Iron deficiency anemia. Iron deficiency anemia (Hypochromic anemia, Microcytic anemia) Anemia clinic diagnostics treatment
Iron deficiency anemia is a syndrome characterized by a decrease in the amount of hemoglobin and/or red blood cells in the blood due to a lack of the microelement iron in the body. This type of anemia is the most common among all, and according to statistics, it accounts for about 78% of the structure of such diseases.
Symptoms of the disease
Symptoms of the disease depend on the severity of the anemic syndrome. There are three degrees:
- Light (hemoglobin within 90-110 g/l)
- Average (hemoglobin within 70-90 g/l)
- Severe (hemoglobin below 70 g/l).
The clinical picture of anemia consists of two syndromes: anemic and sideropenic.
With anemic syndrome, patients complain of increased heart rate, a feeling of lack of air, general weakness, dizziness, drowsiness, headache, loss of performance, difficulty concentrating, tinnitus, irritability, and muscle weakness. Such symptoms are not specific; they can be present in many diseases. Noteworthy is the pallor of the skin and mucous membranes, arterial hypotension.
Sideropenic syndrome is caused by a decrease in the amount of substances that, like hemoglobin, have iron in their structure. Skin changes are characteristic. It becomes dry and flaky. Nails begin to peel and become brittle. Cracks appear in the corners of the mouth. Patients complain of changes in their sense of smell and taste preferences (some begin to eat chalk, coal, dry cereals, inhale the smells of gasoline, acetone, etc.). In some cases, cracks appear in the tongue and ulceration occurs.
Causes of the disease
Iron deficiency in the body can be observed when it is insufficiently obtained from food, at increased costs, or when its absorption in the body is impaired. The main causes of anemia are:
Diagnostics
The main thing in diagnosing iron deficiency anemia is a clinical blood test. Among the doctor’s indicators, the following are of particular interest:
- Hemoglobin amount (will be reduced)
- Red blood cell count (will be reduced)
- Color indicator (below normal - hypochromic anemia)
- When studying the morphology (shape and structure of red blood cells), the following features are noted that indicate IDA - anisocytosis (different sizes of red blood cells in one person; microcytes are more characteristic of the gastrointestinal tract - smaller than ordinary ones), poikilocytosis (various forms of blood cells).
In a biochemical analysis, IDA is indicated by:
- Decreased serum iron levels
- Reducing iron saturation of transferrin (iron transport protein)
- Decreased serum ferritin (depot form of iron)
- Increasing the overall iron-binding function of blood serum.
The above criteria are sufficient to diagnose IDA. But the diagnostic search does not end there. Next, hematologists prescribe a whole range of examinations and consultations to determine the cause of anemia.
Complications
The prognosis with timely diagnosis and adequate therapy is very favorable. If the process has gone far, then various chronic diseases develop against the background of anemia. Most often, patients experience heart failure, chronic hypoxia, diseases of the heart, blood vessels, liver, and brain.
With a critical decrease in hemoglobin in the blood, hypoxic coma, acute cardiovascular failure and death may develop.
Treatment of the disease
Before you begin treatment for anemia itself, you must first eliminate its cause. For example, if the cause of IDA is uterine bleeding, then you first need to be examined and treated by a gynecologist.
A mandatory component of treatment is a diet enriched with iron. But you need to take into account that if a deficiency of a given microelement already exists in the body, then diet alone will not help eliminate it.
Iron supplements are considered the mainstay of treatment for IDA. There are such medications for oral administration (they should be preferred) and in the form of injections (use only in cases of non-absorption of iron in the gastrointestinal tract). The course of treatment is long, ranging from 3 months to 1 year.
Anemia is a clinical and hematological syndrome characterized by a decrease in the number of red blood cells and hemoglobin in the blood.
A wide variety of pathological processes can serve as the basis for the development of anemic conditions, and therefore anemia should be considered as one of the symptoms of the underlying disease. The prevalence of anemia varies significantly, ranging from 0.7 to 6.9%. The cause of anemia can be one of three factors or a combination of them: blood loss, insufficient production of red blood cells, or increased destruction of red blood cells (hemolysis).
Among the various anemic conditions, iron deficiency anemia is the most common and accounts for about 80% of all anemia.
