Anemia disease. Anemia: symptoms. Anemia: causes, treatment, prevention, first signs Mild anemia what

Constant overwork, stress, rare walks and malnutrition have a negative impact on women's health.

Symptoms of many ailments are mistaken for ordinary fatigue and do not go to the doctor. Anemia is a pathology that can be easily confused with overwork.

In this article, we will talk about the symptoms and external signs, treatment, nutrition and consequences of iron deficiency and other types of anemia in adult women, during pregnancy and breastfeeding, in older women over 50 years old.

Kinds

The development of the disease is due to the blood.

- red protein found in red blood cells. It performs the most important function - it delivers oxygen to the internal organs, ensuring their activity.

Anemia occurs when there is loss of blood or a malfunction in the formation of red blood cells. Most often, anemia occurs in children and adult women of reproductive age.

In medicine, 6 types of anemia are distinguished:

All species have common symptoms:

Hemoglobin in the blood in all manifestations of anemia decreases, but a decrease in the number of red blood cells does not always occur.

Anemia is not an independent disease. It is the result of a pathology of the processes of the circulatory system, so it is necessary to take tests so that the doctor determines its type and prescribes treatment.

Severity, blood counts

The reasons

Causes of the development of the disease in women of reproductive age and menopause:

The first signs and external manifestations

You should know how anemia manifests itself in women, because the symptoms differ depending on the type of pathology. Their diversity is shown in the table:

Diagnostic methods, analyzes

If you feel unwell, you should consult a therapist. A general blood test will also help to identify the pathology.

The most common anemia associated with. If there is a suspicion of a different type of it, an examination of the organs of the gastrointestinal tract may be required, to which your doctor will refer you.

A blood test will show all deviations from the norm. In the presence of anemia, red blood cells in the blood will be smaller and less colored than in a healthy person.

The doctor will check the pulse, measure the pressure assess the condition of the skin. After examination and evaluation of the tests, treatment is prescribed.

What is anemia and how to treat it, the program "Live healthy!" will tell:

What is dangerous: consequences and complications

What does anemia lead to and what is terrible for a woman? Possible consequences and complications caused by anemia:

1. Decreased immunity. It is more difficult for the body to fight viruses. As a result, the woman often gets sick.
2. Sleep disorders. Sleepless nights are not the best way to affect well-being and performance.
3. mucous membranes become susceptible and vulnerable, leading to inflammation and infection.
4. Women are more stressed become distracted and vulnerable.
5. Leads to disruption of the cardiovascular system.
6. Prolonged anemia leads to edema, liver disease.
7. The process of absorption of nutrients is disturbed, which leads to diseases of the gastrointestinal tract.
8. When anemia occurs oxygen starvation. This is detrimental to the functioning of the brain.
9. Takes away the beauty- the skin becomes lethargic and dry, the hair brittle and dull, the nails exfoliate.
10. In severe cases anemia leads to fainting, fever,.

How and what to treat: iron supplements, vitamins

In mild forms of anemia, it is enough to revise the diet: include foods rich in iron and B vitamins.

If a special diet is not enough, the specialist will prescribe drugs that compensate for the deficiency in the body of certain substances.

Do not self-medicate - this can aggravate the situation. In the case when therapy does not work, the doctor prescribes drugs containing hormones.

The age of the woman suffering from anemia is also taken into account.. Often, the disease is associated with menopause, when consultation is necessary not only with a therapist, but also with a gynecologist, endocrinologist.

Rules for the use and selection of iron preparations for the treatment of iron deficiency anemia in women:

• taking pills is more effective than intramuscular injections, because. iron is better absorbed if it passes through the intestinal tract;
• the optimal dose of pure iron is 80-160 mg - exceeding the dose is unacceptable;
• taking in the form of tablets is more effective than in liquid form;
• preparations contain ferrous or trivalent iron: in the first case, vitamin C contributes to good absorption, in the second - amino acids;
• use preparations covered with a protective shell, which will save the mucous membrane of the esophagus and stomach from irritation.

Of ferrous iron, the most commonly prescribed drugs are Sorbifer Durules, Tardifferon. They are consumed twice a day, 30 minutes before meals, with a glass of water.

Ferric iron preparations- Ferrum Lek, Biofer - used during meals or after.

Injections are prescribed for patients with diseases of the gastrointestinal tract and with large blood losses.

With complex forms of anemia- posthemorrhagic, hemolytic, hypoplastic - are prescribed:

Uncontrolled treatment is unacceptable. Dosage prescribed by the doctor based on the results of a blood test and diagnostics of narrow specialists.

In order for iron-containing preparations to be absorbed faster, vitamins are prescribed:

• vitamin C;
• vitamin B6;
• folic acid.

Rarely, anemia can be caused by lack of copper or zinc in the body.

Together with vitamins, the intake of mineral complexes (their names will be announced to you by the doctor) helps to alleviate the symptoms of anemia in women and helps to quickly cope with oxygen starvation.

With posthemorrhagic anemia the patient is transfused with blood or its substitutes. After that, iron and vitamins are prescribed until hemoglobin is completely restored.

Folk remedies

With alarming symptoms, it is impossible to self-medicate, because. anemia can be a sign of serious illness, including malignant tumors.

Folk remedies can help relieve symptoms and raise hemoglobin levels in the blood, but for some forms of anemia, home treatment will not work.

If anemia is associated with a lack of iron, natural formulations will give a positive effect without side effects for the body.

Folk methods of treatment of the disease:

Do you know in the blood? Is it necessary and how to reduce its level? Details are in this article.

What cholesterol is considered normal in women? The answer to the question will prompt the material.

About what can cause pulling pains in the lower abdomen in women, read the publication.

What to eat: nutrition and diet

Proper diet plays an important role in the treatment of pathology. Beef will help restore strength- this meat is the champion in the content of nutrients during oxygen starvation.

It is necessary to introduce protein-rich foods into the diet:

• veal;
• liver;
• dairy products;
• fish;
• eggs;
• butter and vegetable oils.

To raise the level of hemoglobin will help included in the menu for iron deficiency anemia in women cereals, especially from buckwheat, apples, honey, dried fruits.

But it is better to refuse fatty foods and semi-finished products. They will only bring harm.

Coffee drinkers should limit the number of cups they drink per day, because it flushes out vitamins and minerals from the body.

If a woman has problems with the gastrointestinal tract, the doctor may prescribe a special diet that excludes certain foods.

Course duration

The treatment regimen may differ depending on the age of the patient. Women of reproductive age most often develop anemia during pregnancy and lactation.

During period and old age the doctor studies the manifestations of anemia in detail, because. often it is associated with specific diseases.

The duration of treatment depends on the form and severity of anemia, as well as on the age of the patient. Older women need more time to heal.

Age-related changes slow down the metabolic processes in the body, so it is difficult to cope with the disease.

Yes, many patients after the age of 60 there is a whole bunch of concomitant diseases, which hinders the positive dynamics of therapy.

During pregnancy and breastfeeding

When a pregnant woman registers at the clinic, she is prescribed a series of tests. If a low hemoglobin level is detected, the expectant mother is prescribed iron supplements and a special diet.

Timely correction and therapy helps to avoid complications in the second half of pregnancy.

Oxygen starvation affects not only the condition of the woman, but also the development of the fetus and placenta. That is why it is so important to follow the doctor's recommendations.

Even mild anemia in women increases the risk of fetal hypoxia leading to developmental disorders of the nervous system of the baby. Pathology can cause weak labor activity.

If a woman loses a lot of blood during childbirth, she is given a transfusion. Thanks to this, hemoglobin can be quickly raised. Iron injections are less effective.

To avoid anemia while breastfeeding, a woman should eat regularly and properly. When discharged from the hospital, they give a list of products that are necessary for use during lactation.

In situations where it is required to raise hemoglobin, iron-containing preparations are prescribed. Do not exceed the dosage prescribed by a specialist in order to avoid irreversible consequences in the baby.

Prevention measures

The main factors that reduce the risk of anemia- Proper nutrition and regular walks in the fresh air. Compliance with preventive measures is especially important for women with heavy and prolonged menstruation.

Dietary intake of vitamins plays an important role. Doctors recommend eating 500 grams of vegetables and fruits daily. This reduces the risk of anemia and other diseases.

Pregnant women and donors are at risk. For prevention, they are often prescribed iron preparations and vitamin complexes.

Timely diagnosis and treatment of anemia can relieve unpleasant symptoms. The main thing is to follow the recommendations of the doctor, review your diet.

Only in this case, you can defeat the disease and continue to enjoy life.

What is dangerous anemia and what are its consequences? This question is asked by many people who are faced with pale skin and weakness. is a common disease that, at first glance, does not pose a danger. In fact, with anemia, a fatal outcome is also possible. Therefore, it is necessary to pay attention to the symptoms of the disease in a timely manner and identify the cause of the occurrence.

Why is anemia dangerous?

Anemia is more related to a female disease, since in men it manifests itself only in 10 cases out of 100. Based on statistics, every fourth inhabitant of the globe suffers from anemia. This is especially true for pregnant women.

At the same time, the body starts compensatory functions, which enhances the work of the heart and circulatory system. Frequent contractions of the heart muscle lead to tissue wear, which causes heart failure. Against the background of a weakened body, the patient becomes overly irritable, an imbalance of the psycho-emotional background is detected, and pathologies of a neurological nature develop. In addition, concentration of attention, memory are disturbed, smell and taste change, the structure of the skin and all mucous membranes is deformed.

Possible Complications:

• decreased immunity and, as a result, frequent morbidity;
• heart palpitations lead to strong loads, as a result of which diseases of the cardiovascular system develop;
• during pregnancy there is a risk of miscarriage, and the fetus stops developing;
• growth and mental development stops in childhood;
• pathologies of the gastrointestinal tract, visual apparatus, and respiratory system develop;
• hypoxic coma occurs, which is dangerous for death. More details about anemic coma - this is one of the types of hypoxic coma.

Consequences of anemia 3 degrees

• cardiogenic shock;
• acute renal failure;
• blood loss;
• heart failure and subsequent stroke, heart attack and so on.

With advanced 3rd degree of anemia, there is a high percentage of the risk of death, so it is important to contact the clinic for an examination and detection of pathology at the slightest suspicion of anemia.

