Sideropenic syndrome in iron deficiency anemia. Sideropenic syndrome in iron deficiency anemia: symptoms, treatment. Increased iron consumption

Lack of iron in the body leads to the development of iron deficiency anemia. Usually the clinical picture of this pathology is described as anemic and sideropenic syndrome.

The main signs are the development of hypoxia, pallor of the skin and mucous membrane, decreased appetite, physical and mental fatigue, and decreased performance. Anemic syndrome is also characterized by changes in the cardiovascular system, dizziness, and tinnitus.

This condition is associated with a lack of tissue iron reserves and insufficient activity of iron-containing enzymes. Sideropenic syndrome is characterized by dystrophic changes in the skin, mucous membrane, angular stomatitis, glossitis, atrophy of the papillae on the tongue, fragility and depletion of the nail plate, perverted taste and smell. People with sideropenic syndrome want to consume earth, clay or ice. Muscle pain and hypotension occur due to lack of myoglobin. This in turn interferes with urination, characterized by an urgent urge to urinate and bedwetting.

Sideropenic syndrome is expressed by disorders of the nervous system. Usually the emotional sphere becomes poorer, a depressive, negative, lethargic state develops, astheno-vegetative disorder, concentration of attention decreases, memory deteriorates, and intellectual development is delayed.

The role of iron in the human body

Iron is considered an essential element that allows the cells of the body to function properly. The biological role of the metal is associated with its ability to participate in reversible redox reactions, for example, in tissue respiration.

Iron in the human body occupies 0.0065% of the total body weight. Its compounds are characterized by different structures and functional activities. The most significant iron-containing compounds are hemoproteins, which contain heme. Such derivatives include hemoglobin, cytochrome, myoglobin, peroxidase, catalase. Non-heme enzymes include succinate dehydrogenase, xanthine oxidase, acetyl-CoA dehydrogenase, ferritin, transferrin, and hemosiderin.

Iron in the human body is found in combination with other compounds. Heme iron accounts for about 70%. Intracellular accumulations, which are ferritin and hemosiderin, account for 18% of deposited iron. The amount of functioning iron in the form of myoglobin and iron-containing enzymes is 12%. The transportable form in the composition of transferrin includes 0.1% of this metal.

There are two types of iron: non-heme and heme. Hemoglobin is formed by heme metal, its content in the diet is insignificant, mainly comes from meat products. The advantage of this form is its good digestibility, which ranges from 20 to 30%.

Non-heme is free iron found in the form of divalent or trivalent ions. This food form of the metal is mainly found in vegetables. Its absorption is much less compared to heme. Only non-heme divalent iron can be absorbed. To restore the trivalent form to the divalent form, reducing agents are used, most often ascorbic acid. The intestinal mucosa serves as a site for the conversion of ferrous iron Fe2+ into the oxide form Fe3+ and its binding to transferrin protein. With the help of such a complex, the ion is transported to the site of hematopoiesis or deposition.

The proteins ferritin and hemosiderin participate in the accumulation of iron, which, if necessary, can actively release the metal for further erythropoiesis.

Types of iron deficiency in the body

Iron deficiency develops in stages. Initially, there is insufficient accumulation of iron or prelatent deficiency, characterized by a decrease in the content of ferritin and iron in bone marrow cells, and an increase in the absorption of its ions. This is followed by latent iron deficiency, called iron deficiency erythropoiesis, caused by a decrease in serum iron concentration and an increase in transferrin levels. The bone marrow loses sideroblasts.

Latent iron deficiency is accompanied by a negative balance in the exchange of iron ions. Metal reserves from depositing organs begin to be consumed. This is followed by tissue iron deficiency, in which enzymatic activity and respiratory function in tissue cells are disrupted. The last stage is iron deficiency anemia with a pronounced lack of this metal, a decrease in the concentration of hemoglobin, red blood cells and hematocrit.

There is a mild degree of severity when the hemoglobin level ranges from 90 to 110 g/liter, a moderate degree with a hemoglobin content of 70 to 90 g/liter and a severe degree when the hemoglobin level is less than 70 g/liter.

Signs of low iron

The latent form of iron deficiency is determined by blood, in which a decrease in red blood cells and its pigment is not yet observed, but changes in the total and iron-binding capacity of the plasma are already noticeable. In the prelatent period, ferritin concentration begins to decrease even with normal levels of iron and serum transferrin.