Iron deficiency anemia is a hypochromic microcytic anemia that develops as a result of an absolute decrease in iron reserves in the body. Iron deficiency anemia occurs, as a rule, with chronic blood loss or insufficient intake of iron into the body.
According to the World Health Organization, every 3rd woman and every 6th man in the world (200 million people) suffer from iron deficiency anemia.
Iron metabolism
Iron is an essential biometal that plays an important role in the functioning of cells in many body systems. The biological significance of iron is determined by its ability to reversibly oxidize and reduce. This property ensures the participation of iron in the processes of tissue respiration. Iron makes up only 0.0065% of body weight. The body of a man weighing 70 kg contains approximately 3.5 g (50 mg/kg body weight) of iron. The iron content in the body of a woman weighing 60 kg is approximately 2.1 g (35 mg/kg body weight). Iron compounds have different structures, have unique functional activity and play an important biological role. The most important iron-containing compounds include: hemoproteins, the structural component of which is heme (hemoglobin, myoglobin, cytochromes, catalase, peroxidase), enzymes of the non-heme group (succinate dehydrogenase, acetyl-CoA dehydrogenase, xanthine oxidase), ferritin, hemosiderin, transferrin. Iron is part of complex compounds and is distributed in the body as follows:
Heme iron - 70%;
- iron depot - 18% (intracellular accumulation in the form of ferritin and hemosiderin);
- functioning iron - 12% (myoglobin and iron-containing enzymes);
- transported iron - 0.1% (iron bound to transferrin).
There are two types of iron: heme and non-heme. Heme iron is part of hemoglobin. It is contained only in a small part of the diet (meat products), is well absorbed (20-30%), its absorption is practically not affected by other food components. Non-heme iron is in free ionic form - ferrous (Fe II) or ferric iron (Fe III). Most dietary iron is non-heme (found primarily in vegetables). The degree of its absorption is lower than that of heme and depends on a number of factors. Only divalent non-heme iron is absorbed from food. To “convert” ferric iron into divalent iron, a reducing agent is needed, the role of which in most cases is played by ascorbic acid (vitamin C). During absorption in the cells of the intestinal mucosa, ferrous iron Fe2+ is converted into oxide Fe3+ and binds to a special carrier protein - transferrin, which transports iron to hematopoietic tissues and sites of iron deposition.
Iron accumulation is carried out by the proteins ferritin and hemosiderin. If necessary, iron can be actively released from ferritin and used for erythropoiesis. Hemosiderin is a ferritin derivative with a higher iron content. Iron is released slowly from hemosiderin. Incipient (prelatent) iron deficiency can be determined by a reduced concentration of ferritin even before the depletion of iron stores, while still maintaining normal concentrations of iron and transferrin in the blood serum.
What causes iron deficiency anemia: The main etiopathogenetic factor in the development of iron deficiency anemia is iron deficiency. The most common causes of iron deficiency conditions are:
1. iron loss due to chronic bleeding (the most common cause, reaching 80%):
- bleeding from the gastrointestinal tract: peptic ulcer, erosive gastritis, esophageal varicose veins, colon diverticula, hookworm infestations, tumors, ulcerative colitis, hemorrhoids;
- long and heavy menstruation, endometriosis, fibroids;
-- macro- and microhematuria: chronic glomerulo- and pyelonephritis, urolithiasis, polycystic kidney disease, kidney and bladder tumors;
- nosebleeds, pulmonary bleeding;
-- blood loss during hemodialysis;
-- uncontrolled donation;
2. insufficient absorption of iron:
-- resection of the small intestine;
- chronic enteritis;
- malabsorption syndrome;
- intestinal amyloidosis;
3. increased need for iron:
-- intensive growth;
-- pregnancy;
- period of breastfeeding;
- playing sports;
4. insufficient intake of iron from food:
-- newborns;
-- small children;
-- vegetarianism.
Pathogenesis (what happens?) during Iron deficiency anemia: Pathogenetically, the development of iron deficiency can be divided into several stages:
1. prelatent iron deficiency (insufficient accumulation) - there is a decrease in ferritin levels and a decrease in iron content in the bone marrow, increased iron absorption;
2. latent iron deficiency (iron deficiency erythropoiesis) - serum iron is further reduced, transferrin concentration increases, and the content of sideroblasts in the bone marrow decreases;
3. severe iron deficiency = iron deficiency anemia - the concentration of hemoglobin, red blood cells and hematocrit further decreases.
