficiency anemia.

The goal of therapy is complete cure.

Of the principles for the treatment of IDA formulated back in the 80s of the last century, most have retained their significance to this day:

• It is impossible to cure iron deficiency anemia without iron supplements with only a diet consisting of iron-rich foods,
• in case of iron deficiency anemia, one should not resort to blood transfusions without vital indications,
• Treatment of iron deficiency anemia should be carried out with iron supplements,
• Iron deficiency anemia should be treated mainly with internal medications,
• do not stop treatment with iron supplements after normalization of hemoglobin and red blood cells.

The exception is point 4. Currently there are highly effective drugs for intravenous use, very rarely causing side effects - Venofer and Ferinject . With intravenous administration of iron, point 5 is also subject to revision.

Treatment with oral medications consists of three stages: 1) restoration of hemoglobin levels, 2) replenishment of iron stores, 3) with ongoing blood loss - maintenance therapy (Table 2).

It is necessary to begin treatment with a minimum dose to ensure that the drug is well tolerated, gradually increasing the dose to the optimal one. It is more advisable to use drugs without additional additives (they do little to increase the effectiveness of therapy, but significantly increase the cost of treatment). Common iron supplements are listed in Tables 3-6.

Table 2. Stages of treatment of iron deficiency anemia with oral medications

Table 3. Iron preparations for oral administration (doses of elemental iron are indicated)

Table 4. Iron preparations for oral administration in solution

(doses of elemental iron are indicated)

Table 5. Iron preparations for oral administration with multivitamins

Table 6. Iron preparations for oral administration with folic acid

The effect of treatment with iron supplements develops slowly, and Clinical signs improvements appear before there is a noticeable increase in hemoglobin. This is due to the supply of iron to enzymes, the deficiency of which causes muscle weakness. On the 6-8th day from the start of treatment, the blood test must be repeated, always with a reticulocyte count. In the future, tests are repeated no more than once every 3 weeks. The hemoglobin level increases noticeably only after 3-3.5 weeks from the start of therapy, and the effect often occurs spasmodically. average speed the increase in hemoglobin usually does not exceed 20 g/l every 3 weeks. An insufficient effect of treatment indicates either unrecognized permanent blood loss, or an incorrect diagnosis, or the patient’s failure to comply with doctor’s orders (very common reason!).

Treatment of IDA with iron preparations for intravenous use.

The course dose must be determined using the formula:

Total iron deficiency [mg] =

body weight [kg] ´ (normal HB - patient’s HB) [g/l] ´ 0.24 + depot [mg],

With a body weight of up to 35 kg, normal hemoglobin is taken as 130 g/l, and depot - 15 mg/kg body weight; with a larger mass, the hemoglobin norm is considered to be 150 g/l, depot - 0.5 g. Calculated coefficient 0.24: 0.24 = 0.0034 ´ 0.07 ´ 1000 [conversion of grams to milligrams].

Venofer is administered 5 ml (100 mg) intravenously, strictly following the attached instructions. The calculated dose should not be exceeded. Ferinject can be administered as a slow stream.

Long-term treatment with oral iron preparations, especially if there is side effects, patients rarely endure it, and treatment often continues for several months. The advantage of using drugs for intravenous use is that the patient avoids dyspeptic disorders and does not have to remember to take next dose. The relatively high price of drugs for intravenous use (oral administration seems cheaper) is compensated by the short duration of therapy. The patient must be told about the duration of therapy for different routes of iron entering the body, about the cost of the drugs, and he must choose the method of treatment himself.

Regardless of the nature of treatment with iron preparations, the patient should be given a number of tips: if necessary, get dentures, eat food slowly, chew it thoroughly (the absorption of iron from food is significantly improved). Food should be complete and varied, but you should not drink a lot of milk and it is advisable to increase the amount of red meat in your diet. Take iron supplements with water (not juices or milk), do not take additional doses unless necessary. ascorbic acid(modern iron supplements are absorbed without other supplements).

Harmful advice for patients with IDA:

• get treatment carrot juice(carotene jaundice and no benefit),
• replace iron supplements with black caviar, walnuts, pomegranates (expensive, although tasty and healthy, but not in terms of replenishing iron deficiency),
• eat raw or half-raw liver (risk of salmonellosis and other infections).

After recovery, patients should undergo blood tests at least once every 3 months.

Patient management tactics.

Iron deficiency anemia is a disease that in most cases does not require the participation of a hematologist in either diagnosis or treatment.

In severe cases (orthostatic syncope), hospitalization is necessary. To quickly increase hemoglobin levels, a transfusion of red blood cells is performed and at the same time treatment with iron supplements is started. In most cases, anemia develops gradually and patients adapt to low level hemoglobin, limiting physical activity. They may not see a doctor even if their hemoglobin level is 60-65 g/l. In these cases, treatment is carried out on an outpatient basis with iron preparations, both orally and intravenously.

Transfusion of donor red blood cells is carried out only in the presence of hemodynamic disorders, as well as in preparation for surgery or childbirth when the hemoglobin level is less than 80 g/l.

Prevention of IDA.

Primary prevention of IDA should be carried out in cases of latent iron deficiency and in risk groups (women of reproductive age, suffering from menorrhagia, pregnant women; personnel donors, workers in hot shops). It is very important to carry out oral sanitation and dental prosthetics for the patient, because... chewing thoroughly food helps improve absorption dietary iron. Even in the absence of clinical and biochemical signs of iron deficiency, people at high risk are recommended to have a varied high-calorie diet including meat, meat products, fruits and berries rich in ascorbic acid.

A lot of iron is found in meat, liver, kidneys, soybeans, parsley, peas, spinach, black currants, gooseberries, dried apricots, prunes, raisins, oatmeal, walnuts, apples (see appendix). The popular belief about the rich iron content in pomegranates and strawberries is not true. A lot of iron is absorbed from red meat. From products plant origin iron absorption is limited.

During pregnancy, prophylactic intake of iron supplements is indicated, especially if pregnancies follow one after another with a short interval (1-2 years), or in cases where a woman suffered from menorrhagia before pregnancy. Start taking iron supplements from the 14th week of pregnancy.

Women with dysfunctional uterine bleeding should take iron supplements for 7-10 days after each menstruation.

In career donors, especially female donors, it is necessary to monitor iron metabolism at least twice a year. If blood is donated regularly in 450 ml doses, then both men and women for preventive purposes should take one or another iron supplement for 2-2.5 weeks after blood donation. Giving 200 ml of blood once or twice during the year does not lead to iron deficiency if there are no other blood losses.

Treatment of latent iron deficiency begins with the second stage (see Table 2). Often it is enough to take a month-long course of oral medications. Then, depending on the situation, stop treatment or carry out maintenance therapy with determination of PVSS or serum ferritin before and after the course of therapy.

NB. Serum iron and TLC cannot be determined while taking iron supplements, and if necessary, no earlier than a week after their discontinuation.

Anemia caused by impaired iron recycling (anemia of chronic disease, ACD)

Anemia of a chronic disease is diagnosed when inflammatory diseases(infectious and aseptic), as well as for severe acute diseases and tumors. It acts as an integral part of the underlying disease. ACD has a complex pathogenesis. Its most important elements are: 1) a decrease in the volume of erythropoiesis and 2) a violation of iron reutilization.