Clear signs of iron deficiency begin to appear in aggregate. Single symptoms cannot indicate disease. Anemia is detected by fatigue, weakness, shortness of breath and palpitations during normal exercise, darkness in the eyes, dizziness, headache, tinnitus, pallor of the skin and mucous membranes. Iron deficiency can cause disruption of tissue nutrition, which leads to dryness and flaking of the skin, deterioration of the condition of nails, teeth, hair, changes in taste preferences, atrophy of the mucous membranes, dry mouth, and frequent stomatitis.

There are deviations in the normal functioning of the digestive system, during which the development of gastritis, colitis, and constipation is possible. The functioning of the liver is disrupted with the development of biliary dyskinesia or hepatosis, cardiovascular and nervous system, which is accompanied by a decrease in blood pressure, palpitations, sleep problems, apathy, and memory loss.

Iron deficiency reduces resistance to infectious diseases and impaired immunity. This leads to a 3-fold increase in the incidence of intestinal, bacterial and acute respiratory viral infections.

How does iron deficiency develop in the body?

The history of the disease “Iron deficiency anemia” boils down to a description of impaired absorption of this metal and its losses. The daily diet for an adult contains from 10 to 15 mg. Iron deficiency is accompanied by the absorption of a small amount, which does not exceed 30%. For normal life, a person needs to consume from 15 to 30 mg of the element per day. With sufficient intake of iron into the body, there are cases of poor absorption, which ranges from 2 to 5 mg, and the rest is excreted.

After the element enters the contents of the stomach, it is ionized. Iron is absorbed through the walls of the duodenum and upper small intestine. In the bloodstream, it combines with transferrin, which transports the metal to bone marrow or liver cells. The history of the disease "Iron deficiency anemia" shows that it often develops under the influence of several factors at once. An imbalance of iron intake and loss with preferential excretion is the reason for the development of this disease.

Main causes of iron deficiency anemia

There are many factors that affect the iron content in the body. Incomplete, poor food, a vegetarian or dairy diet, plant fiber and phytin make it difficult to absorb the element. Various pathologies of the digestive organs lead to disruption of the full absorption of iron and its absorption. For example, in diseases of the small intestine, under the influence of its alkaline contents, insoluble iron phosphate is formed, which prevents the metal from being absorbed. Tetracyclines and antacids, when used simultaneously, can also reduce its absorption.

There are causes of iron deficiency anemia caused by pathological blood loss from the digestive system, during injuries, operations, heavy menstruation, menorrhagia and metrorrhagia, bleeding gums, long-term donation. Metal deficiency is observed with frequent and prolonged infections, which reduce iron stores and its absorption.

Some physiological conditions increase the need for this element, causing iron deficiency. The reasons are due to pregnancy, breastfeeding, and increased growth of the child’s body. The fetus and placenta increase the need for this element, which is also consumed during birth blood loss and lactation. It has been established that the process of restoring normal iron levels after pregnancy and childbirth ends only after 24 months.

The child's body intensively uses iron in the first two years of life for rapid growth, as well as during puberty.

Sideropenic syndrome in iron deficiency anemia develops during an infectious or inflammatory process, burn conditions, tumors and element metabolism.

Diagnostics

Sideropenic syndrome with the development of iron deficiency anemia is determined using laboratory tests based on the following indicators:

Preventing iron deficiency in the body

Prevention of iron deficiency anemia includes measures aimed at eliminating the causes of metal deficiency:

• periodic monitoring of peripheral blood patterns;
• eating foods rich in iron, primarily beef, liver, red vegetables;
• reducing consumption of large amounts of sugars and fats;
• taking medications with iron for people at risk;
• rapid elimination of the source of blood loss.

Treatment of anemia

Serious health problems can be caused by iron deficiency in the body. Treatment of this pathology is reduced to obtaining complete clinical and hematological disappearance of the symptoms of the disease. It usually occurs after restoring the balance of the metal in blood cells and tissues, normalizing the metabolism of red blood cells, eliminating the cause or disease causing a lack of an important element, eliminating visceral damage to the digestive, hepatobiliary, and cardiovascular systems.

It is possible to replenish iron deficiency in iron deficiency anemia only by using drugs containing this element. It is impossible to restore its concentration with food alone.