The consequences of anemia for women

• Violation of digestion and damage to the mucous organs of the gastrointestinal tract.
• Deterioration of the excretory and detoxifying properties of the renal system and liver.
• Pathological changes in the central nervous system, heart, blood vessels.
• The reproductive system of a woman and the genitourinary system are affected against the background of frequent infection.
• The condition of the hair follicles, the nail plate worsens.
• The structure of the mucous membranes and teeth changes.
• Skin diseases appear.

Causes of anemia

1. Genetic abnormalities:

• violations of the production of erythrocytes of congenital form;
• abnormal structure of cells (erythrocytes);
• spherocytosis;
• Bassen-Kronzweig syndrome;
• enzymatic abnormalities.

• frequent strict diets;
• lack of a balanced diet, which leads to a deficiency of vitamin C, B, trace elements (iron, folic acid, etc.).

• pathology of the renal and cardiovascular systems;
• liver disease;
• disorders in the autoimmune apparatus;
• benign and malignant neoplasms.

• hepatitis virus;
• malaria pathogens;
• cytomegalovirus;
• toxoplasmosis;
• obstructive bronchitis;
• tuberculosis bacillus.

Another important factor leading to the development of anemia is intoxication of the body (through pesticides and medications) and injury (burns, frostbite, fractures).

General symptoms of anemia for any age and gender:

• pallor of the skin and lips, further cyanosis;
• weakness and fatigue;
• shortness of breath with little physical activity;
• cramps and numbness in the limbs;
• fragility and delamination of nails, hair loss;
• plaque and cracks in the corners of the lips;
• trembling of the limbs and a change in taste, smell;
• pain in the digestive tract;
• dryness and cracking of the skin (in particular on the shins and hands).

• dizziness, fainting, loss of consciousness;
• sensations of tinnitus, headache and insomnia;
• violation or cessation of the menstrual cycle in women;
• weakening of potency in men;
• aversion to food, as a result of which anorexia develops;
• increased angina pectoris, dementia.

• loss of interest in learning, as concentration decreases and memory deteriorates;
• lethargy in games;
• increased bleeding in the gums;
• lagging behind in physical and mental development;
• disproportionate appearance.

Anemia in newborns and adolescents

For childhood and adolescence, oppression of the heart and vascular system is characteristic, which is manifested by irregular breathing, rapid heartbeat, and changes in blood pressure. Metabolism is disturbed in all tissues and cells, the child suffers from jaundice and frequent catarrhal pathologies.

Learn about the features of anemia in childhood from this video in Dr. Komarovsky's program.

Anemia in pregnancy

Feature - with a mild form of anemia, only the mother's body suffers, since all the nutrients in the required amount are supplied to the child.

During pregnancy, the following unpleasant consequences can join:

• varicose veins and thrombosis;
• the threat of miscarriage and bleeding;
• harm to the unborn child: anemia, mental and physical underdevelopment, lack of immunity, frequent morbidity after birth.

Anemia (grch.αναιμία-anemia) is a clinical and hematological syndrome, which is characterized by a decrease in the concentration of hemoglobin in the blood, with a decrease in the number of red blood cells.

Anemia: causes and development factors

The main causes of anemia include:

• The nature of nutrition. With insufficient intake of iron-containing foods, iron deficiency anemia can develop, this is more common in populations where there is already a high level of nutritional anemia. Anemia can be caused by a diet deficient in iron, vitamin B12, folic acid, or vitamin C.
• Violation of the production of red blood cells in the bone marrow. As a rule, in this case, anemia develops, which is accompanied by kidney disease, protein depletion, endocrine insufficiency, chronic infections and oncological diseases.
• Hemolysis. This is the destruction or shortening of the life span of red blood cells. Normally, erythrocytes live for 4 months, however, with some pathological processes, their lifespan can be significantly reduced. The main cause of hemolysis is a violation of the functions of red blood cells or their defect. In some cases, the cause of hemolysis is the pathology of the spleen.
• Violation of the gastrointestinal tract (with violations of the absorption process). Since the absorption of iron occurs in the stomach and upper small intestine, if the absorption process is disturbed, the mucous membrane of the digestive tract develops anemia.
• Chronic blood loss(gastrointestinal bleeding, nosebleeds, hemoptysis, hematuria, uterine bleeding). Belongs to one of the most important causes of iron deficiency.

There are also degrees of anemia, depending on the level of hemoglobin in the blood:

• mild degree (hemoglobin level is above 90 g/l);
• medium degree (hemoglobin level within 90-70 g/l);
• severe (hemoglobin level is less than 70 g / l).

Symptoms of anemia: how the disease manifests itself

Symptoms of anemia vary depending on the type of anemia. Common symptoms of anemia include:

• weakness, a significant decrease in performance;
• increased fatigue, irritability, drowsiness for no apparent reason;
• headaches, tinnitus, flashing "flies" before the eyes, dizziness;
• dysuric disorders;
• geophagy (irresistible desire to eat chalk or lime);
• trophic disorders of hair, skin, nails;
• pain in the region of the heart of the type of angina pectoris;
• fainting, tinnitus;
• muscle weakness, body aches.

In elderly patients with coronary heart disease, with anemia, there is an increase in angina attacks, even after a little physical exertion.

Specific symptoms of different types of anemia:

• Iron-deficiency anemia. For iron deficiency anemia, a characteristic parorexia (desire to use ice, paper, earth). Also, patients have concave nails (koilonychia), inflammation of the tongue and cracks in the corners of the mouth.
• B12 deficiency anemia. This form of anemia is often manifested by tingling in the limbs (arms and legs), a staggering gait, stiffness in movement, a low sense of touch, impaired thinking, and occasional hallucinations. In severe cases, paranoia and even schizophrenic disorders may develop.
• Anemia caused by lead poisoning. In this case, the patient has dark blue lines on the gums, severe abdominal pain and nausea.
• Chronic destruction of red blood cells. This condition is characterized by emerging jaundice, redness of urine, ulcers on the legs. Children suffering from chronic destruction of red blood cells are late in development. Often, pathology is accompanied by the formation of stones in the gallbladder.
• Sickle cell anemia. This form of anemia is usually accompanied by weakness, paroxysmal pain in the joints and abdominal cavity.

Patient response to anemia

Patients with anemia should include more green vegetables, lettuce, herbs, grains in their diet to get enough iron and folic acid. It is important not to drink caffeinated beverages, especially with meals, as caffeine interferes with iron absorption.

If anemia is suspected, an urgent need to consult a doctor, as anemia can reduce the immune functions of the body, provoke a breakdown, and significantly reduce performance.

Diagnosis of anemia

Methods for diagnosing anemia:

• examination by a doctor with anamnesis;
• laboratory diagnostics. Carrying out a general clinical blood test with the obligatory determination of: the number of erythrocytes, the number of reticulocytes, hemoglobin, hematocrit, the average volume of erythrocytes (MCV), the width of the distribution of erythrocytes by volume (RDW), the average content of hemoglobin in an erythrocyte (MCH), the average concentration of hemoglobin in an erythrocyte ( MCHC), leukocyte count, platelet count.

The tactics of treatment is determined depending on the type of anemia and the reasons that caused it.

For pregnant women, in order to prevent and treat anemia, the doctor prescribes iron supplements and folic acid.

Complications of anemia

In rare cases, iron deficiency anemia can lead to complications in the form of hypoxic coma, which can lead to death in the case of a chronic course of the disease without treatment or with acute blood loss.

Prevention of anemia

In order to prevent the development of anemia, iron-rich foods (whole grain bread, beans, green vegetables, lettuce, herbs, red lean meat) should be included in the diet.

It is also necessary to avoid prolonged contact with toxic substances, chemical agents, oil products, etc.

Anemia is the general name for a specific group of hematological syndromes that are associated with a significant decrease in the level of hemoglobin and red blood cells, when the body absorbs iron poorly or does not absorb at all. Most often, the pathology develops in the female body due to the structural features of the genital organs, which involves monthly menstrual bleeding, and due to frequent diets and dietary restrictions. Anemia in women requires mandatory treatment, since with anemia, intractable oncology can develop.

Among the main causes of the disease are the following factors:

• the presence in the body of abnormal uterine bleeding, a long menstrual cycle that can last up to 10 days, which is already bleeding;
• problems with the work of the gastrointestinal tract, which interferes with the normal absorption and breakdown of iron from products: chronic gastritis in a form in which the amount of hydrochloric acid is significantly reduced, peptic ulcer, including after surgery, resection of the gastrointestinal tract;
• a severely restricted diet, which is associated with a lack of dairy, protein and vegetable products with high or medium iron content.
• in girls: lack of iron at birth and rapid growth of the child, unbalanced nutrition, increased, exceeding the physiological norm, loss of the element during microbleeding in the intestine, due to the early introduction of kefir and whole cow's milk

Attention! To date, the main cause of an insufficient amount of iron in the body, which causes anemia, is abnormal uterine bleeding and gastrointestinal diseases.

You can recognize this condition by the following symptoms:

Attention! The danger of the pathology lies in the fact that it may not manifest itself as acute symptoms that will clearly indicate the serious condition of the woman. Most of the signs are relatively hidden and can be explained by other conditions.

Diet for anemia in women

First of all, if you have a low level of hemoglobin, you should immediately establish nutrition. The principle of diet in the treatment of anemia is similar to proper nutrition. Be sure to eat at least five times a day, of which three are basic, and two are snacks.

For breakfast during the period of active treatment, it is advisable to eat an omelette with beef, cocoa, whole grain bread. Any cereal will do. These products can start the digestion process, do not overstrain the gastrointestinal tract, and are excellent for exacerbation of gastritis, ulcers and other problems with the stomach and intestines. For lunch, it is useful to eat light meat or chicken soup, green vegetable salad. Dinner should consist of dairy products.

It is not necessary to include exclusively iron-containing foods in every meal, but it is worth doing it once a day. Snacks can consist of fermented milk products, nuts, vegetable salad. Such a diet will allow you to notice the first results within a week, your general condition will significantly improve and your working capacity will increase.

The table below shows the foods that contain the highest amount of iron.