Inhibition of erythropoiesis occurs due to an increase in the production of many cytokines (interleukin-1, tumor necrotizing factor-a, b- and g-interferon, transforming growth factor), which inhibit the synthesis of erythropoietin or inhibit it at the level of progenitor cells. Granulocytopoiesis does not suffer, since simultaneous stimulation of the production of colony-stimulating factors of granulocytes and monocytes by interleukin-1 occurs (Fig. 06). Under the influence of microorganisms, immune disorders (increased IL-6) and tumor antigens, hepcidin (hepcidin) is synthesized in the liver, which, like IF-g, disrupts the absorption of iron, and also, more importantly, blocks the release of iron from macrophages, where it accumulates and does not participate in heme synthesis.

Fig.06. Scheme of impaired erythropoiesis in anemia of a chronic disease.

EPO – erythropoietin,

IF – interferon,

IL – interleukin,

TNF – tumor necrosis factor, G-CSF – granulocyte and GM-CSF – granulomonocyte colony-stimulating factors.

Nowadays, the main importance in the development of anemia of a chronic disease is given to the formation of a special peptide in the liver - hepcidin(Fig.07).

Fig.07. The role of hepcidin in the development of anemia of chronic disease.

Hepcidin is a special component of the iron absorption chain. You can compare the relationship between hepcidin and iron in the body like insulin and glucose. There is an enzyme-linked immunosorbent test to determine the precursor of hepcidin in the body in order to determine subsequent treatment tactics (blood serum or urine is taken for testing). Thus, hepcidin is responsible for iron homeostasis in the body.

With anemia of a chronic disease, iron reserves are normal or increased (ferritin), CVS is often reduced, may be normal, but never increased (see Table 1). A decrease in serum iron (a negative acute phase reactant) does not indicate its deficiency.

Treatment of ACD. With anemia of a chronic disease, the main thing is successful therapy of the underlying disease that accompanies it. Treatment with iron supplements is not carried out, despite hypochromia and decreased serum iron levels. If concomitant iron deficiency is convincingly proven, oral iron supplements can be taken. Parenteral use of iron supplements is contraindicated. Red blood cell transfusions should not be performed unless there are other special indications, such as massive blood loss. Currently, erythropoietin preparations are sometimes used to treat ACD.

Alexander Fedorovich Tomilov

Among various anemic conditions iron deficiency anemia are the most common and account for about 80% of all anemias.

Iron-deficiency anemia- hypochromic microcytic anemia, which develops as a result of an absolute decrease in iron reserves in the body. Iron deficiency anemia occurs, as a rule, with chronic blood loss or insufficient intake of iron into the body.

According to World Organization healthcare, every 3rd woman and every 6th man in the world (200 million people) suffer from iron deficiency anemia.

Iron metabolism
Iron is an essential biometal that plays an important role in the functioning of cells in many body systems. Biological significance iron is determined by its ability to reversibly oxidize and reduce. This property ensures the participation of iron in the processes of tissue respiration. Iron makes up only 0.0065% of body weight. The body of a man weighing 70 kg contains approximately 3.5 g (50 mg/kg body weight) of iron. The iron content in the body of a woman weighing 60 kg is approximately 2.1 g (35 mg/kg body weight). Iron compounds have different structures, have unique functional activity and play an important biological role. The most important iron-containing compounds include: hemoproteins, structural component which is heme (hemoglobin, myoglobin, cytochromes, catalase, peroxidase), non-heme group enzymes (succinate dehydrogenase, acetyl-CoA dehydrogenase, xanthine oxidase), ferritin, hemosiderin, transferrin. Iron is part of complex compounds and is distributed in the body as follows:
- heme iron - 70%;
- iron depot - 18% (intracellular accumulation in the form of ferritin and hemosiderin);
- functioning iron - 12% (myoglobin and iron-containing enzymes);
- transported iron - 0.1% (iron bound to transferrin).

There are two types of iron: heme and non-heme. Heme iron is part of hemoglobin. It is contained only in a small part of the diet (meat products), is well absorbed (20-30%), its absorption is practically not affected by other food components. Non-heme iron is found in free ionic form - ferrous (Fe II) or ferric iron (Fe III). Most dietary iron is non-heme (found primarily in vegetables). The degree of its absorption is lower than that of heme and depends on a number of factors. Only divalent non-heme iron is absorbed from food. To “convert” ferric iron into divalent iron, a reducing agent is needed, the role of which in most cases is played by ascorbic acid (vitamin C). During absorption in the cells of the intestinal mucosa, ferrous iron Fe2+ is converted into oxide Fe3+ and binds to a special carrier protein - transferrin, which transports iron to hematopoietic tissues and sites of iron deposition.

Iron accumulation is carried out by the proteins ferritin and hemosiderin. If necessary, iron can be actively released from ferritin and used for erythropoiesis. Hemosiderin is a derivative of ferritin with a higher iron content. Iron is released slowly from hemosiderin. Incipient (prelatent) iron deficiency can be determined by a reduced concentration of ferritin even before the depletion of iron stores, while still maintaining normal concentrations of iron and transferrin in the blood serum.

What causes iron deficiency anemia:

The main etiopathogenetic factor in the development of iron deficiency anemia is iron deficiency. The most common causes of iron deficiency conditions are:
1. iron loss due to chronic bleeding (the most common cause, reaching 80%):
- bleeding from gastrointestinal tract: peptic ulcer, erosive gastritis, esophageal varicose veins, colon diverticula, hookworm infestations, tumors, UC, hemorrhoids;
- long and heavy menstruation, endometriosis, fibroids;
- macro- and microhematuria: chronic glomerulo- and pyelonephritis, urolithiasis disease, polycystic kidney disease, kidney and bladder tumors;
- nosebleeds, pulmonary bleeding;
-- blood loss during hemodialysis;
-- uncontrolled donation;
2. insufficient absorption of iron:
-- resection of the small intestine;
- chronic enteritis;
- malabsorption syndrome;
-- intestinal amyloidosis;
3. increased need for iron:
-- intensive growth;
-- pregnancy;
- period of breastfeeding;
- playing sports;
4. insufficient intake of iron from food:
-- newborns;
-- Small children;
-- vegetarianism.

Pathogenesis (what happens?) during Iron deficiency anemia:

Pathogenetically, the development of iron deficiency can be divided into several stages:
1. prelatent iron deficiency (insufficient accumulation) - there is a decrease in ferritin levels and a decrease in iron content in the bone marrow, increased iron absorption;
2. latent iron deficiency (iron deficiency erythropoiesis) - serum iron is further reduced, transferrin concentration increases, and the content of sideroblasts in the bone marrow decreases;
3. severe iron deficiency = iron deficiency anemia - the concentration of hemoglobin, red blood cells and hematocrit further decreases.

Symptoms of Iron Deficiency Anemia:

During the period of latent iron deficiency, many subjective complaints and clinical signs characteristic of iron deficiency anemia appear. Patients note general weakness, malaise, and decreased performance. Already during this period, there may be a perversion of taste, dryness and tingling of the tongue, difficulty swallowing with a feeling foreign body sore throat, palpitations, shortness of breath.
An objective examination of patients reveals “minor symptoms of iron deficiency”: atrophy of the tongue papillae, cheilitis, dry skin and hair, brittle nails, burning and itching of the vulva. All these signs of impaired trophism of epithelial tissues are associated with tissue sideropenia and hypoxia.

Patients with iron deficiency anemia report general weakness, fatigue, difficulty concentrating, and sometimes drowsiness. Appear headache, dizziness. Severe anemia may cause fainting. These complaints, as a rule, do not depend on the degree of decrease in hemoglobin, but on the duration of the disease and the age of the patients.