Iron preparations are treated according to a strictly prescribed regimen using a specific therapeutic dose. Depending on the medication, the number of tablets may vary. The use of the drug "Ferroplex" as the "gold standard of the last century" involves taking a daily dosage of 6 tablets. The duration of treatment with iron-containing drugs is usually from 2 to 3 months. It is during this period of time that the body will replenish the lack of iron and accumulate the necessary reserves.

The disadvantage of drug therapy is poor tolerance by patients to drugs containing iron. After using medications containing divalent iron salts, undesirable consequences may occur in the form of a feeling of heaviness or pain in the abdomen, nausea, gagging, diarrhea or constipation.

Adverse reactions from treatment with iron preparations cause discomfort, which requires reducing the dose of the drug taken, shortening the duration of therapy, or completely abandoning the medication. Such inadequate use of iron-containing preparations leads to unsatisfactory results, which forces us to reconsider the technique.

Often unsuccessful treatment of iron deficiency is often due to several reasons:

• The iron supplement was prescribed in the wrong therapeutic dose.
• The timing of taking iron-containing medication is inadequately established.
• Use of a small dose of the drug over a short period of time.
• Deviations in compliance with the prescribed drug therapy regimen due to side effects.

Iron supplements

Oral medications containing iron are taken orally throughout the treatment period in order to restore normal hemoglobin levels. The next step will be to reduce the dosage to allow metal deposition to take place over several months. If there is ongoing blood loss, then for prevention, a systematic intake of iron-containing drugs is carried out 2 to 4 times a year, lasting 30 days each.

Parenteral use of iron-based drugs is prescribed only in extreme cases, when the absorption of this metal is impaired, there is enteritis, extensive intestinal resection, intolerance or ineffectiveness of internal use of drugs. This method of administration is suitable in case of contraindication to oral administration, for example, with ulcerative lesions of the digestive system.

During iron deficiency anemia, the functional state of the erythrocyte membrane changes significantly, peroxidation of lipid molecules is activated and the antioxidant protection of the erythrocyte is reduced.

To protect the body from the destructive effects of iron-containing drugs for anemia, they are combined with antioxidants, membrane stabilizers, antihypoxants, and cytoprotectors. Usually, for this purpose, from 100 mg to 150 mg of a-tocopherol are used per day. Other means are the drug "Ascorutin", retinol, ascorbic acid, lipostabil, methionine. Iron supplements combine well with thiamine, riboflavin, pyridoxine, pangamic and lipoic acids. Sometimes used with the drug Ceruloplasmin.

The main iron-containing drugs include the drug “Zhektofer”, produced as an iron-sorbitol-citric acid complex. Each ampoule contains 2 ml of solution for intramuscular administration with a dosage of 0.1 g of iron. The main effect of the drug is aimed at stimulating erythropoiesis thanks to iron, sorbitol, citric acid and dextrin.

Another iron-containing drug is the drug “Conferon”. Refers to complex preparations containing iron oxide sulfate in an amount of 0.25 g and sodium dioctyl sulfosuccinate in a dosage of 0.035 g. The release form is capsules of 0.25 g.

The tablet form is represented by the drug "Tardiferon" with a prolonged action. The sugar-coated tablets contain divalent aqueous ferrous sulfate in the amount of 256.3 mg, which corresponds to 80 mg of the metal. The main purpose of the drug is related to the replenishment of iron deficiency and hematopoietic effect. The combined product “Ferroplex” is produced in the form of dragees. The composition contains 30 mg of ascorbic acid and 50 mg of ferrous sulfate. Thanks to vitamin C, the absorption of the metal is improved and its deficiency in the body is compensated.

Another iron-containing tablet, Ferroceron, is used to stimulate hematopoietic processes. Available in two dosages: 300 mg and 100 mg. Smaller dosage tablets are film-coated and intended for children.

There is also a whole range of antianemic drugs, which include the drugs “Maltofer”, “Feramide”, “Totema”, “Ferrum Lek”, “Sorbifer Durules”, “Ferro-gradumet”.

– a syndrome caused by iron deficiency and leading to impaired hemoglobinopoiesis and tissue hypoxia. Clinical manifestations include general weakness, drowsiness, decreased mental performance and physical endurance, tinnitus, dizziness, fainting, shortness of breath on exertion, palpitations, and pallor. Hypochromic anemia is confirmed by laboratory data: a study of a clinical blood test, serum iron levels, CVSS and ferritin. Therapy includes a therapeutic diet, taking iron supplements, and in some cases, red blood cell transfusion.