Symptoms of Iron Deficiency Anemia: During the period of latent iron deficiency, many subjective complaints and clinical signs characteristic of iron deficiency anemia appear. Patients note general weakness, malaise, and decreased performance. Already during this period, distortion of taste, dryness and tingling of the tongue, difficulty swallowing with the sensation of a foreign body in the throat, palpitations, and shortness of breath may be observed.
An objective examination of patients reveals “minor symptoms of iron deficiency”: atrophy of the tongue papillae, cheilitis, dry skin and hair, brittle nails, burning and itching of the vulva. All these signs of impaired trophism of epithelial tissues are associated with tissue sideropenia and hypoxia.
Patients with iron deficiency anemia report general weakness, fatigue, difficulty concentrating, and sometimes drowsiness. Headache and dizziness appear. Severe anemia may cause fainting. These complaints, as a rule, do not depend on the degree of decrease in hemoglobin, but on the duration of the disease and the age of the patients.
Iron deficiency anemia is also characterized by changes in the skin, nails and hair. The skin is usually pale, sometimes with a slight greenish tint (chlorosis) and with an easy blush on the cheeks, it becomes dry, flabby, peels, and cracks easily form. Hair loses its shine, turns grey, thins, breaks easily, thins and turns gray early. Changes in nails are specific: they become thin, matte, flattened, easily peel and break, and striations appear. With pronounced changes, the nails acquire a concave, spoon-shaped shape (koilonychia). Patients with iron deficiency anemia experience muscle weakness, which is not observed in other types of anemia. It is classified as a manifestation of tissue sideropenia. Atrophic changes occur in the mucous membranes of the digestive canal, respiratory organs, and genital organs. Damage to the mucous membrane of the digestive canal is a typical sign of iron deficiency.
There is a decrease in appetite. There is a need for sour, spicy, salty foods. In more severe cases, distortions of smell and taste (pica chlorotica) are observed: eating chalk, lime, raw cereals, pogophagia (craving for eating ice). Signs of tissue sideropenia quickly disappear after taking iron supplements.
Diagnosis of Iron Deficiency Anemia: The main guidelines in the laboratory diagnosis of iron deficiency anemia are as follows:
1. The average hemoglobin content in an erythrocyte in picograms (normal 27-35 pg) is reduced. To calculate it, the color index is multiplied by 33.3. For example, with a color index of 0.7 x 33.3, the hemoglobin content is 23.3 pg.
2. The average concentration of hemoglobin in the erythrocyte is reduced; Normally it is 31-36 g/dl.
3. Hypochromia of erythrocytes is determined by microscopy of a peripheral blood smear and is characterized by an increase in the zone of central clearing in the erythrocyte; Normally, the ratio of central clearing to peripheral darkening is 1:1; for iron deficiency anemia - 2+3:1.
4. Microcytosis of erythrocytes - reduction in their size.
5. Coloring of erythrocytes of different intensity - anisochromia; the presence of both hypo- and normochromic red blood cells.
6. Different shapes of red blood cells - poikilocytosis.
7. The number of reticulocytes (in the absence of blood loss and a period of ferrotherapy) in iron deficiency anemia remains normal.
8. The leukocyte count is also within normal limits (except in cases of blood loss or oncopathology).
9. The platelet count often remains within normal limits; moderate thrombocytosis is possible with blood loss at the time of examination, and the platelet count decreases when the basis of iron deficiency anemia is blood loss due to thrombocytopenia (for example, with DIC syndrome, Werlhof's disease).
10. Reducing the number of siderocytes until they disappear (a siderocyte is an erythrocyte containing iron granules). In order to standardize the production of peripheral blood smears, it is recommended to use special automatic devices; the resulting monolayer of cells increases the quality of their identification.
Biochemical blood test:
1. Decrease in iron content in blood serum (normally in men 13-30 µmol/l, in women 12-25 µmol/l).
2. The life-saving ratio is increased (reflects the amount of iron that can be bound due to free transferrin; the normal life-value percentage is 30-86 µmol/l).
3. Study of transferrin receptors using the enzyme immunoassay method; their level is increased in patients with iron deficiency anemia (in patients with anemia of chronic diseases - normal or reduced, despite similar indicators of iron metabolism.