Attention! Since some foods with a high iron content have the status of allergenic, the possibility of an allergic reaction should first be excluded. If necessary, allergy tests can be done as part of a complete examination to identify the cause of anemia.

Video - Anemia

Drugs for anemia with iron

You can supplement proper nutrition with a number of vitamin complexes and iron-containing preparations. They are suitable for treatment in childhood and during pregnancy. But still, it is worth going through a preliminary consultation with a doctor in order to choose a more accurate dose, taking into account the current condition, if necessary.

Tardyferon

The drug is available in the form of tablets that can be taken from the age of six. Patients at the classical dosage are recommended to take 1 tablet, regardless of the meal, drinking Tardiferon with clean water. An intensive course of treatment lasts one month, after which you should still drink the medication for 4-8 weeks. In additional time, the patient should take tablets every other day. The average cost of Tardiferon is 300 rubles.

Sorbifer Durules

For anemia, the drug should be taken in the amount of 3-4 tablets per day at regular intervals. After the active phase of treatment, the doctor may recommend taking Sorbifer Durules one tablet per day for a few more weeks as a so-called depot formation. The exact course of use of the drug should be clarified with your doctor. Before use, make sure that there is no vitamin B12 deficiency. The average cost of Sorbifer Durules is 500 rubles.

gestalis

Gestalis is a complete vitamin complex of minerals with a large amount of iron

A complete vitamin complex of minerals with a large amount of iron. It is produced as a medicine for pregnant women, but can be used at any time in life. To get a real result from Gestalis therapy, one capsule per day is taken. The duration of therapy is 4 weeks. The average cost of a vitamin complex is 1000 rubles.

Attention! With the ineffectiveness of drug therapy and diet, a blood transfusion or erythrocyte mass is used.

Anemia during pregnancy and its dangers

During pregnancy, a woman experiences the same symptoms of anemia as at other times in her life. But when carrying a baby, this condition is extremely dangerous, as it can provoke serious pathologies. Most often, the problem appears from 14-20 weeks, when the body begins to experience a solid load on all systems.

With a strong drop in the level of hemoglobin, a woman develops gastritis, which can go into the atrophic stage, during childbirth, contractions may be insignificant or completely absent. Also in this condition, there is a high risk of bleeding and large blood loss, which sometimes requires a transfusion procedure.

For the fetus, a low level of hemoglobin in the mother is fraught with developmental delay and fading. Also, with severe anemia, placental abruption can occur, sometimes a miscarriage occurs.

A woman during this period should also be alert if she has the following symptoms:

• body weight will begin to decrease with normal nutrition;
• there will always be a desire to eat clay, chalk and other substances;
• white spots appear on the nails;
• there is a problem with breathing even at rest;
• the chair will become light in color;
• eye sclera may become very yellow;
• the nail plate will exfoliate and crumble;
• bleeding gums will appear;
• the tongue will become "varnished", the so-called condition in which the mucous membrane becomes smooth and as if painted in a colorless varnish.

All this indicates a rather serious drop in hemoglobin levels, which requires immediate consultation with a gynecologist and therapist.

Attention! It is mandatory to follow the diet and other preventive measures for the occurrence of anemia when carrying a child in order to prevent serious pathologies during pregnancy.

To prevent possible problems, doctors recommend undergoing an annual medical examination, but ideally, it is advisable to take a complete blood count twice a year to monitor the level of hemoglobin. It is desirable for women to do this in the middle of the cycle, when the body has managed to recover from menstruation. If even minor deviations appear, you should immediately establish nutrition and, if necessary, seek medical help.

Anemia is a clinical and hematological syndrome characterized by a decrease in hemoglobin content per unit volume of blood, more often with a simultaneous decrease in the number of red blood cells, which leads to the development of oxygen starvation of tissues.

Anemia classification

Pathogenetic classification of anemia:

I. Anemia due to blood loss (posthemorrhagic).

2. Chronic

II. Anemia due to impaired formation of red blood cells and hemoglobin.

1. Iron deficiency anemia.

2. Megaloblastic anemia associated with impaired DNA synthesis. (B 12 - and folate deficiency anemia)

3. Anemia associated with bone marrow failure (hypoplastic).

Sh. Anemia due to increased blood destruction (hemolytic).

IV. Mixed anemia.

Classification of anemia by color index:

I. Hypochromic anemia, color. indicator below 0.8.

Iron-deficiency anemia;

Thyroid anemia (with hypofunction of the thyroid gland).

II. Anemia normochromic, tsv. indicator 0.85-1.05:

Anemia in chronic renal failure;

Hypoplastic (aplastic) anemia;

Drug and radiation cytostatic disease;

Anemia in malignant neoplasms and hemoblastoses;

Anemia in systemic connective tissue diseases;

Anemia in chronic active hepatitis and liver cirrhosis;

Hemolytic anemia (except thalassemias);

Acute pothemorrhagic anemia.

III. Anemia hyperchromic, tsv. score above 1.05:

B 12 - deficiency anemia.

Folate deficiency anemia.

ANEMIA DUE TO EDUCATIONAL DISORDERS

erythrocytes and hemoglobin

IRON-DEFICIENCY ANEMIA

Iron deficiency anemia is an anemia caused by iron deficiency in the blood serum, bone marrow and depot. People suffering from latent iron deficiency and iron deficiency anemia make up 15-20% of the world's population. Most often, iron deficiency anemia occurs among children, adolescents, women of childbearing age, and the elderly. It is generally accepted to distinguish two forms of iron deficiency states: latent iron deficiency and iron deficiency anemia. Latent iron deficiency is characterized by a decrease in the amount of iron in its depot and a decrease in the level of transport iron in the blood with normal levels of hemoglobin and erythrocytes.

Basic information about iron metabolism

Iron in the human body is involved in the regulation of metabolism, in the processes of oxygen transfer, in tissue respiration and has a huge impact on the state of immunological resistance. Almost all iron in the human body is part of various proteins and enzymes. Two main forms can be distinguished: heme (part of the heme - hemoglobin, myoglobin) and non-heme. Heme iron in meat products is absorbed without the participation of hydrochloric acid. However, achilia can to some extent contribute to the development of iron deficiency anemia in the presence of significant losses of iron from the body and a high need for iron. Iron absorption is carried out mainly in the duodenum and upper jejunum. The degree of absorption of iron depends on the body's need for it. With severe iron deficiency, its absorption can occur in other parts of the small intestine. With a decrease in the body's need for iron, the rate of its entry into the blood plasma decreases and deposition in enterocytes in the form of ferritin increases, which is eliminated during physiological desquamation of intestinal epithelial cells. In the blood, iron circulates in combination with plasma transferrin. This protein is synthesized mainly in the liver. Transferrin captures iron from enterocytes, as well as from depots in the liver and spleen, and transfers it to receptors on bone marrow erythrocytes. Normally, transferrin is approximately 30% saturated with iron. The transferrin-iron complex interacts with specific receptors on the membrane of erythrokaryocytes and bone marrow reticulocytes, after which it penetrates into them by endocytosis; iron is transferred to their mitochondria, where it is incorporated into protoporphyrin and thus participates in the formation of heme. Freed from iron, transferrin is repeatedly involved in the transfer of iron. The cost of iron for erythropoiesis is 25 mg per day, which greatly exceeds the capacity of iron absorption in the intestine. In this regard, iron is constantly used for hematopoiesis, which is released during the breakdown of red blood cells in the spleen. Storage (deposition) of iron is carried out in the depot - in the composition of ferritin and hemosiderin proteins.

The most common form of iron deposition in the body is ferritin. It is a water-soluble glycoprotein complex consisting of a centrally located iron coated with a protein coat of apoferritin. Each ferritin molecule contains from 1000 to 3000 iron atoms. Ferritin is determined in almost all organs and tissues, but its largest amount is found in macrophages of the liver, spleen, bone marrow, erythrocytes, in blood serum, in the mucous membrane of the small intestine. With a normal balance of iron in the body, a peculiar balance is established between the content of ferritin in plasma and depot (primarily in the liver and spleen). The level of ferritin in the blood reflects the amount of deposited iron. Ferritin creates reserves of iron in the body, which can be quickly mobilized with an increase in tissue demand for iron. Another form of iron deposition is hemosiderin, a poorly soluble ferritin derivative with a higher iron concentration, consisting of aggregates of iron crystals that do not have an apoferritin shell. Hemosiderin accumulates in macrophages of the bone marrow, spleen, and Kupffer cells of the liver.

Physiological iron loss

The loss of iron from the body of men and women occurs in the following ways:

• with feces (iron not absorbed from food; iron excreted in bile; iron in the composition of the desquamating intestinal epithelium; iron in erythrocytes in feces);
• with exfoliating skin epithelium;
• with urine.

In these ways, about 1 mg of iron is released per day. In addition, in women of the childbearing period, additional iron losses occur due to menstruation, pregnancy, childbirth, and lactation.

Etiology

Chronic blood loss

Chronic blood loss is one of the most common causes of iron deficiency anemia. The most characteristic are not abundant, but prolonged blood loss, which is invisible to patients, but gradually reduces iron stores and leads to the development of anemia.

The main sources of chronic blood loss

Uterine blood loss is the most common cause of iron deficiency anemia in women. In patients of reproductive age, most often we are talking about prolonged and profuse blood loss during menstruation. Menstrual blood loss of 30-60 ml (15-30 mg of iron) is considered normal. With a full nutrition of a woman (with the inclusion of meat, fish and other iron-containing products), a maximum of 2 mg can be absorbed from the intestines daily, and 60 mg of iron per month and, therefore, with normal menstrual blood loss, anemia does not develop. With a larger amount of monthly menstrual blood loss, anemia will develop.

Chronic bleeding from the gastrointestinal tract is the most common cause of iron deficiency anemia in men and non-menopausal women. Sources of gastrointestinal bleeding can be erosions and ulcers of the stomach and duodenum, stomach cancer, gastric polyposis, erosive esophagitis, diaphragmatic hernia, gingival bleeding, cancer of the esophagus, varicose veins of the esophagus and cardia of the stomach (with cirrhosis of the liver and other forms portal hypertension), bowel cancer; diverticular disease of the gastrointestinal tract, colon polyps, bleeding hemorrhoids.