ICD-10

D50

General information

Iron deficiency (microcytic, hypochromic) anemia is anemia caused by a lack of iron necessary for normal hemoglobin synthesis. Its prevalence in the population depends on gender, age and climatic geographical factors. According to general information, about 50% of young children, 15% of women of reproductive age and about 2% of men suffer from hypochromic anemia. Hidden tissue iron deficiency is detected in almost every third inhabitant of the planet. Microcytic anemia accounts for 80–90% of all anemias in hematology. Since iron deficiency can develop in a variety of pathological conditions, this problem is relevant for many clinical disciplines: pediatrics, gynecology, gastroenterology, etc.

Causes

Every day, about 1 mg of iron is lost through sweat, feces, urine, and exfoliated skin cells and approximately the same amount (2-2.5 mg) enters the body with food. An imbalance between the body's need for iron and its supply or loss from outside contributes to the development of iron deficiency anemia. Iron deficiency can occur both under physiological conditions and as a result of a number of pathological conditions and can be caused by both endogenous mechanisms and external influences:

Blood loss

Most often, anemia is caused by chronic blood loss: heavy menstruation, dysfunctional uterine bleeding; gastrointestinal bleeding from erosions of the gastric and intestinal mucosa, gastroduodenal ulcers, hemorrhoids, anal fissures, etc. Hidden but regular blood loss is observed with helminthiasis, pulmonary hemosiderosis, exudative diathesis in children, etc.

A special group consists of people with blood diseases - hemorrhagic diathesis (hemophilia, von Willebrand disease), hemoglobinuria. It is possible to develop posthemorrhagic anemia caused by immediate but massive bleeding during injuries and operations. Hypochromic anemia can occur due to iatrogenic causes - in donors who frequently donate blood; patients with chronic renal failure undergoing hemodialysis.

Impaired intake, absorption and transport of iron

Nutritional factors include anorexia, vegetarianism and following diets with limited meat products, poor nutrition; in children - artificial feeding, late introduction of complementary foods. Decreased iron absorption is typical for intestinal infections, hypoacid gastritis, chronic enteritis, malabsorption syndrome, conditions after resection of the stomach or small intestine, gastrectomy. Much less often, iron deficiency anemia develops as a result of impaired transport of iron from the depot with insufficient protein-synthetic function of the liver - hypotransferrinemia and hypoproteinemia (hepatitis, cirrhosis of the liver).

Increased iron consumption

The daily requirement for a microelement depends on gender and age. The greatest need for iron is in premature infants, young children and adolescents (due to high rates of development and growth), women of the reproductive period (due to monthly menstrual losses), pregnant women (due to the formation and growth of the fetus), nursing mothers ( due to consumption in milk). It is these categories that are most vulnerable to the development of iron deficiency anemia. In addition, an increase in the need and consumption of iron in the body is observed in infectious and tumor diseases.

Pathogenesis

Due to its role in ensuring the normal functioning of all biological systems, iron is the most important element. The level of iron determines the supply of oxygen to cells, the course of redox processes, antioxidant protection, the functioning of the immune and nervous systems, etc. On average, the iron content in the body is at the level of 3-4 g. More than 60% of iron (>2 g) is included in the composition of hemoglobin, 9% - in the composition of myoglobin, 1% - in the composition of enzymes (heme and non-heme). The rest of the iron in the form of ferritin and hemosiderin is located in tissue depots - mainly in the liver, muscles, bone marrow, spleen, kidneys, lungs, and heart. Approximately 30 mg of iron continuously circulates in the plasma, partly bound by the main plasma iron-binding protein, transferrin.

With the development of a negative iron balance, microelement reserves contained in tissue depots are mobilized and consumed. At first, this is enough to maintain adequate levels of Hb, Ht, and serum iron. As tissue reserves are depleted, the erythroid activity of the bone marrow increases compensatoryly. With complete depletion of endogenous tissue iron, its concentration in the blood begins to decrease, the morphology of erythrocytes is disrupted, and the synthesis of heme in hemoglobin and iron-containing enzymes decreases. The oxygen transport function of the blood suffers, which is accompanied by tissue hypoxia and degenerative processes in the internal organs (atrophic gastritis, myocardial dystrophy, etc.).