Iron deficiency anemia is also characterized by changes in the skin, nails and hair. The skin is usually pale, sometimes with a slight greenish tint (chlorosis) and with an easy blush on the cheeks, it becomes dry, flabby, peels, and cracks easily form. Hair loses its shine, turns grey, thins, breaks easily, thins and turns gray early. Changes in nails are specific: they become thin, matte, flattened, easily peel and break, and striations appear. With pronounced changes, the nails acquire a concave, spoon-shaped shape (koilonychia). Patients with iron deficiency anemia experience muscle weakness, which is not observed in other types of anemia. It is classified as a manifestation of tissue sideropenia. Atrophic changes occur in the mucous membranes of the digestive canal, respiratory organs, and genital organs. Damage to the mucous membrane of the digestive canal is a typical sign of iron deficiency conditions.
There is a decrease in appetite. There is a need for sour, spicy, salty foods. In more severe cases, distortions of smell and taste (pica chlorotica) are observed: eating chalk, lime, raw cereals, pogophagia (craving for eating ice). Signs of tissue sideropenia quickly disappear after taking iron supplements.

Diagnosis of Iron Deficiency Anemia:

Basic landmarks in laboratory diagnostics iron deficiency anemia the following:
1. The average hemoglobin content in an erythrocyte in picograms (normal 27-35 pg) is reduced. To calculate it, the color index is multiplied by 33.3. For example, with a color index of 0.7 x 33.3, the hemoglobin content is 23.3 pg.
2. The average concentration of hemoglobin in the erythrocyte is reduced; Normally it is 31-36 g/dl.
3. Hypochromia of erythrocytes is determined by microscopy of a peripheral blood smear and is characterized by an increase in the zone of central clearing in the erythrocyte; Normally, the ratio of central clearing to peripheral darkening is 1:1; for iron deficiency anemia - 2+3:1.
4. Microcytosis of erythrocytes - reduction in their size.
5. Coloring of erythrocytes of different intensity - anisochromia; the presence of both hypo- and normochromic red blood cells.
6. Different shape erythrocytes - poikilocytosis.
7. The number of reticulocytes (in the absence of blood loss and a period of ferrotherapy) in iron deficiency anemia remains normal.
8. The leukocyte count is also within normal limits (except in cases of blood loss or cancer pathology).
9. The platelet count often remains within normal limits; moderate thrombocytosis is possible with blood loss at the time of examination, and the platelet count decreases when the basis of iron deficiency anemia is blood loss due to thrombocytopenia (for example, with DIC syndrome, Werlhof's disease).
10. Reducing the number of siderocytes until they disappear (a siderocyte is an erythrocyte containing iron granules). In order to standardize the production of peripheral blood smears, it is recommended to use special automatic devices; the resulting monolayer of cells increases the quality of their identification.

Blood chemistry:
1. Decrease in iron content in blood serum (normally in men 13-30 µmol/l, in women 12-25 µmol/l).
2. The total life-value percentage is increased (reflects the amount of iron that can be bound due to free transferrin; the normal level of total life-value percentage is 30-86 µmol/l).
3. Study of transferrin receptors using the enzyme immunoassay method; their level is increased in patients with iron deficiency anemia (in patients with anemia chronic diseases- normal or reduced, despite similar indicators of iron metabolism.
4. The latent iron-binding capacity of blood serum is increased (determined by subtracting the serum iron content from the TLC indicators).
5. The percentage of transferrin saturation with iron (the ratio of the serum iron index to the total life-saving value; normally 16-50%) is reduced.
6. The level of serum ferritin is also reduced (normally 15-150 mcg/l).

At the same time, in patients with iron deficiency anemia, the number of transferrin receptors is increased and the level of erythropoietin in the blood serum is increased (compensatory reactions of hematopoiesis). The volume of erythropoietin secretion is inversely proportional to the oxygen transport capacity of the blood and directly proportional to the oxygen demand of the blood. It should be taken into account that serum iron levels are higher in the morning; before and during menstruation it is higher than after menstruation. The iron content in blood serum in the first weeks of pregnancy is higher than in its last trimester. Serum iron levels increase on days 2-4 after treatment with iron-containing drugs and then decrease. Significant consumption of meat products on the eve of the study is accompanied by hypersideremia. These data must be taken into account when assessing the results of serum iron studies. It is equally important to follow the technique laboratory research, rules for blood sampling. Thus, the tubes in which blood is collected must first be washed with hydrochloric acid and double-distilled water.

Myelogram study reveals a moderate normoblastic reaction and a sharp decline content of sideroblasts (erythrokaryocytes containing iron granules).

Iron reserves in the body are judged by the results of the desferal test. U healthy person after intravenous administration of 500 mg of desferal, 0.8 to 1.2 mg of iron is excreted in the urine, while in a patient with iron deficiency anemia, iron excretion is reduced to 0.2 mg. The new domestic drug defericolixam is identical to desferal, but circulates in the blood longer and therefore more accurately reflects the level of iron reserves in the body.

Taking into account the level of hemoglobin, iron deficiency anemia, like other forms of anemia, is divided into severe, moderate and mild degree. With mild iron deficiency anemia, the hemoglobin concentration is below normal, but more than 90 g/l; with moderate iron deficiency anemia, the hemoglobin content is less than 90 g/l, but more than 70 g/l; with severe iron deficiency anemia, the hemoglobin concentration is less than 70 g/l. However, clinical signs of the severity of anemia (symptoms of a hypoxic nature) do not always correspond to the severity of anemia according to laboratory criteria. Therefore, a classification of anemia according to the severity of clinical symptoms has been proposed.

Based on clinical manifestations, there are 5 degrees of severity of anemia:
1. anemia without clinical manifestations;
2. anemic syndrome moderate severity;
3. severe anemic syndrome;
4. anemic precoma;
5. anemic coma.

Moderate severity of anemia is characterized by general weakness, specific signs (for example, sideropenic or signs of vitamin B12 deficiency); with a pronounced degree of severity of anemia, palpitations, shortness of breath, dizziness, etc. appear. Precomatose and comatose states can develop in a matter of hours, which is especially typical for megaloblastic anemia.

Modern clinical studies show that laboratory and clinical heterogeneity is observed among patients with iron deficiency anemia. Thus, in some patients with signs of iron deficiency anemia and concomitant inflammatory and infectious diseases, the level of serum and erythrocyte ferritin does not decrease, but after the exacerbation of the underlying disease is eliminated, their content drops, which indicates the activation of macrophages in the processes of iron consumption. In some patients, the level of erythrocyte ferritin even increases, especially in patients with long-term iron deficiency anemia, which leads to ineffective erythropoiesis. Sometimes there is an increase in the level of serum iron and erythrocyte ferritin, a decrease in serum transferrin. It is assumed that in these cases the process of iron transfer to heme-synthesizing cells is disrupted. In some cases, a deficiency of iron, vitamin B12 and folic acid is simultaneously determined.

Thus, even the level of serum iron does not always reflect the degree of iron deficiency in the body in the presence of other signs of iron deficiency anemia. Only the level of THC in iron deficiency anemia is always increased. Therefore, not a single biochemical indicator, incl. OZHSS cannot be considered as absolute diagnostic criterion with iron deficiency anemia. At the same time, the morphological characteristics of peripheral blood erythrocytes and computer analysis of the main parameters of erythrocytes are decisive in the screening diagnosis of iron deficiency anemia.