In addition, iron can be lost with nosebleeds, with blood loss as a result of lung diseases (with pulmonary tuberculosis, bronchiectasis, lung cancer).

Iatrogenic blood loss- this is blood loss due to medical manipulations. These are rare causes of iron deficiency anemia. These include frequent bleeding in patients with polycythemia, blood loss during hemodialysis procedures in patients with chronic renal failure, as well as donation (leads to the development of latent iron deficiency in 12% of men and 40% of women, and with many years of experience provokes the development of iron deficiency anemia) .

Increased need for iron

An increased need for iron can also lead to the development of iron deficiency anemia.

Pregnancy, childbirth and lactation - during these periods of a woman's life, a significant amount of iron is consumed. Pregnancy - 500 mg of iron (300 mg for the child, 200 mg for the placenta). In childbirth, 50-100 mg of Fe is lost. During lactation, 400 - 700 mg of Fe is lost. It takes at least 2.5-3 years to restore iron reserves. Consequently, women with birth intervals of less than 2.5-3 years easily develop iron deficiency anemia.

The period of puberty and growth is often accompanied by the development of iron deficiency anemia. The development of iron deficiency anemia is due to an increase in the need for iron due to the intensive growth of organs and tissues. In girls, factors such as the appearance of blood loss due to menstruation and poor nutrition due to the desire to lose weight also play a role.

An increased need for iron in patients with B 12 deficiency anemia can be observed during treatment with vitamin B 12, which is explained by the intensification of normoblastic hematopoiesis and the use of large amounts of iron for these purposes.

Intensive sports in some cases can contribute to the development of iron deficiency anemia, especially if there was a hidden iron deficiency previously. The development of anemia during intense sports activities is due to an increase in the need for iron during high physical exertion, an increase in muscle mass (and, consequently, the use of more iron for myoglobin synthesis).

Insufficient intake of iron from food

Alimentary iron deficiency anemia, caused by insufficient intake of iron from food, develops in strict vegetarians, in people with a low socio-economic standard of living, in patients with mental anorexia.

Iron malabsorption

The main reasons leading to impaired absorption of iron in the intestine and the development of iron deficiency anemia as a result are: chronic enteritis and enteropathy with the development of malabsorption syndrome; resection of the small intestine; resection of the stomach according to the Billroth II method (“end to side”), when part of the duodenum is turned off. At the same time, iron deficiency anemia is often combined with B 12 - (folic) deficiency anemia due to malabsorption of vitamin B 12 and folic acid.

Iron transport disorders

Iron deficiency anemia, caused by a decrease in the content of transferrin in the blood and, consequently, a violation of iron transport, is observed with congenital hypo- and atransferinemia, hypoproteinemias of various origins, and the appearance of antibodies to transferrin.

Pathogenesis

All clinical manifestations of iron deficiency anemia are based on iron deficiency, which develops when iron losses exceed its intake with food (2 mg / day). Initially, iron stores in the liver, spleen, and bone marrow decrease, which is reflected in a decrease in the level of ferritin in the blood. At this stage, there is a compensatory increase in iron absorption in the intestine and an increase in the level of mucosal and plasma transferrin. The content of serum iron is not yet reduced, there is no anemia. However, in the future, depleted iron depots are no longer able to provide the erythropoietic function of the bone marrow and, despite the continuing high level of transferrin in the blood, the iron content in the blood (transport iron), hemoglobin synthesis, develop anemia and subsequent tissue damage.

With iron deficiency, the activity of iron-containing and iron-dependent enzymes in various organs and tissues decreases, and the formation of myoglobin also decreases. As a result of these disorders and a decrease in the activity of tissue respiration enzymes (cytochrome oxidases), dystrophic lesions of epithelial tissues (skin, its appendages, mucous membrane, gastrointestinal tract, often urinary tract) and muscles (myocardium and skeletal muscles) are observed.

A decrease in the activity of some iron-containing enzymes in leukocytes disrupts their phagocytic and bactericidal functions and inhibits protective immune responses.

Classification of iron deficiency anemia

Stage

Stage 1 - iron deficiency without anemia clinic (latent anemia)

Stage 2 - iron deficiency anemia with a detailed clinical and laboratory picture

Severity

1. Light (Hb content 90-120 g/l)

2. Medium (Hb content 70-90 g/l)

3. Heavy (Hb content below 70 g/l)

Clinical picture

Clinical manifestations of iron deficiency anemia can be grouped into two major syndromes - anemic and sideropenic.

Anemia syndrome

Anemia syndrome is caused by a decrease in hemoglobin content and the number of erythrocytes, insufficient provision of tissues with oxygen and is represented by nonspecific symptoms. Patients complain of general weakness, increased fatigue, decreased performance, dizziness, tinnitus, flies before the eyes, palpitations, shortness of breath during physical exertion, the appearance of fainting. There may be a decrease in mental performance, memory, drowsiness. Subjective manifestations of anemic syndrome first disturb patients during exercise, and then at rest (as anemia grows).

An objective examination reveals pallor of the skin and visible mucous membranes. Often, some pastosity is found in the area of ​​\u200b\u200bthe legs, feet, face. Typical morning swelling - "bags" around the eyes.

Anemia causes the development of myocardial dystrophy syndrome, which is manifested by shortness of breath, tachycardia, often arrhythmia, moderate expansion of the borders of the heart to the left, deafness of heart sounds, low systolic murmur at all auscultatory points. In severe and prolonged anemia, myocardial dystrophy can lead to severe circulatory failure. Iron deficiency anemia develops gradually, so the patient's body gradually adapts and subjective manifestations of anemic syndrome are not always pronounced.

sideropenic syndrome

Sideropenic syndrome (hyposiderosis syndrome) is caused by tissue iron deficiency, which leads to a decrease in the activity of many enzymes (cytochrome oxidase, peroxidase, succinate dehydrogenase, etc.). Sideropenic syndrome is manifested by numerous symptoms:

• taste perversion (pica chlorotica) - an irresistible desire to eat something unusual and inedible (chalk, tooth powder, coal, clay, sand, ice), as well as raw dough, minced meat, cereals; this symptom is more common in children and adolescents, but quite often in adult women;
• addiction to spicy, salty, sour, spicy foods;
• perversion of smell - addiction to smells that most people around perceive as unpleasant (gasoline, acetone, the smell of varnishes, paints, shoe polish, etc.);
• severe muscle weakness and fatigue, muscle atrophy and a decrease in muscle strength due to a deficiency of myoglobin and tissue respiration enzymes;
• dystrophic changes in the skin and its appendages (dryness, peeling, a tendency to quickly form cracks on the skin; dullness, brittleness, loss, early graying of hair; thinning, brittleness, transverse striation, dullness of nails; symptom of koilonychia - spoon-shaped concavity of nails);
  • angular stomatitis - cracks, "jamming" in the corners of the mouth (occur in 10-15% of patients);
  • glossitis (in 10% of patients) - characterized by a feeling of pain and fullness in the region of the tongue, reddening of its tip, and further atrophy of the papillae ("varnished" tongue); often there is a tendency to periodontal disease and caries;
  • atrophic changes in the mucous membrane of the gastrointestinal tract - this is manifested by dryness of the mucous membrane of the esophagus and difficulty, and sometimes pain when swallowing food, especially dry (sideropenic dysphagia); development of atrophic gastritis and enteritis;
  • the symptom of "blue sclera" is characterized by a bluish color or a pronounced blueness of the sclera. This is due to the fact that with iron deficiency, collagen synthesis in the sclera is disrupted, it becomes thinner and the choroid of the eye shines through it.
  • imperative urge to urinate, the inability to hold urine when laughing, coughing, sneezing, perhaps even bedwetting, which is due to the weakness of the sphincters of the bladder;
  • "Sideropenic subfebrile condition" - characterized by a prolonged increase in temperature to subfebrile values;
  • a pronounced predisposition to acute respiratory viral and other infectious and inflammatory processes, chronic infections, which is due to a violation of the phagocytic function of leukocytes and a weakening of the immune system;
  • reduction of reparative processes in the skin, mucous membranes.

Laboratory data

Diagnosis of latent iron deficiency

Latent iron deficiency is diagnosed on the basis of the following signs:

• anemia is absent, hemoglobin content is normal;
• there are clinical signs of sideropenic syndrome due to a decrease in the tissue fund of iron;
• serum iron is reduced, which reflects a decrease in the transport fund of iron;
• the total iron-binding capacity of blood serum (OZHSS) is increased. This indicator reflects the degree of "starvation" of blood serum and iron saturation of transferrin.

With iron deficiency, the percentage of saturation of transferrin with iron is reduced.

Diagnosis of iron deficiency anemia

With a decrease in the hemoglobin fund of iron, changes characteristic of iron deficiency anemia appear in the general blood test:

• decrease in hemoglobin and erythrocytes in the blood;
• decrease in the average content of hemoglobin in erythrocytes;
• decrease in color index (iron deficiency anemia is hypochromic);
• hypochromia of erythrocytes, characterized by their pale staining and the appearance of enlightenment in the center;
• predominance in the smear of peripheral blood among erythrocytes of microcytes - erythrocytes of reduced diameter;
• anisocytosis - unequal size and poikilocytosis - a different form of red blood cells;
• normal content of reticulocytes in the peripheral blood, however, after treatment with iron preparations, an increase in the number of reticulocytes is possible;
  • tendency to leukopenia; the platelet count is usually normal;
  • with severe anemia, a moderate increase in ESR (up to 20-25 mm / h) is possible.

Biochemical analysis of blood - a decrease in the level of serum iron and ferritin is characteristic. There may also be changes due to the underlying disease.

Treatment of iron deficiencyanemia

The treatment program includes:

1. Elimination of etiological factors.
2. Medical nutrition.
3. Treatment with iron-containing drugs.

3.1. Elimination of iron deficiency and anemia.

3.2. Replenishment of iron stores (satiation therapy).

3.3. anti-relapse therapy.

4. Prevention of iron deficiency anemia.

4.1. Primary.

4.2. Secondary.

1. Elimination of etiological factors

The elimination of iron deficiency and, therefore, the cure of iron deficiency anemia is possible only after the elimination of the cause leading to a permanent iron deficiency.