4. The latent iron-binding capacity of blood serum is increased (determined by subtracting the serum iron content from the TLC indicators).
5. The percentage of transferrin saturation with iron (the ratio of the serum iron indicator to the total life-saving value; normally 16-50%) is reduced.
6. The level of serum ferritin is also reduced (normally 15-150 mcg/l).
At the same time, in patients with iron deficiency anemia, the number of transferrin receptors is increased and the level of erythropoietin in the blood serum is increased (compensatory reactions of hematopoiesis). The volume of erythropoietin secretion is inversely proportional to the oxygen transport capacity of the blood and directly proportional to the oxygen demand of the blood. It should be taken into account that serum iron levels are higher in the morning; before and during menstruation it is higher than after menstruation. The iron content in blood serum in the first weeks of pregnancy is higher than in its last trimester. Serum iron levels increase on days 2-4 after treatment with iron-containing drugs and then decrease. Significant consumption of meat products on the eve of the study is accompanied by hypersideremia. These data must be taken into account when assessing the results of serum iron studies. It is equally important to follow laboratory testing techniques and blood sampling rules. Thus, the tubes in which blood is collected must first be washed with hydrochloric acid and double-distilled water.
A myelogram examination reveals a moderate normoblastic reaction and a sharp decrease in the content of sideroblasts (erythrokaryocytes containing iron granules).
Iron reserves in the body are judged by the results of the desferal test. In a healthy person, after intravenous administration of 500 mg of desferal, 0.8 to 1.2 mg of iron is excreted in the urine, while in a patient with iron deficiency anemia, iron excretion decreases to 0.2 mg. The new domestic drug defericolixam is identical to desferal, but circulates in the blood longer and therefore more accurately reflects the level of iron reserves in the body.
Taking into account the level of hemoglobin, iron deficiency anemia, like other forms of anemia, is divided into severe, moderate and mild anemia. With mild iron deficiency anemia, the hemoglobin concentration is below normal, but more than 90 g/l; with moderate iron deficiency anemia, the hemoglobin content is less than 90 g/l, but more than 70 g/l; with severe iron deficiency anemia, the hemoglobin concentration is less than 70 g/l. However, clinical signs of the severity of anemia (symptoms of a hypoxic nature) do not always correspond to the severity of anemia according to laboratory criteria. Therefore, a classification of anemia according to the severity of clinical symptoms has been proposed.
Based on clinical manifestations, there are 5 degrees of severity of anemia:
1. anemia without clinical manifestations;
2. moderate anemic syndrome;
3. severe anemic syndrome;
4. anemic precoma;
5. anemic coma.
Moderate severity of anemia is characterized by general weakness, specific signs (for example, sideropenic or signs of vitamin B12 deficiency); with a pronounced degree of severity of anemia, palpitations, shortness of breath, dizziness, etc. appear. Precomatose and comatose states can develop in a matter of hours, which is especially typical for megaloblastic anemia.
Modern clinical studies show that laboratory and clinical heterogeneity is observed among patients with iron deficiency anemia. Thus, in some patients with signs of iron deficiency anemia and concomitant inflammatory and infectious diseases, the level of serum and erythrocyte ferritin does not decrease, but after the exacerbation of the underlying disease is eliminated, their content drops, which indicates the activation of macrophages in the processes of iron consumption. In some patients, the level of erythrocyte ferritin even increases, especially in patients with long-term iron deficiency anemia, which leads to ineffective erythropoiesis. Sometimes there is an increase in the level of serum iron and erythrocyte ferritin, a decrease in serum transferrin. It is assumed that in these cases the process of iron transfer to heme-synthesizing cells is disrupted. In some cases, a deficiency of iron, vitamin B12 and folic acid is determined simultaneously.
Thus, even the level of serum iron does not always reflect the degree of iron deficiency in the body in the presence of other signs of iron deficiency anemia. Only the level of THC in iron deficiency anemia is always elevated. Therefore, not a single biochemical indicator, incl. OZHSS cannot be considered as an absolute diagnostic criterion for iron deficiency anemia. At the same time, the morphological characteristics of peripheral blood erythrocytes and computer analysis of the main parameters of erythrocytes are decisive in the screening diagnosis of iron deficiency anemia.