Diagnosis of iron deficiency conditions is difficult in cases where the hemoglobin level remains normal. Iron deficiency anemia develops in the presence of the same risk factors as for iron deficiency anemia, as well as in individuals with an increased physiological need for iron, especially in premature infants. early age, in adolescents with a rapid increase in height and body weight, in blood donors, with nutritional dystrophy. In the first stage of iron deficiency clinical manifestations are absent, and iron deficiency is determined by the content of hemosiderin in bone marrow macrophages and by the absorption of radioactive iron in the gastrointestinal tract. At the second stage (latent iron deficiency), an increase in the concentration of protoporphyrin in erythrocytes is observed, the number of sideroblasts decreases, morphological signs appear (microcytosis, hypochromia of erythrocytes), the average content and concentration of hemoglobin in erythrocytes decreases, the level of serum and erythrocyte ferritin, and transferrin saturation with iron decrease. The hemoglobin level at this stage remains quite high, and clinical signs are characterized by a decrease in tolerance to physical activity. The third stage is manifested by obvious clinical and laboratory signs of anemia.

Examination of patients with iron deficiency anemia
To exclude anemia that has common features with iron deficiency anemia, and identifying the cause of iron deficiency requires a complete clinical examination of the patient:

General blood analysis with the obligatory determination of the number of platelets, reticulocytes, and the study of erythrocyte morphology.

Blood chemistry: determination of the level of iron, TLC, ferritin, bilirubin (bound and free), hemoglobin.

In all cases it is necessary examine bone marrow aspirate before prescribing vitamin B12 (primarily for differential diagnosis with megaloblastic anemia).

To identify the cause of iron deficiency anemia in women, a preliminary consultation with a gynecologist is required to exclude diseases of the uterus and its appendages, and in men, an examination by a proctologist to exclude bleeding hemorrhoids and a urologist to exclude pathology of the prostate gland.

There are known cases of extragenital endometriosis, for example in respiratory tract. In these cases, hemoptysis is observed; fiberoptic bronchoscopy with histological examination of a biopsy of the bronchial mucosa makes it possible to establish a diagnosis.

The examination plan also includes x-ray and endoscopic examination of the stomach and intestines to exclude ulcers, tumors, incl. glomic, as well as polyps, diverticulum, Crohn's disease, ulcerative colitis etc. If pulmonary siderosis is suspected, X-ray and tomography of the lungs and sputum examination for alveolar macrophages containing hemosiderin are performed; in rare cases it is necessary histological examination lung biopsy. If kidney pathology is suspected, a general urine test, blood serum testing for urea and creatinine are required, and, if indicated, an ultrasound and x-ray examination of the kidneys. In some cases it is necessary to exclude endocrine pathology: myxedema, in which iron deficiency can develop secondary to damage to the small intestine; polymyalgia rheumatica - rare disease connective tissue in older women (less often in men), it is characterized by pain in the muscles of the shoulder or pelvic girdle without any objective changes in them, and in a blood test - anemia and an increase in ESR.

Differential diagnosis of iron deficiency anemia
When diagnosing iron deficiency anemia, it is necessary to carry out a differential diagnosis with other hypochromic anemias.

Iron redistribution anemia is a fairly common pathology and in terms of frequency of development it ranks second among all anemias (after iron deficiency anemia). It develops in acute and chronic infectious and inflammatory diseases, sepsis, tuberculosis, rheumatoid arthritis, liver diseases, oncological diseases, IHD, etc. The mechanism of development of hypochromic anemia in these conditions is associated with the redistribution of iron in the body (it is located mainly in the depot) and a violation of the mechanism of reutilization of iron from the depot. In the above diseases, activation of the macrophage system occurs, when macrophages, under activation conditions, firmly retain iron, thereby disrupting the process of its reutilization. A general blood test shows a moderate decrease in hemoglobin (<80 г/л).

The main differences from iron deficiency anemia are:
- increased level of serum ferritin, which indicates an increased iron content in the depot;
- serum iron levels may remain within normal limits or be moderately reduced;
- TIHR remains within normal values ​​or decreases, which indicates the absence of serum Fe starvation.

Iron-saturated anemia develops as a result of a violation of heme synthesis, which is caused by heredity or can be acquired. Heme is formed from protoporphyrin and iron in erythrokaryocytes. In iron-saturated anemia, the activity of enzymes involved in the synthesis of protoporphyrin occurs. The consequence of this is a violation of heme synthesis. Iron, which was not used for heme synthesis, is deposited in the form of ferritin in macrophages of the bone marrow, as well as in the form of hemosiderin in the skin, liver, pancreas, and myocardium, resulting in the development of secondary hemosiderosis. A general blood test will record anemia, erythropenia, and a decrease in color index.

Indicators of iron metabolism in the body are characterized by an increase in the concentration of ferritin and serum iron levels, normal indicators of life-saving blood test, and an increase in transferrin saturation with iron (in some cases reaching 100%). Thus, the main biochemical indicators that allow us to assess the state of iron metabolism in the body are ferritin, serum iron, total body mass and % transferrin saturation with iron.

Using indicators of iron metabolism in the body allows the clinician to:
- identify the presence and nature of iron metabolism disorders in the body;
- identify the presence of iron deficiency in the body at the preclinical stage;
- carry out differential diagnosis of hypochromic anemia;
- evaluate the effectiveness of the therapy.

Treatment of Iron Deficiency Anemia:

In all cases of iron deficiency anemia, it is necessary to establish the immediate cause of this condition and, if possible, eliminate it (most often, eliminate the source of blood loss or treat the underlying disease, complicated by sideropenia).

Treatment of iron deficiency anemia should be pathogenetically substantiated, comprehensive and aimed not only at eliminating anemia as a symptom, but also at eliminating iron deficiency and replenishing its reserves in the body.

Iron deficiency anemia treatment program:
- eliminating the cause of iron deficiency anemia;
- therapeutic nutrition;
- ferrotherapy;
- prevention of relapses.

Patients with iron deficiency anemia are recommended to have a varied diet, including meat products (veal, liver) and products of plant origin (beans, soy, parsley, peas, spinach, dried apricots, prunes, pomegranates, raisins, rice, buckwheat, bread). However, it is impossible to achieve an antianemic effect with diet alone. Even if the patient eats high-calorie foods containing animal protein, iron salts, vitamins, and microelements, iron absorption of no more than 3-5 mg per day can be achieved. The use of iron supplements is necessary. Currently, the doctor has at his disposal a large arsenal of iron medications, characterized by different compositions and properties, the amount of iron they contain, the presence of additional components that affect the pharmacokinetics of the drug, and various dosage forms.

According to the recommendations developed by WHO, when prescribing iron supplements, preference is given to drugs containing divalent iron. The daily dose should reach 2 mg/kg of elemental iron in adults. The total duration of treatment is at least three months (sometimes up to 4-6 months). An ideal iron supplement should have a minimum amount side effects, have a simple scheme of application, the best efficiency/price ratio, optimal iron content, it is desirable to have factors that enhance absorption and stimulate hematopoiesis.

Indications for parenteral administration of iron preparations arise in case of intolerance to all oral drugs, malabsorption (ulcerative colitis, enteritis), gastric and duodenal ulcers during an exacerbation, with severe anemia and the vital need to quickly replenish iron deficiency. The effectiveness of iron supplements is judged by changes in laboratory parameters over time. By the 5-7th day of treatment, the number of reticulocytes increases by 1.5-2 times compared to the initial data. Starting from the 10th day of therapy, the hemoglobin content increases.