Classification

Iron deficiency anemia does not occur immediately. Initially, prelatent iron deficiency develops, characterized by depletion of only deposited iron reserves while the transport and hemoglobin pools are preserved. At the stage of latent deficiency, there is a decrease in transport iron contained in the blood plasma. Hypochromic anemia itself develops with a decrease in all levels of metabolic iron reserves - stored, transport and erythrocyte. In accordance with the etiology, anemia is distinguished: post-hemorrhagic, nutritional, associated with increased consumption, initial deficiency, insufficiency of resorption and impaired iron transport. According to the severity, iron deficiency anemia is divided into:

• Lungs(Hb 120-90 g/l). They occur without clinical manifestations or with their minimal severity.
• Medium-heavy(Hb 90-70 g/l). Accompanied by circulatory-hypoxic, sideropenic, hematological syndromes of moderate severity.
• Heavy(Hb

Symptoms

Circulatory-hypoxic syndrome is caused by a violation of hemoglobin synthesis, oxygen transport and the development of hypoxia in tissues. This is expressed in a feeling of constant weakness, increased fatigue, and drowsiness. Patients are plagued by tinnitus, flashing spots before the eyes, dizziness that turns into fainting. Characteristic complaints are palpitations, shortness of breath that occurs during physical activity, and increased sensitivity to low temperatures. Circulatory-hypoxic disorders can aggravate the course of concomitant ischemic heart disease and chronic heart failure.

The development of sideropenic syndrome is associated with a deficiency of tissue iron-containing enzymes (catalase, peroxidase, cytochromes, etc.). This explains the occurrence of trophic changes in the skin and mucous membranes. Most often they manifest themselves as dry skin; striations, brittleness and deformation of nails; increased hair loss. On the part of the mucous membranes, atrophic changes are typical, which is accompanied by the phenomena of glossitis, angular stomatitis, dysphagia, and atrophic gastritis. There may be an addiction to strong odors (gasoline, acetone), distortion of taste (the desire to eat clay, chalk, tooth powder, etc.). Signs of sideropenia also include paresthesia, muscle weakness, dyspeptic and dysuric disorders. Asthenovegetative disorders are manifested by irritability, emotional instability, decreased mental performance and memory.

Complications

Since IgA loses its activity under conditions of iron deficiency, patients become susceptible to frequent incidence of ARVI and intestinal infections. Patients are plagued by chronic fatigue, loss of strength, decreased memory and concentration. Long-term course of iron deficiency anemia can lead to the development of myocardial dystrophy, recognized by inversion of T waves on the ECG. With extremely severe iron deficiency, anemic precoma develops (drowsiness, shortness of breath, severe pallor of the skin with a cyanotic tint, tachycardia, hallucinations), and then coma with loss of consciousness and lack of reflexes. With massive rapid blood loss, hypovolemic shock occurs.

Diagnostics

The presence of iron deficiency anemia can be indicated by the patient’s appearance: pale, alabaster-tinged skin, pasty face, legs and feet, puffy “bags” under the eyes. Auscultation of the heart reveals tachycardia, dullness of tones, soft systolic murmur, and sometimes arrhythmia. To confirm anemia and determine its causes, a laboratory examination is performed.

• Laboratory tests. The iron deficiency nature of anemia is supported by a decrease in hemoglobin, hypochromia, micro- and poikilocytosis in a general blood test. When assessing biochemical parameters, a decrease in serum iron levels and ferritin concentration (60 µmol/l), a decrease in transferrin saturation with iron (
• Instrumental techniques. To determine the cause of chronic blood loss, an endoscopic examination of the gastrointestinal tract (EGD, colonoscopy), and X-ray diagnostics (irrigoscopy, radiography of the stomach) should be performed. Examination of the reproductive system organs in women includes pelvic ultrasound, chairside examination, and, if indicated, hysteroscopy with RDV.
• Bone marrow puncture examination. Smear microscopy (myelogram) shows a significant decrease in the number of sideroblasts, characteristic of hypochromic anemia. Differential diagnosis is aimed at excluding other types of iron deficiency conditions - sideroblastic anemia, thalassemia.

Treatment

The basic principles of treatment for iron deficiency anemia include the elimination of etiological factors, correction of diet, and replenishment of iron deficiency in the body. Etiotropic treatment is prescribed and carried out by gastroenterologists, gynecologists, proctologists, etc.; pathogenetic - hematologists. For iron deficiency conditions, a nutritious diet is indicated with the mandatory inclusion in the diet of foods containing heme iron (veal, beef, lamb, rabbit meat, liver, tongue). It should be remembered that ascorbic, citric, and succinic acids contribute to increased ferrosorption in the gastrointestinal tract. Oxalates and polyphenols (coffee, tea, soy protein, milk, chocolate), calcium, dietary fiber and other substances inhibit the absorption of iron.