Diagnosis of iron deficiency conditions is difficult in cases where the hemoglobin level remains normal. Iron deficiency anemia develops in the presence of the same risk factors as for iron deficiency anemia, as well as in individuals with an increased physiological need for iron, especially in premature infants at an early age, in adolescents with a rapid increase in height and body weight, in blood donors, with nutritional dystrophy. At the first stage of iron deficiency, there are no clinical manifestations, and iron deficiency is determined by the content of hemosiderin in bone marrow macrophages and by the absorption of radioactive iron in the gastrointestinal tract. At the second stage (latent iron deficiency), an increase in the concentration of protoporphyrin in erythrocytes is observed, the number of sideroblasts decreases, morphological signs appear (microcytosis, hypochromia of erythrocytes), the average content and concentration of hemoglobin in erythrocytes decreases, the level of serum and erythrocyte ferritin, and transferrin saturation with iron decrease. The hemoglobin level at this stage remains quite high, and clinical signs are characterized by a decrease in exercise tolerance. The third stage is manifested by obvious clinical and laboratory signs of anemia.
Examination of patients with iron deficiency anemia
To exclude anemia that has common features with iron deficiency anemia and to identify the cause of iron deficiency, a complete clinical examination of the patient is necessary:
A general blood test with mandatory determination of the number of platelets, reticulocytes, and study of the morphology of red blood cells.
Biochemical blood test: determination of the level of iron, TBC, ferritin, bilirubin (bound and free), hemoglobin.
In all cases, it is necessary to examine bone marrow aspirate before prescribing vitamin B12 (primarily for differential diagnosis with megaloblastic anemia).
To identify the cause of iron deficiency anemia in women, a preliminary consultation with a gynecologist is required to exclude diseases of the uterus and its appendages, and in men, an examination by a proctologist to exclude bleeding hemorrhoids and a urologist to exclude prostate pathology.
There are known cases of extragenital endometriosis, for example in the respiratory tract. In these cases, hemoptysis is observed; fiberoptic bronchoscopy with histological examination of a biopsy of the bronchial mucosa makes it possible to establish a diagnosis.
The examination plan also includes x-ray and endoscopic examination of the stomach and intestines to exclude ulcers, tumors, incl. glomic, as well as polyps, diverticulum, Crohn's disease, ulcerative colitis, etc. If pulmonary siderosis is suspected, X-ray and tomography of the lungs and sputum examination for alveolar macrophages containing hemosiderin are performed; in rare cases, histological examination of a lung biopsy is necessary. If kidney pathology is suspected, a general urine test, blood serum testing for urea and creatinine are required, and, if indicated, an ultrasound and x-ray examination of the kidneys. In some cases, it is necessary to exclude endocrine pathology: myxedema, in which iron deficiency can develop secondary to damage to the small intestine; polymyalgia rheumatica is a rare connective tissue disease in older women (less often in men), characterized by pain in the muscles of the shoulder or pelvic girdle without any objective changes in them, and in a blood test - anemia and an increase in ESR.
Differential diagnosis of iron deficiency anemia
When diagnosing iron deficiency anemia, it is necessary to carry out a differential diagnosis with other hypochromic anemias.
Iron redistribution anemia is a fairly common pathology and in terms of frequency of development it ranks second among all anemias (after iron deficiency anemia). It develops in acute and chronic infectious and inflammatory diseases, sepsis, tuberculosis, rheumatoid arthritis, liver diseases, cancer, ischemic heart disease, etc. The mechanism of development of hypochromic anemia in these conditions is associated with the redistribution of iron in the body (it is located mainly in the depot) and a violation mechanism for recycling iron from the depot. In the above diseases, activation of the macrophage system occurs, when macrophages, under activation conditions, firmly retain iron, thereby disrupting the process of its reutilization. A general blood test shows a moderate decrease in hemoglobin (
The main differences from iron deficiency anemia are:
- increased level of serum ferritin, which indicates an increased iron content in the depot;
- serum iron levels may remain within normal limits or be moderately reduced;
- TIHR remains within normal values or decreases, which indicates the absence of serum Fe starvation.