2. Medical nutrition

With iron deficiency anemia, the patient is shown a diet rich in iron. The maximum amount of iron that can be absorbed from food in the gastrointestinal tract is 2 g per day. Iron from animal products is absorbed in the intestines in greater quantities than from plant products. Divalent iron, which is part of the heme, is best absorbed. Meat iron is absorbed better, and liver iron is worse, since iron in the liver is found mainly in the form of ferritin, hemosiderin, and also in the form of heme. Small amounts of iron are absorbed from eggs and fruits. Iron is best absorbed from veal (22%), fish (11%). From eggs, beans, fruits, only 3% of iron is absorbed.

For normal hematopoiesis, it is necessary to receive with food, in addition to iron, also other microelements. The diet of a patient with iron deficiency anemia should include 130 g of proteins, 90 g of fat, 350 g of carbohydrates, 40 mg of iron, 5 mg of copper, 7 mg of manganese, 30 mg of zinc, 5 mcg of cobalt, 2 g of methionine, 4 g of choline, B vitamins and FROM.

With iron deficiency anemia, a phyto-collection can also be recommended, including leaves of nettle, string, strawberry, black currant. At the same time, it is recommended to take a decoction or infusion of rose hips, 1 cup per day. Rosehip infusion contains iron and vitamin C.

3. Treatment with iron-containing drugs

3.1. Elimination of iron deficiency

The intake of iron with food can only compensate for its normal daily loss. The use of iron preparations is a pathogenetic method for the treatment of iron deficiency anemia. Currently, preparations containing ferrous iron (Fe ++) are used, since it is much better absorbed in the intestine. Iron supplements are usually taken orally. To ensure a progressive increase in hemoglobin levels, it is necessary to take daily such an amount of iron-containing preparations that it corresponds to a daily dose of ferrous iron from 100 mg (minimum dose) to 300 mg (maximum dose). The choice of a daily dose in the indicated doses is determined mainly by the individual tolerance of iron preparations and the severity of iron deficiency. It is useless to prescribe more than 300 mg of ferrous iron per day, since the volume of its absorption does not increase.

Ferrous preparations are prescribed 1 hour before a meal or not earlier than 2 hours after a meal. For better absorption of iron, ascorbic or succinic acid is simultaneously taken, absorption also increases in the presence of fructose.

Ferro-foil gamma (iron sulfate complex 100 mg + ascorbic acid 100 mg + folic acid 5 mg + cyanocobalamin 10 mg). Take 1-2 caps 3 times a day after meals.

Ferroplex - a complex of iron sulfate and ascorbic acid, is prescribed 2-3 tablets 3 times a day.

Hemofer prolongatum is a long-acting drug (iron sulfate 325 mg), 1-2 tablets per day.

Treatment with iron-containing drugs is carried out at the maximum tolerated dose until the hemoglobin content is completely normalized, which occurs after 6-8 weeks. Clinical signs of improvement appear much earlier (after 2-3 days) compared to the normalization of hemoglobin levels. This is due to the entry of iron into enzymes, the deficiency of which causes muscle weakness. The content of hemoglobin begins to increase at the 2-3rd week from the start of treatment. Iron supplements are usually taken orally. In case of violation of the absorption of iron from the gastrointestinal tract, drugs are prescribed parenterally.

3.2. Replenishment of iron stores (satiation therapy)

Iron stores (iron depot) in the body are represented by iron of ferritin and hemosiderin of the liver and spleen. To replenish iron reserves, after reaching a normal level of hemoglobin, treatment with iron-containing drugs is carried out for 3 months at a daily dose that is 2-3 times less than the dose used at the stage of anemia relief.

3.3. Anti-relapse (maintenance) therapy

With continued bleeding (for example, heavy menstruation), iron preparations are indicated in short courses of 7-10 days monthly. With recurrence of anemia, a repeated course of treatment is indicated for 1-2 months.

4. Prevention of iron deficiency anemia

Persons with previously cured iron deficiency anemia in the presence of conditions that threaten the development of recurrence of iron deficiency anemia (heavy menstruation, uterine fibromyoma, etc.) are prevented from anemia. A prophylactic course lasting 6 weeks (daily dose of iron 40 mg) is recommended, then two 6-week courses per year or 30-40 mg of iron daily for 7-10 days after menstruation are carried out. In addition, it is necessary to consume at least 100 grams of meat daily.

MEGALOBLASTIC ANEMIA

Megaloblastic anemia is a group of anemias caused by a violation of DNA synthesis in erythrokaryocytes due to a deficiency of vitamin B 12 and / or folic acid and characterized by a megaloblastic type of hematopoiesis.

B 12 deficiency anemia

Basic information about vitamin metabolismAT 12

Vitamin B 12 enters the human body with food. It is found in meat, liver, kidneys, egg yolk, cheese, milk, caviar. In food, vitamin B 12 is associated with protein. During cooking, as well as in the stomach, under the action of hydrochloric acid and proteolytic enzymes, vitamin B 12 is released from food. Further in the stomach, vitamin B 12 (Castle's external factor) combines with R proteins (Rapid-binders). Then the complex “vitamin B 12 + protein “R”” enters the duodenum, where, under the influence of proteolytic enzymes of pancreatic juice, the protein “R” is cleaved off and the released B 12 combines with gastromucoprotein (Castle’s internal factor), which came here from the stomach. Gastromucoprotein is produced by parietal cells in the fundic part and in the area of ​​the body of the stomach. The alkaline environment of the contents of the duodenum enhances the relationship between vitamin B12 and gastromucoprotein. Gastromucoprotein protects vitamin B 12 from the effects of proteolytic enzymes. Further, the “vitamin B 12 + gastromucoprotein” complex moves along the small intestine and enters the ileum, where in the presence of Ca 2+ ions it interacts with specific receptors, after which it is cleaved, and vitamin B 12 enters the mitochondria of mucosal cells. From here, vitamin B 12 penetrates into the blood, where it combines with transport proteins - transcobalamins and is delivered to the liver and bone marrow. In these organs, vitamin B 12 is released from the vitamin B 12 + transcobalamin complex. Part of the complex is eliminated with bile. In the bone marrow, vitamin B 12 is used for hematopoiesis, in the liver it is deposited and then enters the blood if necessary. Part of vitamin B 12 from the liver in the composition of bile again enters the duodenum 12 and is subsequently absorbed according to the mechanism described above.

With good nutrition, the daily diet of a person contains up to 30 μg of vitamin B 12. The daily requirement for it is 2-7 mcg. About 6-9 μg of vitamin B 12 is absorbed in the intestine per day. The body of a healthy person contains about 2-5 mg of vitamin B 12. The main organ that contains the largest amount of cobalamin is the liver. Stocks of vitamin B 12 in the liver are enough for 3-5 years after the cessation of its absorption.

Vitamin B 12 performs its biological role in the form of two coenzymes - methylcobalamin and deoxyadenosylcobalamin. The transformation of free vitamin B 12 into B 12 coenzymes proceeds in several stages with the participation of specific enzymes. With the help of these coenzymes, vitamin B 12 carries out two important reactions.

The first reaction proceeds with the participation of the coenzyme methylcobalamin and ensures the maturation, development and reproduction of the cells of the hematopoietic system, primarily the red hematopoietic germ and the epithelium of the gastrointestinal tract.

The second reaction - the breakdown and synthesis of fatty acids proceeds with the participation of the coenzyme deoxyadenosylcobalamin and ensures the conversion of the metabolic product of fatty acids methylmalonic acid into succinic acid. The normal course of this reaction ensures optimal myelin metabolism in the nervous system and requires the presence of the active form of folic acid.

Etiology

The main reasons for the development of B 12 deficiency anemia:

I. Violation of secretion by the stomach of the "intrinsic factor" - gastromucoprotein occur in atrophic autoimmune gastritis with the production of antibodies to parietal cells and gastromucoprotein, total gastrectomy (less often subtotal resection of the stomach), cancer and gastric polyposis, and the toxic effect of high doses of alcohol on the gastric mucosa.

II. Malabsorption of vitamin B 12 in the small intestine in patients with resection of the ileum (more than 60 cm), with malabsorption syndrome of various origins (enzymatic enteropathy, celiac disease, tropical sprue, enteritis, Crohn's disease, intestinal amyloidosis), and small intestine lymphoma. The absorption of B12 is slowed down in patients with chronic pancreatitis with impaired trypsin secretion. Reduce the absorption of vitamin B 12 a number of drugs (colchicine, neomycin, biguanides, cimetidine, etc.).

III. Competitive consumption of vitamin B 12 occurs when infested with worms (wide tapeworm, whipworm, etc.).

IV. Increased consumption of vitamin B 12 observed in multiple pregnancies, chronic hemolytic anemia, myeloproliferative diseases, neoplasms, thyrotoxicosis.

v. Violation of the intake of vitamin B 12 with food due to malnutrition or a strict vegetarian diet.

VI. Decrease in vitamin B 12 stores occurs in severe cirrhosis of the liver.

Pathogenesis

With a deficiency of vitamin B 12, the following disorders develop.

The lack of coenzyme vitamin B 12 methylcobalamin leads to a violation of the synthesis of thymidine, which is included in DNA, as a result, DNA synthesis and mitosis processes in the cells of the body are disrupted. Fast-growing tissues - bone marrow cells, epithelium of the gastrointestinal tract - suffer the most. Bone marrow cells lose their ability to mature normally. Violations of the red hematopoietic germ are especially pronounced. A large number of megaloblasts appear. Megaloblastic erythropoiesis is characterized by a delay in the maturation of erythrokaryocyte nuclei compared to the degree of hemoglobinization of the cytoplasm, a reduction in the lifespan of red hematopoietic cells, and an increased breakdown of megaloblasts in the bone marrow.

Erythropoiesis in B 12 deficiency anemia becomes ineffective, which is confirmed by the discrepancy between the increased number of erythrocaryocytes in the bone marrow and a sharp decrease in the content of reticulocytes in the peripheral blood, an increase in serum iron and a decrease in the inclusion of radioactive iron in erythrokaryocytes.