At the same time, even a balanced diet is not able to eliminate an already developed iron deficiency, so patients with hypochromic anemia are recommended to undergo replacement therapy with ferrodrugs. Iron supplements are prescribed for a course of at least 1.5-2 months, and after normalization of Hb levels, maintenance therapy is carried out for 4-6 weeks with half the dose of the drug. For the pharmacological correction of anemia, ferrous and ferric iron preparations are used. If there are vital indications, blood transfusion therapy is used.

Prognosis and prevention

In most cases, hypochromic anemia can be successfully corrected. However, if the cause is not eliminated, iron deficiency can recur and progress. Iron deficiency anemia in infants and young children can cause delayed psychomotor and intellectual development (RDD). In order to prevent iron deficiency, annual monitoring of clinical blood test parameters, nutritious nutrition with sufficient iron content, and timely elimination of sources of blood loss in the body are necessary. It should be taken into account that iron contained in meat and liver in the form of heme is best absorbed; Non-heme iron from plant foods is practically not absorbed - in this case it must first be reduced to heme iron with the participation of ascorbic acid. People at risk may be advised to take prophylactic iron supplements as prescribed by a specialist.

Vydyborets S.V. , Doctor of Medical Sciences, Professor of the Department of Hematology and Transfusiology

National Medical Academy of Postgraduate Education named after. P.L. Shupika Ministry of Health of Ukraine

Clinical picture of iron deficiency anemia

Clinical manifestations of IDA consist of general symptoms of anemia, which are caused by hemic hypoxia, signs of tissue iron deficiency (sideropenic syndrome) and metabolic disorders (endogenous metabolic intoxication syndrome).

General symptoms of anemia are dizziness, weakness, headache (usually in the evening), shortness of breath, palpitations, a tendency to faint, especially in stuffy rooms, often a moderate increase in temperature, often drowsiness during the day and insomnia at night. Sometimes there are feelings of heaviness in the epigastric region, loss of appetite, dyspeptic symptoms, nausea, flatulence, constipation or a tendency to diarrhea. Due to poor blood supply to the skin, patients are sensitive to cold. In older people with coronary heart disease, an increase in anemia can provoke an increase in angina attacks and increased signs of heart failure.

Sideropenic syndrome . Since iron is part of many enzymes, its deficiency causes a decrease in the activity of these enzymes and disruption of the normal course of metabolic processes in the body. Sideropenia contributes to the development of various symptoms, which can be grouped as follows.

1. Changes in the muscular system. A lack of myoglobin and enzymes in the muscles increases muscle weakness and fatigue. In children and adolescents, the presence of IDA is accompanied by delayed growth and physical development. As a result of weakening of the muscular apparatus of the sphincters, an imperative urge to urinate appears, the inability to hold urine when laughing, coughing, and girls sometimes experience bedwetting (enuresis).

2. Changes in the skin and its derivatives. Iron deficiency may cause dry and flaky skin. The skin becomes parchment-like and cracks easily. Cracks in the anus, cracks in the corners of the mouth, on the feet, and palms appear. Hair becomes brittle (“split”), turns gray early and falls out rapidly. In 20-25% of patients, changes in the nails in the form of thinning, brittleness, transverse striations, and sometimes spoon-shaped concavity (koilonychia).

3. Changes in the mucous membranes of the digestive tract. When examining the mouth and oral cavity, 10-15% of patients have cracks in the corners of the mouth, “jams” (cheilosis); erosion (angular stomatitis). There may be an increased tendency to periodontal disease and caries.

4. Changes in the perception of odors. Some patients develop an addiction to unusual odors: gasoline, gas, newsprint, fuel oil, acetone, varnish, shoe polish, mothballs, damp earth after rain.

5. Changes in taste sensations(pica chlorotika) most often occurs in children and adolescents in the form of an indomitable desire to consume non-food products: earth (geophagy), chalk, tooth powder, coal, clay, sand, ice (pagophagy), raw dough, minced meat, cereals, seeds. Often patients have a desire to eat spicy, salty, sour or spicy foods.