Considering the pro-oxidant and lysosomotropic effect of iron preparations, their parental administration can be combined with intravenous drip administration of rheopolyglucin (400 ml - once a week), which protects the cell and avoids iron overload of macrophages. Considering significant changes in the functional state of the erythrocyte membrane, activation of lipid peroxidation and a decrease in antioxidant protection of erythrocytes in iron deficiency anemia, it is necessary to introduce antioxidants, membrane stabilizers, cytoprotectors, antihypoxants into the treatment regimen, such as a-tocopherol up to 100-150 mg per day (or ascorutin, vitamin A, vitamin C, lipostabil, methionine, mildronate, etc.), and also combined with vitamins B1, B2, B6, B15, lipoic acid. In some cases, it is advisable to use ceruloplasmin.

List of drugs used in the treatment of iron deficiency anemia:

Definition. A disease, the leading symptom of which is a decrease in the number of erythrocytes less than 4.0x10 12 / l and hemoglobin less than 120 g/l with a color index below 0.8 and a serum iron level less than 13 µmol/l.

Statistics. One of the most common human diseases. Up to 25% of the total population is affected, 40% of women of childbearing age, 33% of people of both sexes over 60 years of age.

Etiology.

Chronic blood loss exceeding re
Generative capabilities of the body:

Menorrhagia (menstruation lasting
6-7 days, abundant; or with clots -
any duration);

Hemorrhoidal bleeding;

Gastrointestinal bleeding with
erosive and ulcerative lesions.

Chronic gastrointestinal diseases
tract, especially at reduced sec
retort function of the stomach, leading to
disruption of the absorption of dietary iron.

Poor nutrition (starvation, anorexia
and etc.)

Hyper- and hypothyroid conditions.

Pregnancy, lactation, early childhood
rast.

Long-term uncontrolled use of some
ry medications, especially non-steroidal ones
anti-inflammatory drugs (ibupro-
hair dryer, diclofenac, etc.), analgin, biseptol.

Clinic, diagnostics. In women, the disease often occurs with chlorosis syndrome. Complaints of fainting, low-grade fever, pain in the tongue, perversion of taste and smell; irresistible

the desire to eat chalk, lime, clay, earth, whitewash from the walls, I like heavy spicy aromas. Brittle nails and hair. The nails are flattened in appearance, soft and layered to the touch. Hair is dry, split ends, dull. In men, the disease always occurs without chlorosis syndrome. Pale skin, sometimes with a greenish tint. Heart sounds are muffled, gentle systolic murmur at all points. Tachycardia, hypotension. Nervous system- signs of asthenodepressive, asthenoneurotic, asthenohypochondriacal syndromes. Laboratory indicators: decrease in the number of erythrocytes, hemoglobin, color index, serum iron, increase in ESR, anisocytosis, poikilocytosis of erythrocytes.

Classification. The degree of severity is specified, etiological factor, phase of the disease (exacerbation, remission).

Anemia severity:

Light (erythrocytes 3.0-3.5x10 |2 /l, Hb 100 g/l
and higher);

Moderate (erythrocytes 2.0-3.0x10 |2 /l,
Hb 80-100 g/l);

Severe (erythrocytes 1.0-2.0x10"7l, Hb 55-
80 g/l);

Extremely severe, threatening development
anemic coma (red blood cells<1,0х10 12 /л, НЬ
<55 г/л).

Exacerbation criteria: a decrease in the numbers of erythrocytes and Hb in women below 4.0x10" 2 /l and 120 g/l, in men below 4.5x10 12 /l and 130 g/l, respectively.

Remission criterion: return of erythrocyte and Hb numbers to normal values. Any increase in red blood numbers that does not reach the norm should be considered not a remission, but an improvement.

Outpatient hematology

Formulation of the diagnosis.

due to menorrhagia, moderate severity,
friction.

Chronic iron deficiency anemia
Shanky genesis due to menorrhagia and gas
trogenic, severe, exacerbation.

Psychological, social status form
are regulated according to general principles.

Differential diagnosis

To exclude hemoblastosis should ube
to be treated in the absence of hemorrhagic and ulcerative
crotic syndromes, laboratory - in the absence
in the patient's leukogram changes characteristic of
leukemia.

To exclude oncological pathology
first level screening is carried out: close-up
vaya fluorography (FCF), fluoroscopy of the gastric
no-intestinal tract or fibrogastroduodenoscopy
(FGDS), examination by a gynecologist is mandatory for women.
If the history does not reveal the source, no
indications of gastrointestinal diseases
that the patient is elderly, then additionally for
exclusion of malignant neoplasm
radiography of organs is carried out chest, ir-
rigoscopy, sigmoidoscopy, ultrasound
follow-up (ultrasound) of the abdominal organs.

Vitamin B 12 and folate deficiency anemia
hyperchromic, the number of reticulopitis is reduced,
Serum iron is normal, high levels are common
identification of the liver, in sternal punctate megalo-
blast hematopoiesis.

At hemolytic anemia: icterus
skin, enlarged spleen and liver,
laboratory - normochromic anemia, sudden increase
decrease in the number of reticulocytes, serum
Lez is normal or increased, I also eat hyperbilirubin
due to indirect bilirubin, hemosiderin in the urine,
in the bone marrow punctate there is pronounced hyperplasia
erythroid germ.

At hypoplastic anemia hemorrhages
chelic and (or) purulent-necrotic syndrome, res
some decrease in all blood parameters (erythrocytes,
leukocytes, platelets), in punctate inhibition of all
germs of hematopoiesis.

Sideroachrestic anemias by clinic
and data general analysis blood is no different
are from iron deficiency, but the jelly content
behind V the blood serum of such patients is high (50-
90 µmol/l). Treatment with iron supplements for
leads to hemosiderosis of organs without relieving symptoms
volumes of disease.

Patient management

Goal of treatment: recovery (complete clinical and hematological remission for 5 years). Tasks:

Restoring normal values
red blood and serum iron;

Maintaining normal levels
at the proper level.

Organization of treatment. Most patients are treated on an outpatient basis, except in cases of severe or etiologically unclear iron deficiency anemia. In such cases, patients are hospitalized, based on the principle of the most likely nature of anemia, in gynecological, gastroenterological or other departments.

Treatment monitoring. During the period of first detection or exacerbation of the disease, blood is monitored once every 10-14 days, and the frequency of medical examinations should be the same. You should not count on an increase in the numbers of red blood cells and hemoglobin after 3-5 days.

During the period of partial remission, when the patient is able to work, but the hematological norm has not been achieved, blood monitoring and medical examination are carried out monthly. During the period of complete remission with normal red blood composition, monitoring is carried out quarterly during the first year, then once every 6 months. Recovery is considered to be the absence of exacerbations for 5 years. Consultation with a hematologist during an exacerbation - once every 2 months, then once every 4-6 months.

Planned therapy

Information for the patient and his family:

The reason for the development of anemia in this patient.

Fundamental curability of the disease.

Duration of drug therapy (initial
iron therapy course - 2-3 months, full course - up to
1 year).

Possibility of self-control (red norms)
blood and serum iron).

Explanation of harm for this category of pas
unqualified treatment patients, vegetarians
ancestry, fasting, “recipes” for self-medication.

Advice for the patient and his family:

Start treatment with iron supplements with
moment of detection of the disease, with the exception of
We eat the very initial stages, when red blood cells
>3.5x10 |2 /l, and Hb >P0 g/l. In these cases you can
use diet and herbal medicine as a stand-alone
telny method, but in its case it is ineffective
sti within 1 month. it is necessary to convince the patient of the need
the need for drug therapy.