Iron-saturated anemia develops as a result of a violation of heme synthesis, which is caused by heredity or can be acquired. Heme is formed from protoporphyrin and iron in erythrokaryocytes. In iron-saturated anemia, the activity of enzymes involved in the synthesis of protoporphyrin occurs. The consequence of this is a violation of heme synthesis. Iron, which was not used for heme synthesis, is deposited in the form of ferritin in macrophages of the bone marrow, as well as in the form of hemosiderin in the skin, liver, pancreas, and myocardium, resulting in the development of secondary hemosiderosis. A general blood test will record anemia, erythropenia, and a decrease in color index.
Indicators of iron metabolism in the body are characterized by an increase in the concentration of ferritin and serum iron levels, normal indicators of life-saving blood test, and an increase in transferrin saturation with iron (in some cases reaching 100%). Thus, the main biochemical indicators that make it possible to assess the state of iron metabolism in the body are ferritin, serum iron, TLC and % transferrin saturation with iron.
Using indicators of iron metabolism in the body allows the clinician to:
- identify the presence and nature of iron metabolism disorders in the body;
- identify the presence of iron deficiency in the body at the preclinical stage;
- carry out differential diagnosis of hypochromic anemia;
- evaluate the effectiveness of the therapy.
Treatment of Iron Deficiency Anemia: In all cases of iron deficiency anemia, it is necessary to establish the immediate cause of this condition and, if possible, eliminate it (most often, eliminate the source of blood loss or treat the underlying disease, complicated by sideropenia).
Treatment of iron deficiency anemia should be pathogenetically substantiated, comprehensive and aimed not only at eliminating anemia as a symptom, but also at eliminating iron deficiency and replenishing its reserves in the body.
Iron deficiency anemia treatment program:
- eliminating the cause of iron deficiency anemia;
- therapeutic nutrition;
- ferrotherapy;
- prevention of relapses.
Patients with iron deficiency anemia are recommended to have a varied diet, including meat products (veal, liver) and products of plant origin (beans, soy, parsley, peas, spinach, dried apricots, prunes, pomegranates, raisins, rice, buckwheat, bread). However, it is impossible to achieve an antianemic effect with diet alone. Even if the patient eats high-calorie foods containing animal protein, iron salts, vitamins, and microelements, iron absorption of no more than 3-5 mg per day can be achieved. The use of iron supplements is necessary. Currently, the doctor has at his disposal a large arsenal of iron medications, characterized by different compositions and properties, the amount of iron they contain, the presence of additional components that affect the pharmacokinetics of the drug, and various dosage forms.
According to the recommendations developed by WHO, when prescribing iron supplements, preference is given to drugs containing divalent iron. The daily dose should reach 2 mg/kg of elemental iron in adults. The total duration of treatment is at least three months (sometimes up to 4-6 months). An ideal iron-containing drug should have a minimum number of side effects, have a simple regimen of use, the best efficiency/price ratio, optimal iron content, and preferably the presence of factors that enhance absorption and stimulate hematopoiesis.
Indications for parenteral administration of iron preparations arise in case of intolerance to all oral drugs, malabsorption (ulcerative colitis, enteritis), gastric and duodenal ulcers during an exacerbation, with severe anemia and the vital need to quickly replenish iron deficiency. The effectiveness of iron supplements is judged by changes in laboratory parameters over time. By the 5-7th day of treatment, the number of reticulocytes increases by 1.5-2 times compared to the initial data. Starting from the 10th day of therapy, the hemoglobin content increases.
Considering the pro-oxidant and lysosomotropic effect of iron preparations, their parental administration can be combined with intravenous drip administration of rheopolyglucin (400 ml - once a week), which helps protect the cell and avoid overload of macrophages with iron. Considering significant changes in the functional state of the erythrocyte membrane, activation of lipid peroxidation and a decrease in the antioxidant protection of erythrocytes in iron deficiency anemia, it is necessary to introduce antioxidants, membrane stabilizers, cytoprotectors, antihypoxants into the treatment regimen, such as a-tocopherol up to 100-150 mg per day (or ascorutin, vitamin A, vitamin C, lipostabil, methionine, mildronate, etc.), and also combined with vitamins B1, B2, B6, B15, lipoic acid. In some cases, it is advisable to use ceruloplasmin.