At the same time, there is a violation and inefficiency of granulocytopoiesis and thrombocytopoiesis. Giant forms of thrombocytes and granulocytes appear, phagocytosis of neutrophils by bone marrow macrophages increases. Autoantibodies to neutrophils may appear, which also contributes to the development of neutropenia in patients with B12 deficiency anemia.

Thus, vitamin B12 deficiencyleads to inefficiency of hematopoiesis with the development of megaloblastic anemia, leukopenia and thrombocytopenia. In addition, there is a violation of the maturation of epithelial cells of the gastrointestinal tract, which leads to the development of atrophy of the mucous membrane of the stomach and small intestine.

The lack of coenzyme vitamin B 12 deoxyadenosylcobalamin leads to a disruption in the metabolism of fatty acids and the accumulation of methylmalonic and propionic acids that are toxic to the nervous system in large quantities. In the absence of vitamin B12, methylmalonic acid does not convert to succinic acid. As a result, damage to the posterior and lateral columns of the spinal cord develops, and myelin synthesis in the nerve fibers decreases.

Clinical picture

The development of the disease is characteristic mainly for the age of 60-70 years. The clinical picture In 12-deficiency anemia is characterized by damage to three systems: digestive, hematopoietic and nervous.

Damage to the digestive system

In the vast majority of patients, symptoms of damage to the digestive system (primarily subjective) may be the earliest signs of the disease. Patients complain of a decrease or lack of appetite, a feeling of heaviness in the epigastric region after eating, belching of food and air eaten, pain and burning in the tongue, in the gums, lips, and sometimes in the rectum. These complaints of patients are due to the development of glossitis, atrophic gastritis and atrophic changes in the intestinal mucosa.

When examining the oral cavity, attention is drawn to inflammatory-atrophic changes in the mucous membrane of the oral cavity and tongue. B12-deficiency anemia is characterized by a smooth "varnished" tongue with atrophied papillae, cracked, with areas of inflammation of a bright red color (the entire tongue may be inflamed and red), sometimes with ulceration. Glossitis is observed only with a significant and prolonged deficiency of vitamin B 12, in approximately 25% of patients. Glossitis is characteristic not only for B12-deficiency anemia, it can also be observed with iron deficiency anemia. The mucous membrane of the oral cavity is pale, there may be phenomena of aphthous stomatitis. On palpation of the abdomen, mild pain in the epigastric region can be determined, often an increase in the liver and spleen.

Damage to the hematopoietic system

Violation of the hematopoietic system is the leading one in the clinical picture of the disease and is characterized by anemia of varying severity. Patients present complaints characteristic of anemic syndrome. The skin is usually pale, very often with a lemon yellow tint (due to hyperbilirubinemia due to hemolysis). Sometimes with B 12 - deficiency anemia, the body temperature rises (not higher than 38 ° C).

Damage to the nervous system

Changes in the nervous system in B 12 deficiency anemia are a characteristic feature of this disease and, as a rule, are observed in severe and prolonged course. Damage to the nervous system in B 12 deficiency anemia is called funicular myelosis and is characterized by involvement of the posterior and lateral columns of the spinal cord in the process. Demyelination occurs, and then degeneration of nerve fibers in the spinal cord and spinal nerves. Patients complain of weakness in the legs, especially when climbing stairs, when walking fast, a feeling of crawling on the legs, numbness of the legs. It seems to patients that they do not feel support under their feet when walking. It seems that the foot is not stepping on solid ground, but on something loose, soft, like cotton wool. These complaints are due to a violation of proprioceptive sensitivity.

With the predominance of damage to the posterior columns, deep, spatial, vibrational sensitivity is disturbed; there are sensory ataxia, difficulty walking; tendon reflexes decrease; there is atrophy of the muscles of the lower extremities. Pelvic organ dysfunction (urinary incontinence, fecal incontinence) may occur.

With damage to the lateral columns of the spinal cord, neurological symptoms are different: lower spastic paraparesis develops with a sharp increase in tendon reflexes and muscle tone of the lower extremities; dysfunction of the pelvic organs is characterized by urinary retention and defecation.

Laboratory data

The study of peripheral blood and bone marrow are of decisive importance in the diagnosis of the disease.

General blood analysis. The development of hyperchromic macrocytic anemia is characteristic (color index more than 1.1). Rarely, anemia may be normochromic. Erythrocytes are large (macrocytes), there is anisocytosis (different size of erythrocytes, along with macrocytes there are normocytes), poikilocytosis (change in the shape of erythrocytes). In many megalocytes (macrocytes), remnants of the nucleus (Jolly bodies, Cabot rings) are found, and basophilic punctuation is possible. Often, normoblasts are found in the peripheral blood, the number of reticulocytes in most patients is reduced or normal. The number of leukocytes is reduced, neutropenia, eosinopenia, relative lymphocytosis are determined. For B12-deficient anemia, the appearance of large segmented neutrophils with a polysegmented nucleus is extremely characteristic. The number of platelets is reduced, but there are usually no hemorrhagic manifestations, because thrombocytopenia does not reach a critical value.

Myelogram. The characteristic signs of B 12 deficiency anemia, which allow to verify the diagnosis, are:

• hyperplasia of the red hematopoietic germ; cells of the red row predominate over the cells of the white row;
• the appearance of a megaloblastic type of hematopoiesis;

Changes in myeloid cells - they increase in size, there are large metamyelocytes (young), stab, segmented neutrophils; the appearance of hypersegmented neutrophils is characteristic;

Violation of the maturation of megakaryocytes, expressed in violation of platelet lacing (non-permanent symptom).

Blood chemistry- there are no specific changes. However, with B 12 deficiency anemia, a hemolytic syndrome is often observed, due to the intramedullary decay of erythrokaryocytes, as well as a shortening of the lifespan of peripheral erythrocytes. This is manifested by unconjugated hyperbilirubinemia. It is possible to increase the content of LDH in the blood, and LDH 2. Often there is a moderate increase in the content of iron in the blood serum (with the development of hemolysis).

Analysis of urine and feces- with the development of hemolysis in the urine, urobilin is detected, in the feces - the amount of stercobilin is increased.

Instrumental Research

Esophagogastroduodenoscopy- there are atrophic changes in the mucous membrane of the digestive tract. The development of diffuse atrophic gastritis, duodenitis, less often atrophic esophagitis is characteristic.

Examination of gastric secretion- a decrease in the amount of gastric juice is detected, the absence of hydrochloric acid (akhiliya) and pepsin, sometimes a decrease in hydrochloric acid.

Fluoroscopy of the stomach- violations of the evacuation function of the stomach, flattening and smoothing of the folds of the mucous membrane are detected.

Diagnosis

Diagnostic criteria for B12 deficiency anemia:

I. Basic diagnostic criteria.

1. Hyperchromic character of anemia (occasionally the color index is normal).
2. Characteristic changes in peripheral blood erythrocytes: an increase in diameter (macrocytosis), volume, preservation of the remains of the nucleus (Jolly bodies, Cabot rings), reticulocytopenia.
3. Characteristic changes in peripheral blood leukocytes: leukopenia, neutrophil hypersegmentation.
4. thrombocytopenia.
5. Characteristic changes in the myelogram: the appearance of megaloblasts in the bone marrow, hyperplasia of the red hematopoietic germ, hypersegmentation of neutrophils (sternal puncture should be performed before treatment with vitamin B 12, since even 1-2 injections of vitamin B 12 lead to the disappearance of megaloblasts).
6. The development of the clinical picture of funicular myelosis (as a rule, with severe and prolonged course of the disease).
7. Low levels of vitamin B 12 in the blood.

II. Additional diagnostic criteria.

1. Atrophic gastritis, absence of hydrochloric acid, pepsin and gastromucoprotein in gastric juice.

2. Detection in the blood of antibodies to the parietal cells of the stomach, gastromucoprotein or the complex "vitamin B 12 gastromucoprotein".

3. Reticulocyte crisis (on the 5th-7th day of treatment, B 12 sharply increases the number of reticulocytes in the peripheral blood).

folate deficiency anemia (FDA)

FDA belongs to the group of megaloblastic anemias. The development of the megaloblastic type of hematopoiesis is due to the fact that with a deficiency of folic acid, the effect of vitamin B 12 on DNA synthesis is disrupted.

Fundamentals of Folic Acid Metabolism

Folic acid is a water-soluble, heat-labile vitamin. In foods and in the cells of the body, folic acid is found in the form of folic acid salts - polyglutamates (folates). Folates are found in meat, liver, plant foods (spinach, asparagus, lettuce, legumes, vegetables, fruits, mushrooms), yeast, milk. During cooking, long-term cooking, more than 50% of folates are destroyed, therefore, to meet the body's needs for folates, it is necessary to consume fresh vegetables and fruits. Folate absorption occurs in the duodenum and proximal jejunum. In the blood, 5-methyltetrahydrofolate binds to various proteins, enters the liver and rapidly proliferating bone marrow cells. The penetration of folates through the membrane and their accumulation in the cell occurs with the participation of vitamin B 12.

Folic acid is involved in the following biochemical reactions:

• together with vitamin B 12 is involved in the synthesis of thymidine monophosphate from uridine phosphate. Thymidine monophosphate is involved in the synthesis of pyrimidine bases and DNA. Therefore, folic acid is essential for DNA synthesis;
• participates in the synthesis of purine bases, which are part of DNA and RNA;
• takes part in the formation of glutamic acid from histidine. With a deficiency of folic acid, DNA synthesis in hematopoietic cells is disrupted, and megaloblastic anemia develops.

Indicators of normal folic acid metabolism:

The daily requirement for folic acid is 100-200 mcg. The total amount of folic acid ingested with food with good nutrition is 500-600 mcg / day. The amount of folate absorbed in the intestine is 400-480 mcg / day. The total folate content in the body is 5-10 mg. The period during which the depot provides the need for folic acid when it stops entering the body is 4-5 months.

Etiology

Insufficient dietary folate intake

Dietary folate deficiency is a common cause of FDA. It develops with insufficient consumption of vegetables and fruits, meat and other foods containing folates, as well as with improper cooking. FDA can develop in infants fed with goat's milk, various formulas containing little or no folate; with the exclusion from the diet of vegetables, fruits, meat.