Chronic iron deficiency anemia

If possible, eliminate etiological
factors: use hemostatic herbal medicine
in case of menorrhagia; treat chronic
diseases of the gastrointestinal tract, kidneys;
convince the patient (tku) of the need for surgery
who treats hemorrhoids or uterine fibroids with
persistent bleeding.

Organize therapeutic nutrition with predominantly
consumption of meat products and natural sources
of vitamins (black currants, lemons,
piha). For women with heavy periods - grana
you and nuts.

Eliminate chronic household and occupational
onal and, if possible, medicinal
toxicity during the treatment period (gasoline, dyes,
non-steroidal anti-inflammatory drugs,
biseptol).

Drug therapy

Iron supplements should be prescribed in sufficient doses and for a long period of time. Due to low efficiency and severe side effects Not should be prescribed: reduced iron, aloe syrup with iron, hemostimulin, ferramide. Nutritional supplements, containing iron, for therapeutic purposes are unsuitable because the iron content in them is not higher than 18 mg, with a requirement of at least 250 mg/day. Their use is possible only during the period of complete remission to prevent relapses.

Tardiferon(hypotardiferon for pregnant women). Prescribed 1-2 tablets. per day, strictly after meals. Contains mucoprotease, which protects the gastric mucosa and has high bioavailability. Hypotardiferon contains folic acid necessary for pregnant women.

Sorbifer. Prescribed 1 tablet. 2 times a day, after meals. Well tolerated, contains ascorbic acid, which facilitates absorption of the drug.

Actiferrin. Depending on the severity of anemia, it is prescribed from 1 to 3 caps per day. There are forms for children: syrup and drops. The drug is highly effective, but individual intolerance is possible.

Ferroplex. Prescribed 2 tablets. 4 times a day. Compared to the retard forms described above, it is ineffective, but is well tolerated and has almost no side effects. Possible use for anemia in pregnant women.

NB! Warn the patient about the change in color of the stool to black and that all iron supplements, without exception, are taken strictly after meals, regardless of the manufacturer's instructions.

Parenteral use of iron (the drug Ferrumlek) is limited to two situations:

Complete intolerance to oral medications
rats;

The need to quickly and briefly stabilize
zirate the numbers of red blood, for example, with
preparation for emergency surgery. Maybe challenges
cause anaphylactic reactions, hypercoagus
lation. Prescribes on an outpatient basis
only intramuscularly, injections (containing
pressing one ampoule) are carried out every other day,
course of 10-15 injections.

Auxiliary drugs

To improve iron absorption and stimulate erythropoiesis - multivitamin preparations with the addition of microelements: complivit 1 tablet. per day, during meals.

To correct protein metabolism - potassium orotate, 1 table. (0.5 g) 3 times a day for 20 days. Prescribing B vitamins in injection form is not justified.

Phytotherapy.Rose hip decoction. Chop the berries and pour boiling water at the rate of 1 cup of boiling water per 1 tbsp. l. berries, leave for 20-30 minutes. Drink during the day.

Antianemic collection. Mix nettles, string, currant leaves, strawberry leaves equally, pour cold water(1 glass of water per 1 tablespoon of mixture) for 2-3 hours, then put on fire, boil for 5-7 minutes, cool, strain. Drink during the day.

An approximate treatment regimen for iron deficiency anemia in pregnant women:

Hypotardiferon 1 tablet. in the morning and in the evening
after meal; will take 1 caps. 2 times a day, orotate
potassium 1 table. (0.5 g) 3 times a day for
20 days; phytotherapy; diet therapy.

An approximate treatment regimen for iron deficiency anemia in the elderly:

Sorbifer 1 tablet. morning and evening after
food; undevit 1 tablet 2 times a day, potassium orotate
1 table each (0.5 g) 3 times a day for 20 days;
herbal medicine, diet therapy.

Rehabilitation therapy

During the period of partial remission, when the patient is able to work, daily medication should be continued until hemoglobin levels normalize. When the amount of hemoglobin reaches 120 g/l, one of the iron preparations is prescribed for 7 days after menstruation or 7 days of each month, up to a year.

During the period of complete remission, when hemoglobin numbers are normal without treatment, one-month anti-relapse courses of ferroplex or tardiferon in the spring and autumn.

Outpatient hematology

Criteria for the effectiveness of rehabilitation therapy: maintaining normal numbers of red blood and serum iron for three years during one-month anti-relapse courses of treatment in spring and autumn.

Medical examination

Examination of temporary disability
you. The terms of labor losses are determined by medical
(clinic, numbers of red blood cells and hemoglobin) and with
cial factor - the nature of the patient’s work.
During heavy physical labor and hazardous work
in industries, men’s ability to work was restored
occurs at hemoglobin levels of 130 g/l, in women -
120 g/l. For light physical work are allowed
hemoglobin numbers per 10 g/l, in mental workers
yes - 20 g/l lower than given.

Medical and social expertise. At MSEC
patients with severe, difficult correction are referred
controlled by anemia. In diagnostic formulation
anemia takes the place of a symptom or complication
underlying disease.

Military medical examination. For anemia
(according to Article 11), quickly or slowly progressing

with significant changes in blood composition and periodic exacerbations, conscripts are considered unfit to serve military service, with anemia accompanied by moderate dysfunction of the hematopoietic system and rare exacerbations - of limited use.

Preliminary and periodic medical examinations. According to medical contraindications (in addition to general medical contraindications) persons suffering from anemia should not be allowed to work in contact with lead (1.25.1), aromatic hydrocarbons(1.33), naphthalene, naphthols (1.34), organochlorine pesticides (2.2.1), organofluorine pesticides (2.2.2), carbamic acid derivatives (2.2.4), chlorobenzoic acid derivatives (2.2.6), chlorophenoxyacetic acid derivatives (2.2 .7), derivatives of chlorophenoxybutyric acid (2.2.8), halogenated anilides of carboxylic acids (2.2.9), derivatives of urea and guanidine (2.2.10), polystyrenes (2.4.7), antitumor drugs (2.7.2), ionizing radiation (5.1).

Vitamin B 12 - and folate deficiency anemia (code D 51.9)

Definition. Anemia associated with impaired DNA and RNA synthesis caused by deficiency of vitamin B]2 or folic acid and manifested by megaloblastic hematopoiesis, hyperchromia and macrocytosis of erythrocytes. Combined deficiency of vitamin B 12 and folic acid is rare, but forms with isolated deficiency of both factors are clinically and laboratory indistinguishable, and therefore are considered together.

Statistics. In Russia, the incidence of the disease (20-60 cases per 100,000 population) varies significantly depending on the region: northerners are more likely to get sick, residents of the middle zone are less likely to get sick, and residents of the Far East are very rarely affected. Starting from the age of 45-55 years, in older age groups the incidence increases progressively. No significant differences in pathological involvement due to gender differences were identified.

Etiology and pathogenesis. Megaloblastic anemias are considered to be the result of a genetic defect that causes an immunological disorder manifested by the production of autoantibodies against gastric epithelial cells. This leads to degenerative lesions of the mucous membranes of the digestive tract due to insufficient absorption of vitamin B 12 and (or) folic acid. Vitamin B2 deficiency is a cause of severe damage spinal cord(funicular myelosis).