6. Changes in the mucous membranes of the upper and lower respiratory tract. Iron deficiency is accompanied by the development of chronic atrophic rhinitis and atrophic pharyngitis.

7. Changes in the mucous membranes of the organ of vision. The “blue sclera symptom” occurs in 87% of patients with IDA. The blueness of the sclera is due to the fact that with iron deficiency, the hydroxylation of proline and lysine is disrupted, which leads to disruption of collagen synthesis. Therefore, vessels begin to appear through the thinned sclera, which creates the effect of blue sclera.

8. Symptoms that arise as a result of changes in the digestive tract:

a) dryness of the esophageal mucosa, its atrophy, spastic condition of the upper esophagus leads to sideropenic dysphagia - Plummer-Winson syndrome. Patients have difficulty swallowing dry food in the evening or when overtired.

b) disruption of tissue respiration leads to gradual atrophy of the gastric mucosa with the development of atrophic gastritis, a decrease in gastric secretion up to achylia.

9. Changes in thermoregulation. Sometimes patients experience a constant low-grade fever (according to various authors, from 3 to 5% of cases). This symptom is probably a sign of severe endogenous metabolic intoxication and hypoxia of thermoregulation centers.

10. Dystrophic changes in internal organs. For example, secondary anemic sideropenic myocardial dystrophy, which is manifested by an expansion of the border of percussion dullness of the heart to the left, an increase in the first sound at the apex, and changes in repolarization according to ECG data.

11. Changes in the immune system. In patients, the level of lysozyme, B-lysines, the complement component system, and some immunoglobulins decreases. The phagocytic activity of neutrophils and cellular immunity are disrupted (a decrease in the number of T- and B-lymphocytes is observed).

Endogenous metabolic intoxication syndrome occurs in patients with IDA as a result of long-term disruption of metabolic processes. In tissues, there is a violation of the synthesis, deposition, release and inactivation of such physiologically active compounds as molecules of average mass, lactic and pyruvic acids, histamine, serotonin, heparin, etc. Clinical manifestations of endogenous metabolic intoxication are probably fatigue, weakness, disturbances in thermoregulation, disturbances of taste and smell, psycho-emotional disorders, etc.

Laboratory diagnostics

There are a number of indicators that can help verify the diagnosis of IDA, but only an integrated approach to diagnosis, a thorough analysis of the results obtained, and taking into account the clinical picture can correctly establish the diagnosis.

Table 4

Basic criteria for laboratory diagnosis of IDA

Differential diagnosis

Differential diagnosis of IDA is carried out with those diseases that are accompanied by iron deficiency - thalassemia, anemia in chronic diseases. Thalassemia is characterized by clinical and laboratory signs of hemolysis of erythrocytes: reticulocytosis, increased levels of indirect bilirubin, increased size of the spleen, high iron content in the blood serum and in the depot, hypochromic anemia.

The term "anemia associated with chronic diseases" It is customary to designate a group of anemias that occur against the background of inflammatory diseases (abscesses, emphysema, tuberculosis, pneumonia, etc.), with subacute bacterial endocarditis, pelvic inflammation, meningitis. For the development of anemic syndrome it takes 1-2 months from the onset of clinical manifestations of the main pathological process. A characteristic sign of such anemia is a low level of serum iron, a decrease in the total life-value, an increase in bone marrow iron reserves, a decrease in the formation of red blood cells, and an increase in the concentration of free erythrocyte porphyrin.

For quotation: Tikhomirov A.L., Sarsania S.I., Nochevkin E.V. Iron deficiency conditions in gynecological and obstetric practice // RMZh. 2003. No. 16. P. 941

MGMSU named after. ON THE. Semashko

Epidemiology

Currently, there is a high prevalence of iron deficiency anemia (IDA) worldwide. According to WHO, 600 million people suffer from IDA. Anemia most often occurs in women of childbearing age, pregnant women and children of various age groups. In Europe and Russia, 10-12% of women of childbearing age develop IDA .

1. Arkadyeva G.V. Diagnosis and treatment of IDA.-M., 1999.

2. Harrison G.R. In the book: Internal diseases. Volume 7.- M.: Medicine, 1996, p. 572-587.

4. Dvoretsky L.I. WAITING. - M.: “Newdiamid-AO”, 1998.

5. Shekhtman M.M. In the book: Extragenital pathology and pregnancy. -Medicine, 1987, pp. 143-155.