Folate malabsorption in the small intestine

The reasons for the violation of the absorption of folates in the intestine are similar to those that violate the absorption of vitamin B 12: congenital disorders of the transport of folates through the wall of the small intestine; extensive resection of the small intestine, especially the lean one; enzyme deficiency enteropathy; malabsorption syndrome of various origins; blind gut syndrome; tumor diseases of the small intestine.

Increased need for folate

An increased need for folate is observed in children of any age, but especially often in children of the first year of life, as well as during periods of intensive growth, puberty. An increased need for folate is characteristic of pregnancy, chronic inflammatory diseases, chronic hemolytic anemia, exfoliative dermatitis, malignant neoplasms, including hemoblastoses.

Chronic alcohol intoxication

Alcohol impairs folate absorption in the small intestine, so chronic alcohol abuse can lead to FDA.

Increased folate loss

It can be observed with severe cirrhosis of the liver (the depot of folates in the liver decreases), hemodialysis, heart failure.

Taking medications

• Some drugs (biseptol, sulfalazine, aminopterin and methotrexate, triamterene, etc. can cause the development of FDA.

Pathogenesis

The above etiological factors lead to a decrease in the formation of the active form of folic acid - 5,10-methylenetetrahydrofolic acid. As a result, DNA synthesis in hematopoietic cells is disrupted and megaloblastic anemia develops.

Clinical picture

The disease most often develops in children, young people and pregnant women.

Patients present with complaints characteristic of anemia of any origin - there is a nonspecific anemic syndrome. However, unlike B 12 -deficiency anemia, there are no complaints due to damage to the nervous system. On examination, attention is drawn to the pallor of the skin, subicteric. When examining internal organs, one can detect a slight enlargement of the spleen (a non-permanent sign) and myocardial dystrophy syndrome (muffled heart tones, a soft systolic murmur at the apex, a violation of the repolarization phase of the left ventricular myocardium on the ECG in the form of a decrease in the amplitude of the T waves). In contrast to B12-deficiency anemia, FDA is characterized by the absence of atrophic glossitis, atrophic gastritis, and achylia.

Laboratory data

General blood analysis- the same symptoms are characteristic as in B 12 deficiency anemia.

Blood chemistry- there may be an increase in the amount of unconjugated bilirubin (due to hemolysis of erythrocytes), a decrease in the content of folic acid in the blood and erythrocytes.

Myelogram- characterized by hyperplasia of the red hematopoietic germ, the appearance of a large number of megaloblasts, hypersegmented neutrophils.

Test with histidine- the patient takes 15 g of histidine, after which the urinary excretion of formiminglutamic acid is determined 8 hours after taking histidine. Normally, the main part of histidine is converted with the participation of folic acid into glutamic acid, from 1 to 18 mg of formiming-lutamic acid is excreted in the urine. With folic acid deficiency anemia, the excretion of formiminglutamic acid is significantly increased.

Diagnostic criteriaFDA.

1. General analysis of peripheral blood: hyperchromic anemia, erythrocyte macrocytosis, neutrophil hypersegmentation, leukopenia, thrombocytopenia.

2. Myelogram - detection of megaloblasts, hypersegmented neutrophils.

3. Absence of glossitis, atrophic gastritis.

4. Absence of funicular myelosis.

5. Normal blood levels of vitamin B 12.

6. Reduced content of folic acid in blood serum and erythrocytes.

7. Normal daily urinary excretion of methylmalonic acid.

Treatment for B12 deficiencyandFDA

Treatment of B 12 deficiency anemia with vitamin B 12 can only be started after the diagnosis has been established and verified using a myelogram. Even 1-2 injections of vitamin B 12, without eliminating the syndrome of anemia, can transform megaloblastic hematopoiesis into normoblastic and make sternal puncture uninformative.

Treatment of B 12 deficiency anemia is carried out by intramuscular injections of vitamin B 12. There are two preparations of vitamin B 12 - cyanocobalamin and oxycobalamin.

Cyanocobalamin is prescribed 400-500 mcg intramuscularly 1 time per day (oxycobalamin 1 mg / day every other day). The duration of the course of treatment is 4-6 weeks. On the 3-4th day from the start of treatment with vitamin B 12, an increase in the content of reticulocytes in the blood begins. After the course of treatment, a course of fixing therapy is prescribed: cyanocobalamin is administered once a week for 2 months, and then constantly 2 times a month, 400-500 mcg. Oxycobalamin: for 3 months it is administered 1 time per week, and then constantly 1 time per month, 500 mcg.

In funicular myelosis, large doses of vitamin B 12 (1000 μg daily) are prescribed in combination with vitamin B 12 coenzyme cobamamide (500 μg 1 time per day intramuscularly), which is involved in the metabolism of fatty acids and improves the functional state spinal cord and nerve fibers. This dose of vitamin B 12 is administered until the disappearance of the myelosis clinic.

Folic acid preparations are prescribed only for patients with FDA. Assign folic acid inside in a daily dose of 5-15 mg. With B 12 deficiency anemia, folic acid treatment is not indicated.

Treatment of B 12-deficiency anemia is carried out for life, dispensary observation should be carried out constantly.

HYPO AND APLASTIC ANEMIA

Hypo and aplastic anemias are disorders of hematopoiesis characterized by a reduction in erythroid, myeloid and megakaryocyte hematopoietic bone marrow and pancytopenia in the blood, not accompanied by hepatosplenomegaly, in the absence of myelofibrosis, acute leukemia or myelodysplastic syndrome.

The pathomorphological basis of hypo and aplastic anemia is a sharp reduction in the active hematopoietic bone marrow and its replacement with adipose tissue. The disease occurs with a frequency of 5-10 cases per 1 million inhabitants per year.

Etiology

Depending on the etiological factors, congenital (hereditary) and acquired hypo- and aplastic anemia are distinguished. In turn, acquired hypo- and aplastic anemia is subdivided into an idiopathic (with unknown etiology) form and a form with known etiological factors. The idiopathic form accounts for 50-65% of all cases of aplastic anemia.

Known Causes of Acquired Aplastic Anemia:

I. Chemical factors: benzene, inorganic arsenic compounds, leaded gasoline (contains tetraethyl lead, heavy metals - mercury, bismuth, etc.), organochlorine compounds, etc.

II. Physical factors: ionizing radiation and x-rays.

III. Medicines: antibiotics (chloramphenicol, methicillin, etc.), sulfonamides, non-steroidal anti-inflammatory drugs (butadione, indomethacin, analgin), gold preparations, mercasolil, cytostatics, antiarrhythmic drugs (quinidine), antihypertensive drugs (captopril, enalapril; dopegyt), etc. .

IV. Infectious agents: viruses of infectious mononucleosis, hepatitis, influenza, Epstein-Barr, human immunodeficiency, cytomegaloviruses, herpes, mumps.

V. Immune diseases: graft-versus-host disease, eosinophilic fasciitis, thymoma, and thymic carcinoma.

Pathogenesis

Currently, the main pathogenetic factors of aplastic anemia are:

• damage to a pluripotent stem hematopoietic cell;
• damage to the cellular microenvironment of the hematopoietic stem cell and indirect impairment of its function;
• immune depression of hematopoiesis and apoptosis of stem hematopoietic cells;
• shortening the life of red blood cells;
• violation of the metabolism of hematopoietic cells.

Defeat of a pluripotent hematopoietic stem cell — the most important pathogenetic factor of aplastic anemia. The stem cell is the ancestor of all hematopoietic cells. With aplastic anemia, the colony-forming ability of the bone marrow is significantly reduced, the proliferation of hematopoietic cells is disturbed, and eventually pancytopenia syndrome is formed - leukopenia, anemia, thrombocytopenia. Finally, the mechanism of inhibition of the activity of pluripotent stem hematopoietic cells has not been elucidated.

Damage to the cellular microenvironment of the stem hematopoietic cell ki . It has now been established that the functional state of the hematopoietic stem cell and pluripotent progenitor cells is greatly influenced by the microenvironment, i.e., the stroma of the bone marrow. Cells of the microenvironment determine the division and differentiation of stem cells. The main cellular components of the stem cell microenvironment are osteoblasts, fibroblasts, endosteal, adventitial, endothelial and fat cells. In connection with the large role of the microenvironment in hematopoiesis, the term “hematopoiesis-inducing microenvironment” (ICM) has been proposed. For the normal development of hematopoietic cells, hematopoietic growth factors (HFR) and colony stimulating growth factors (CSF) are needed, glycoprotein hormones, of which about twenty have been identified. Under the influence of GRF and CSF, division and differentiation of hematopoietic cells occurs. In aplastic anemia, an internal defect in a pluripotent stem cell is a primary disorder that manifests itself or intensifies when various etiological factors act on hematopoietic cells through a change in the ICM.

Great importance in the development of aplastic anemia is attached to immune mechanisms. It is assumed that T-lymphocytes block differentiation of stem cells, antibodies are formed to stem cells, erythrocytes, cells - precursors of different blood lines, which leads to depression of hematopoiesis. When hematopoietic stem cells interact with activated cytotoxic T-lymphocytes and some cytokines, apoptosis (programmed cell death) of hematopoietic stem cells is stimulated.

In aplastic anemia, violations of enzyme systems in erythrocytes can occur, which makes them hypersensitive to various damaging factors and leads to their intracerebral destruction. The metabolism of hematopoietic cells undergoes significant changes, as a result of which the cells of all hematopoietic germs do not adequately absorb the substances necessary for optimal hematopoiesis (iron, vitamin B 12).

A decrease in the intensity of proliferation and differentiation of cells of the red series of hematopoiesis, increased destruction of erythrocytes, suboptimal use of iron and impaired hemoglobin formation lead to the accumulation of iron in the body with the deposition of iron-containing pigments in various organs and tissues (liver, spleen, skin, myocardium, adrenal glands, etc.) - that is, secondary hemochromatosis develops.

Classification

I. Hereditary forms

II. Acquired Forms

1. Hypoplastic anemia with damage to all three hematopoietic sprouts:

2. Partial hypoplastic anemia with a selective lesion of erythropoiesis.

III. The role of immune factors in the development of anemia

1. Immune form

2. Non-immune form.

Clinical picture

The main clinical and laboratory symptoms of acquired hypo- and aplastic anemia with damage to all three hematopoietic sprouts of the bone marrow are due to total inhibition of hematopoiesis, as well as hypoxia of organs and tissues, and hemorrhagic syndrome. The severity of symptoms depends on the severity and variant of the course of anemia.