Clinic. As a rule, older people are affected. General weakness, change in skin color (pallor with a jaundiced tint), pain in the tongue and increased taste sensitivity to the point of discomfort, numbness of the feet and palms. The history indicates chronic gastritis, colitis and other diseases of the gastrointestinal tract. On examination, patients are “more jaundiced than pale,” with bright red areas on the tongue. Palpation of the abdomen may reveal pain in the epigastric region, in the hypochondrium, along the intestine in the presence of chronic diseases of the gastrointestinal tract. Blood test: hyperchromic macrocytic anemia, usually significant. The color index can increase to 1.3. The number of reticulocytes is reduced, the number of leukocytes is also reduced, due to neutrophils. Sometimes I observe

24. Denisov

significant thrombocytosis without bleeding is observed. Moderate hyperbilirubinemia (up to 28-47 µmol/l) due to indirect bilirubin. The iron content in the blood serum is normal or slightly increased. Sterial punctate - megaloblastic hematopoiesis.

Formulation of the diagnosis. Vitamin B2 - deficiency anemia of moderate severity.

Differential diagnosis

First of all, it is necessary to exclude it
ecological disease. For this purpose they carry out
first level screening: CCF, fluoroscopy
stomach or FGDS, for women - examination by a gynecologist,
for persons over 50 years old - irrigoscopy and ultrasound examination
new abdominal cavity.

How does hyperchromic anemia syndrome occur?
yes in acute erythromyelosis. To exclude
of this disease it is necessary to make sure that there is no hepatitis
morrhagic and purulent-necrotic syndrome
mov, and also, since with this hemoblastosis the
stench cells appear in the peripheral blood
not immediately, the patient should undergo sternal
puncture.

At iron deficiency anemia Unlike
vitamin B 12 - deficiency - pale skin with gray
greenish tint, the presence of chlorosis syndrome (in
women). Laboratory: color index 0.8 and
lower, the number of reticulocytes is increased, aniso-
cytosis and poikilocytosis of erythrocytes, in the sternal
punctate - moderate hyperplasia of the erythroid
sprout.

At hemolytic anemia Unlike
vitamin B 12 - deficiency - severe jaundice
skin, significant hepato- and splenomegaly. Labo
Ratory: normochromic anemia, sharply increased blood
the number of reticulocytes, the number of leukocytes is higher
but, hyperbilirubinemia more than 50 µmol/l due to
indirect bilirubin, in urine - hemosiderin, in sterile
onal punctate - pronounced hyperplasia erythritis
roid sprout.

Hypoplastic anemia from vitamin B 12 -
deficient is characterized by the severity of the general condition
niya, the presence of hemorrhagic or purulent-non-

Outpatient hematology

Crotic syndrome, absence of liver enlargement. Laboratory examination: normochromic anemia, all blood parameters are sharply reduced, there is no hyperbilirubinemia, in the sternal puncture there is inhibition of all hematopoietic germs.

Patient management

Goal of treatment: achieving and maintaining stable clinical and hematological remission. Tasks:

Transfer of hematopoiesis from megaloblastic-
go to normoblastic;

Lifelong maintenance of normoblastic
what type of hematopoiesis is permanent injection
vitamin B 12 and (or) folic acid deficiency
lots.

Organization of treatment. Megaloblastic anemia is treated on an outpatient basis. However, in cases requiring transfusion therapy for life-saving reasons, hospitalization in a therapeutic or hematology department is necessary. Consultation with a hematologist is advisable when the disease is first detected, when remission occurs, and then once a year.

Planned therapy

Informationfor the patient And his families:

Brief information about the essence of the disease.

It is fundamentally possible to create a sustainable
howl clinical and hematological remission with adek
cotton maintenance therapy.

It is necessary to control the blood test once every
3 months, administration of vitamin B 12 monthly even in
period of stable remission.

. Advice for the patient and to his family:

Nutrition complete in protein and vitamins
mu composition.

If necessary, you must complete the coursework
treatment of chronic gastric diseases
but-intestinal tract.

Drug therapy

During the period of first detection and exacerbation of the disease, it is necessary home mode. The diet is the same as for iron deficiency anemia. Vitamin B 12 500 mcg intramuscularly daily for 7-10 days, then another 7-10 injections every other day. Improvement occurs after the first or second injection. On days 3-7 - reticulocyte crisis. Remission is induced quickly and is stable. Folic acid is prescribed at 5-15 mg/day. During the period of partial remission, when the patient is able to work, but the hematological norm has not yet been achieved, it is necessary to introduce

vitamin B 12 500 mcg intramuscularly once a week, 3 months. During the period of complete remission - lifelong administration of 500 mcg of vitamin B 12 once a month.

Approximate treatment plan for pregnant women:

200 mcg once every 10 days;

Folic acid 15 mg/day from 1st to 30th day
from the start of treatment with vitamin B 12;

Hypotardiferon 1 tablet. per day from the 30th day
within 1-2 months.

Iron supplements are necessary because In pregnant women, anemia is usually mixed origin.

Approximate treatment plan for the elderly:

Vitamin B 12,500 mcg intramuscularly daily
gently for 10 days, then every other day 10 injections, then
500 mcg once a week, 2-3 months, then once every 2 weeks.
- 2 months, then 1 time per month. for life;

Folic acid 10 mg/day;

Multivitamin preparation (undevit) 1 tablet.
2 times a day from the 30th day from the start of vitamin treatment
At 12, for 1-2 months, with breaks for 2-3 months.

Phytotherapy- see section “Iron deficiency anemia”.

Rehabilitation therapy

During the period of complete remission, 500 mcg of vitamin B12 is administered once a month. If necessary (if there are signs of megal regional hematopoiesis), vitamin B 12 is administered in the spring and autumn, 200 mcg, once every 10 days. In 12 - and folate deficiency anemia during the period of clinical and hematological remission is not a contraindication to sanatorium treatment and does not entail restrictions in receiving physical procedures.

Criteriaefficiency rehabilitation no therapy:

Preservation of normoblastic hematopoiesis
(normal red blood cell numbers, Hb, color
howl indicator is not higher than 1.1; lack of poppy
rocytosis) if present, I only support
cabbage soup therapy.

Absence of neurological disorders: from
rotation of taste, numbness of the feet and palms,
paresthesia, etc.

Medical examination

The patient is temporarily disabled until signs of megaloblastic hematopoiesis completely disappear and red blood counts are restored to normal.

Medical and social examination, military medical examination, preliminary and periodic medical examinations - see the section “Chronic iron deficiency anemia”.

Hemolytic anemia (codes D 58.9, D 59)

Definition. A group of anemic conditions in which the process of destruction of red blood cells prevails over the process of their reproduction. In hemolytic anemia, red blood cells live less than 100 days.

Statistics. Pathological incidence is low, amounting to 0.6-2.8 cases per 100,000 population. Congenital hemolytic anemia is more common in Dagestan, acquired - in large centers with a developed chemical industry.

Etiology, pathogenesis. Among causal factors highlighted:

Intraerythrocytic (erythrocytopathies,
fermentopathy, hemoglobinopathies).

Extra-erythrocyte:

Infectious;

Chemical (medicinal, professional
nal and household intoxications);

Physical (burns, presence of dental prostheses)
bowel valves);

Immunological (auto- and heteroimmune-
new forms);

Unknown (hemolysis in pathology,
liver and kidney pathologies).

In the pathogenesis, the leading role is played by the peripheral destruction of erythrocytes, the appearance of decay products in the circulatory system and, as a consequence, according to the analysis of peripheral blood, the bone marrow regenerative reaction and its markers.