List of drugs used in the treatment of iron deficiency anemia:
- Jectofer;
- Conferon;
- Maltofer;
- Sorbifer durules;
- Tardiferon;
- Feramidum;
- Ferro-gradumet;
- Ferroplex;
- Ferroceron (Ferroceronum);
- Ferrum lek.
- Tothema
Prevention of Iron Deficiency Anemia:- Periodic monitoring of the blood picture;
- eating foods high in iron (meat, liver, etc.);
- preventive administration of iron supplements in risk groups.
- prompt elimination of sources of blood loss.
This type of anemia is caused by iron deficiency in the human body or large blood loss. Iron deficiency anemia does not have strictly specific symptoms. Most often it is accompanied by pallor of the skin and mucous membranes, causeless weakness, and dizziness.
Iron in the human body is an essential component of blood, or more precisely, hemoglobin, which is part of red blood cells. It is this metal that binds oxygen atoms and carries them from the lungs to the tissues of the body, allowing the body to breathe, and on the way back it removes carbon dioxide.
Sources of iron in the body
Iron enters the body with food and is excreted in very small quantities. The balance of iron is so important that there is an iron depot in the liver - an emergency reserve that is used only in emergency cases. Such a case may be acute bleeding or a long break in the supply of iron from food, for example, during fasting. Only after all iron reserves are used up does its deficiency affect the blood and anemia begins.
Causes of iron deficiency anemia
There are two main causes of iron deficiency anemia: blood loss and impaired intake of iron into the body from food. All of the following are variations:
Loss of a large amount of blood at one time, for example during injuries, so that iron is lost with the blood and its depot does not have time to recover.
Uterine bleeding in women due to endometriosis, fibroids, etc.
Long and heavy periods.
Hidden prolonged bleeding from the digestive tract, from hemorrhoids.
Poor nutrition over a long period of time, food low in iron (eg vegetarian food, diets with insufficient amounts of iron, folic acid, vitamin B12).
In case of sufficient intake of iron from food, the following obstacles to the absorption of iron by the body may be: celiac disease, Crohn's disease, gastric bypass surgery, old age.
Taking medications that impair iron absorption (antacids containing calcium; Almagel, omeprazole, ranitidine, etc.)
Anemia during pregnancy
Pregnancy without additional intake of vitamins and microelements is very often accompanied by anemia, since the expectant mother’s need for vitamins, iron and other microelements increases, but the supply remains at the same level.
Also, in very rare cases, iron deficiency anemia can be caused by certain hereditary diseases, such as deficiency of transferrin (the protein that transports iron in the blood).
Hidden anemia
Before iron deficiency anemia gives its first symptoms, it is in a hidden (latent) stage. During this period, the lack of iron is compensated by its reserves in the liver depot; this does not affect a person’s well-being in any way and the blood hemoglobin is within normal limits. Hidden anemia is most often discovered accidentally, after a blood test for ferritin. Many people remain in this stage of preanemia for years without knowing it.
An overt period of anemia occurs after iron stores have been completely depleted. Hemoglobin and the number of red blood cells in the blood decrease, and unpleasant symptoms appear.
Symptoms of iron deficiency anemia
Iron deficiency anemia does not have strictly specific symptoms. Most often it is accompanied by pallor of the skin and mucous membranes (in the mouth, inside the eyelids), causeless weakness, and dizziness. All this can be observed in other diseases, so if you suspect anemia, you should consult a doctor and do a blood test.
Diagnosis of iron deficiency anemia
The most characteristic diagnostic sign of anemia is a decrease in hemoglobin in a blood test. The diagnosis and stage are determined by the doctor based on the amount of hemoglobin in the blood:
Absence of anemia: hemoglobin above 120 g/l in women and 130 g/l in men.
First degree: decrease in hemoglobin to 90−120 g/l. The reserves in the depot are used up, hemoglobin begins to decrease. It is necessary to consult a doctor and take iron supplements.
Second degree: hemoglobin 60−90 g/l - you should seriously think about the reasons, consult a doctor and immediately begin treatment.
Third stage: hemoglobin below 60 g/l - urgent hospitalization and intensive treatment are required. In the absence of qualified medical care, an unfavorable outcome is possible.
Iron deficiency anemia is diagnosed by blood tests, which include a complete blood count (CBC). Additional studies include: measurement of serum ferritin levels, serum iron levels, total iron-binding capacity and/or transferrin.