Patients present complaints characteristic of anemic syndrome. Bleeding (gingival, nasal, gastrointestinal, renal, uterine bleeding) and frequent infectious and inflammatory diseases are characteristic. In the acute form, the symptoms develop quickly and the course of the disease is severe from the very beginning. But in most patients, the disease develops rather slowly, gradually, to a certain extent, patients adapt to anemia. The disease is usually recognized with severe symptoms.

When examining patients, attention is drawn to the pronounced pallor of the skin and visible mucous membranes, often with an icteric tint; hemorrhagic rashes on the skin, often in the form of bruises of various sizes. Often at the injection site (intramuscular, intravenous, subcutaneous) extensive hematomas are formed. Hemorrhagic rash is localized mainly in the area of ​​the legs, thighs, abdomen, sometimes on the face. There may be hemorrhages in the conjunctiva and visible mucous membranes - lips, oral mucosa. There may be severe nasal, gastrointestinal, renal, pulmonary, uterine, intracerebral bleeding. Peripheral lymph nodes are not enlarged.

When examining internal organs, the following changes can be detected:

• Respiratory system - frequent bronchitis, pneumonia.
• Cardiovascular system - myocardial dystrophy syndrome.
• Digestive system - with severe hemorrhagic syndrome, erosions can be found on the mucous membrane of the stomach, duodenum 12.

Hemosiderosis of internal organs often develops due to increased destruction of defective erythrocytes, a decrease in the use of iron by the bone marrow, impaired heme synthesis, and frequent transfusions of erythrocyte mass.

Laboratory data and instrumentalresearch

General blood analysis- pronounced decrease in the number of erythrocytes and hemoglobin; anemia in most patients is normochromic, normocytic; characterized by the absence or a sharp decrease in the number of reticulocytes (regenerative anemia); there is leukopenia due to granulocytopenia with relative lymphocytosis; characterized by thrombocytopenia. Thus, the most significant laboratory manifestation of hypo- and aplastic anemia is pancytopenia. ESR increased.

Blood chemistry- the content of serum iron is increased, the percentage of transferrin saturation with iron is significantly increased.

Examination of sternal punctate (myelogram)- a pronounced decrease in cells of the erythrocyte and granulocytic rows, lymphocytes and a significant reduction in the megakaryocytic germ. In severe cases, the bone marrow looks “empty”, and only single cells can be found in the sternal punctate. In the bone marrow, the content of iron, located both extracellularly and intracellularly, increases significantly.

Diagnostic criteria

• Normochromic normocytic regenerating anemia with a sharp decrease or complete absence of reticulocytes, an increase in ESR.
• Leukocytopenia, absolute granulocytopenia, relative lymphocytosis.
• thrombocytopenia.
• A pronounced absolute deficit in the myelogram of erythro-, leuko- and thrombopoiesis cells, a delay in their maturation.

An increase in the content of iron inside erythrokaryocytes and extracellularly.

• A sharp decrease in the number or complete disappearance of hematopoietic cells and the replacement of hematopoietic bone marrow with adipose tissue in the trepanobioptate of the ilium is the main method for verifying the diagnosis of hypo- and aplastic anemia).
• Increased serum iron levels.

Treatment of hypoplastic (aplastic) anemias

Treatment program:

1. Treatment with glucocorticoids.
2. Treatment with anabolic drugs.
3. Androgen treatment.
4. Treatment with cytostatics (immunosuppressants).
5. Splenectomy.
6. Treatment with antilymphocyte globulin.

7. Treatment with cyclosporine.

1. Bone marrow transplantation.
2. Treatment with colony-stimulating factors.
3. RBC transfusions.
4. Desferal therapy.
5. Platelet transfusions.
6. Treatment with immunoglobulin.

1. Treatment with glucocorticoids

Glucocorticoid therapy is most effective if hypoplastic anemia is caused by autoimmune mechanisms, the appearance of antibodies against blood cells. However, glucocorticoids are also used in other variants of bone marrow depression due to the ability to stimulate erythrocyte, neutrophilic and megakaryocytic hematopoietic sprouts. The daily dose of prednisolone is 1-2 mg/kg of the patient's weight per day, most often the dose ranges from 60 to 120 mg per day. The duration of therapy with prednisolone depends on the effect in the first 2 weeks from the start of treatment. If there is an effect, then treatment with prednisolone is continued with a transition to maintenance doses of 15-20 mg after a significant improvement in the hemogram. If there is no effect, then further treatment with prednisolone (more than 2 weeks) is useless. Treatment with prednisolone can last from 4 weeks to 3-4 months.

2. Treatment with anabolic drugs

Anabolic steroid drugs, on the one hand, neutralize the catabolic effects of glucocorticoids, on the other hand, stimulate hematopoiesis. Assign nerobol 20 mg / day or more effective anadrol (oxymetholone) 200 mg / day for 5-6 months. Anabolic treatment is also indicated after splenectomy.

3. Androgen treatment

Androgens have an anabolic effect and stimulate erythropoiesis. An increase in the level of hemoglobin is noted in 50% of patients, neutrophilic leukocytes - in 30%, platelets - in 25% of patients. Daily doses of androgens are 1-2 mg/kg, sometimes 3-4 mg/kg. Testosterone propionate 5% solution is injected 1 ml 2 times a day or a long-acting drug Sustanon-250 1 time per month (1 ml contains 250 mg of male sex hormones). The effect of androgens occurs gradually, so the treatment is carried out for a long time for several months. With a decrease in the dose or the abolition of androgens in some patients, an exacerbation of the disease is possible. Treatment with androgens is carried out only for men.

4. Treatment with cytostatics (immunosuppressants)

Immunosuppressant therapy is prescribed only in the absence of the effect of other methods of treatment in patients with an autoimmune form of hypoplastic anemia. Azathioprine (Imuran) 0.05 g 2-3 times a day with a gradual decrease in dose after the effect is obtained. The duration of the course of treatment can be 2-3 months.

5. Splenectomy

Splenectomy is indicated in the absence of the effect of glucocorticoids in all patients, if they do not have septic complications. The positive effect of splenectomy is observed in 84% of patients and is due to a decrease in the production of antibodies against hematopoietic cells, as well as a decrease in the sequestration of blood cells.

6. Treatment with antilymphocyticglobulin

Treatment with antilymphocyte globulin is recommended if splenectomy and other treatments fail. The drug inhibits the formation of antibodies against blood cells. 120-160 mg of antilymphocytic globulin is administered intravenously, drop by drop, once a day for 10-15 days.

Immunosuppressive therapy with anti-lymphocyte globulin, moderate doses of glucocorticoids, and androgens is the treatment of choice in patients with aplastic anemia who do not have an HLA-identical donor and who therefore cannot receive bone marrow transplantation.

7. Treatment with cyclosporine

Cyclosporine A - has an immunosuppressant effect. It is an effective treatment for aplastic anemia, hematological remission is achieved in 40-50% of patients. It is used orally as an oily solution or in capsules at a dose of 4 mg/kg/day in 2 divided doses. In the absence of toxic effects, treatment can continue for several months.

8. Bone marrow transplantation

Currently, bone marrow transplantation is the main treatment for hypoplastic anemia in the absence of the effect of other treatments. The bone marrow selected and compatible according to the HLA system is transplanted. Before transplantation, preliminary immunosuppression with cytostatics and radiation is performed. Achieving remission after myelotransplantation was noted in 80-90% of patients with severe aplastic anemia. The best results are obtained in persons not older than 30 years. Transplantation should be used no later than 3 months after the diagnosis of severe aplasia.

9. Treatment with colony-stimulating factors

Colony stimulating factors (CSF) are glycoproteins that stimulate the proliferation and differentiation of progenitor cells of various types.

Preparations of granulocytic CSF filgrastim, lenograstim, nartograstim mainly stimulate the formation of neutrophils; preparations of granulocyte-macrophage CSF molgramostim, sargramostim, leukomax stimulate the production of eosinophils, neutrophils, monocytes. The main indication for the appointment of CSF is neutropenia of various nature, including aplastic anemia, which increases the risk of life-threatening infections. CSFs are used in addition to other therapies. Recombinant CSF preparations are used intravenously at a dose of 5 µg/kg/day for 14 days.

10. RBC transfusions

Indications for erythrocyte transfusion are severe anemia, signs of cerebral hypoxia, and hemodynamic disorders. Frequent transfusions of erythrocytes create the risk of developing hypersiderosis and a depressive effect on erythrocytopoiesis. In this regard, blood transfusions are strictly limited by the level of hemoglobin. Its increase to 80-90 g/l is sufficient to eliminate tissue hypoxia. If 250-450 ml of erythrocyte mass transfused during the week maintains the hemoglobin content at the level of 90-100 g/l, then more frequent blood transfusions are not needed.

11. Desferal Therapy

With hypoplastic (aplastic) anemia, there is a significant accumulation of iron in the cells of hematopoiesis, especially erythropoiesis. This is due to a depression of hematopoiesis, a decrease in iron utilization, and insufficient formation of protoporphyrin IX. Excess iron can disrupt the function of hematopoietic cells up to their death. Therefore, the complex therapy of hypoplastic anemia includes the drug desferrioxalin (desferal), which selectively binds and removes ferric iron from human organisms. The drug is rapidly excreted through the kidneys in the form of ferroxamine, giving the urine a reddish tint. Desferal is administered intramuscularly or intravenously, 500 mg 2 times a day for at least 2-3 weeks. After a break of 3-4 weeks, it is advisable to conduct another 2-4 such such courses. In 50% of patients after treatment with desferal, hematopoiesis indicators improve.

12. Platelet transfusions

Platelet transfusion is performed with severe hemorrhagic syndrome caused by thrombocytopenia. The platelets received from one donor are transfused.

13. Treatment with immunoglobulin

In recent years, for the treatment of hypoplastic anemia, intravenous administration of immunoglobulin at a dose of 400 μg/kg of body weight for 5 consecutive days has been recommended. The drug stimulates erythro- and thrombopoiesis.