Clinic, diagnostics. Hemolytic syndrome consists of three symptoms: anemia, jaundice and splenomegaly. Diagnosis is often difficult; many patients are diagnosed with chronic hepatitis or cirrhosis for many years, and anemia is taken as a consequence of these diseases. In

In all cases of jaundice with an enlarged spleen, a thorough examination of patients is required, regardless of hemoglobin numbers, since anemia can be mild. Laboratory indicators: anemia, often normochromic, multiple increase in the number of reticulocytes, severe hyperbilirubinemia due to indirect bilirubin, hemosiderin in the urine, pronounced hyperplasia of the erythroid lineage in the sternal punctate.

Classification. There are two large groups of hemolytic anemias: congenital and acquired. Congenital forms are often familial and hereditary, inherited in an autosomal dominant and autosomal recessive manner.

The main cause of skin disorders in allergic urticaria is massive degranulation of tissue basophils (mast cells). The granules of these cells contain histamine, heparin, leukotrienes and a number of other biologically active compounds that can significantly change metabolic processes in tissues. They mainly lead to expansion blood vessels, increase the permeability of their walls, cause the accumulation of tissue fluid, stimulate pain receptors in the skin, which leads to itching. In most cases, such reactions in allergic urticaria are local in nature and affect only a certain area of ​​the skin or, less commonly, the entire surface of the body. However, sometimes such a massive release of active compounds can lead to general reactions type anaphylactic shock and Quincke's edema.
The reasons that cause mast cell degranulation differ among various forms allergic urticaria. Usually this is a reagin type of hypersensitivity (type 1 allergy), mediated by type E immunoglobulins. Allergens for this type of allergic urticaria are food components, pollen, household dust, some medications and other factors. In this case, skin manifestations are just one of the symptoms of a food or other allergy. In some cases, type 2 allergies can also cause such skin disorders - this mainly happens with blood transfusions. Intravenous administration some medicines with the development of an immunocomplex intolerance reaction, it can also cause allergic urticaria.
It has been noticed that some infectious diseases, endocrine disorders, disorders of the psycho-emotional sphere increase the likelihood of developing allergic urticaria. This is especially true in relation to idiopathic, or chronic form pathology. The pathogenesis of the development of skin disorders in this case has been poorly studied; both immune and non-immune mechanisms of activation of tissue basophils of the skin are assumed. Therefore, in the presence of allergic urticaria of unspecified etiology, full examination the patient’s body in order to identify hidden and chronic diseases and disorders.
In pseudoallergic urticaria, the pathogenesis is largely similar - massive activation of skin tissue basophils occurs with the release of biologically active compounds. However, the reasons and mechanisms of this process are somewhat different - it may be congenital or acquired instability of mast cell membranes, their abnormal response to various physical or humoral factors. In addition, in some cases of pseudoallergic urticaria, the patient has increased sensitivity skin tissue to histamine and other components of basophil granules. Therefore, even a slight release of these substances can lead to the clinical picture of urticaria.

Statistics. One of the most common human diseases. Up to 25% of the total population is affected, 40% of women of childbearing age, 33% of people of both sexes over 60 years of age.

Etiology.

Chronic blood loss exceeding the body's regenerative capabilities:

Menorrhagia (menstruation lasting 6-7 days, heavy; or with clots - of any duration);

Hemorrhoidal bleeding;

Gastrointestinal bleeding with erosive and ulcerative lesions.

Chronic diseases of the gastrointestinal tract, especially with reduced secretory function of the stomach, leading to impaired absorption of dietary iron.

Poor nutrition (starvation, anorexia, etc.)

Hyper- and hypothyroid conditions.

Pregnancy, lactation, early childhood.

Long-term uncontrolled use of certain medications, especially non-steroidal anti-inflammatory drugs (ibuprofen, diclofenac, etc.), analgin, biseptol.

Clinic, diagnostics. In women, the disease often occurs with chlorosis syndrome. Complaints of fainting, low-grade fever, pain in the tongue, perversion of taste and smell; irresistible

The desire to eat chalk, lime, clay, earth, whitewash from the walls, I like heavy spicy aromas. Brittle nails and hair. The nails are flattened in appearance, soft and layered to the touch. Hair is dry, split ends, dull. In men, the disease always occurs without chlorosis syndrome. Pale skin, sometimes with a greenish tint. Heart sounds are muffled, gentle systolic murmur at all points. Tachycardia, hypotension. Nervous system - signs of asthenodepressive, asthenoneurotic, asthenohypochondriacal syndromes. Laboratory indicators: decrease in the number of erythrocytes, hemoglobin, color index, serum iron, increase in ESR, anisocytosis, poikilocytosis of erythrocytes.

Classification. The degree of severity, etiological factor, and phase of the disease (exacerbation, remission) are specified.

Anemia severity:

Light (erythrocytes 3.0-3.5x10|2/l, Hb 100 g/l and above);

Moderate severity (erythrocytes 2.0-3.0x10|2/l, Hb 80-100 g/l);

Severe (erythrocytes 1.0-2.0x10"7l, Hb 55-80 g/l);

Extremely severe, threatening the development of anemic coma (red blood cells
Criteria for exacerbation: a decrease in the numbers of erythrocytes and Hb in women below 4.0x10"2/l and 120 g/l, in men below 4.5x1012/l and 130 g/l, respectively.

Remission criterion: return of red blood cell and Hb numbers to normal values. Any increase in red blood numbers that does not reach the norm should be considered not a remission, but an improvement.

Formulation of the diagnosis.

Chronic iron deficiency anemia due to menorrhagia, moderate severity, exacerbation.

Chronic iron deficiency anemia of mixed origin due to menorrhagia and gastrogenic, severe, exacerbation.

Psychological and social status are formulated according to general principles.

Differential diagnosis

To exclude hemoblastosis, one should verify the absence of hemorrhagic and ulcerative-necrotic syndromes, and laboratory tests should ensure that there are no changes in the patient’s leukogram characteristic of leukemia.

To exclude oncological pathology, first-level screening is carried out: large-frame fluorography (CCF), fluoroscopy of the gastrointestinal tract or fibrogastroduodenoscopy (FGDS); for women, an examination by a gynecologist is required. If the source is not identified when collecting anamnesis, there is no indication of diseases of the gastrointestinal tract, the patient elderly, then in addition to exclude a malignant neoplasm, chest X-ray, irrigoscopy, sigmoidoscopy, ultrasonography(ultrasound) of the abdominal organs.

Vitamin B12 and folate deficiency anemia is hyperchromic, the number of reticulopitis is reduced, serum iron is normal, liver enlargement is common, megaloblastic hematopoiesis is found in the sternal punctate.

With hemolytic anemia: icterus of the skin, enlargement of the spleen and liver, laboratory tests - normochromic anemia, a sharp increase in the number of reticulocytes, serum iron is normal or increased, hyperbilirubinemia due to indirect bilirubin, hemosiderin in the urine, pronounced hyperplasia of the erythroid lineage in bone marrow punctate.

With hypoplastic anemia, hemorrhagic and (or) purulent-necrotic syndrome, a sharp decrease in all blood parameters (erythrocytes, leukocytes, platelets), in the punctate, inhibition of all hematopoietic germs.

Sideroachrestic anemia, according to the clinical picture and data from a general blood test, is no different from iron deficiency, but the iron content in the blood serum of such patients is high (50-90 µmol/l). Treatment with iron preparations leads to hemosiderosis of organs without relieving the symptoms of the disease.