In the case of iron deficiency anemia, tests usually show the following results:
low hemoglobin (Hg) and hematocrit (0.8−0.9 and below); - low average volume of red blood cells; - low ferritin levels; - low serum iron content in the blood serum;
high level of transferrin or total serum iron binding capacity (TIBC); - low coefficient of transferrin saturation with iron.
If there is doubt about the diagnosis or suspicion of hidden anemia, the doctor may recommend a test that checks the amount of iron in the blood and liver. It is reflected by indicators such as serum iron, the amount of transferrin and ferritin, and TIBC (total iron-binding capacity of serum). If the blood level is increased and the amount of ferritin is decreased, there is most likely hidden iron deficiency anemia.
Treatment of iron deficiency anemia
Treating iron deficiency anemia can be quite a challenging task, but in most cases it can be done. The main goals are to eliminate the cause of blood loss and replenish iron deficiency. An indicator of improvement is normal hemoglobin and red blood cells, so several repeat tests must be done during treatment. Depending on the conditions and medical history, treatment can last from a couple of months to lifelong.
If the main cause of anemia is bleeding, then the first priority is to stop it. When bleeding from the digestive tract, a complete and thorough examination by a gastroenterologist is necessary to determine the level and source of blood loss. In case of uterine bleeding, treatment is carried out by a gynecologist.
Replenishment of iron deficiency is required in any case. For mild anemia, taking tablets is sufficient; for severely ill patients, iron supplements are administered intravenously. The more iron contained in the tablet, the better, but in any case, their use should be under the supervision of a doctor. An overdose of iron can be just as dangerous as a deficiency.
Absorption of iron in the body during anemia
The absorption of iron in the body worsens if it is taken simultaneously with tea, coffee, or milk. However, it is recommended to drink milk if nausea occurs after taking the pills. Calcium supplements and stomach medications also impair iron absorption.
If you have a choice, preference should be given to drugs that combine iron with ascorbic acid - it improves its absorption. You should not drink iron at the same time as zinc and copper, as they compete in the intestines for absorption.
According to recent studies, taking large doses of iron can reduce the body's resistance to bacterial infections. Therefore, treatment should be carried out under the supervision of a doctor.
– 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.
Reasons
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 needs 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, being partially 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, insufficient 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 acute respiratory viral infections 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 obligatory 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, therefore, 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.
Contents of the article
Iron deficiency anemia characterized by a decrease in iron content in the blood serum (bone marrow and depot), resulting in impaired hemoglobin formation.Iron deficiency anemia is widespread in the world, especially among women. According to summary statistics from different countries, iron deficiency anemia occurs in approximately 11% of women of childbearing age, and hidden iron deficiency in tissues occurs in 20-25%, while among adult men, patients with iron deficiency anemia account for about 2%.
Etiology and pathogenesis of iron deficiency anemia
The adult human body contains approximately 4 g of iron, with about 70% in hemoglobin, 4% in myoglobin, 25% in the storage pool (ferritin, hemosiderin) and labile pool (blood plasma), the rest in iron-containing enzymes of various cells.The most common cause of iron deficiency anemia is chronic blood loss. Normally, only a small amount (about 1 mg per day) of this unique element is excreted from the body (with desquamated cells of the intestinal epithelium, skin, bile) and is replenished by intake (1 -1.3 mg, maximum 2 mg per day). Each millimeter of blood contains about 0.5 mg of iron, so women lose on average about 17 mg of additional iron during menstruation (equivalent to 34 ml of normal menstrual blood loss). With heavy or prolonged uterine bleeding, iron losses are large and, not compensated by intake, can lead to sideropenia - a gradual depletion of reserves, a decrease in serum iron levels, and anemia. In addition to uterine blood loss, bleeding from the gastrointestinal tract (duodenal and gastric ulcers, hiatal hernia, hemorrhoids, benign and malignant tumors, diverticula, helminthic infestations, especially hookworm infection), lungs (paragonimiasis, isolated pulmonary siderosis) Iron deficiency anemia can be caused by increased iron consumption in pregnant women: the period of pregnancy and lactation requires about 400 mg of iron for the construction of the fetus, 150 mg for the placenta, about 100 mg (200 ml of blood) is lost during childbirth and about 0. 5 mg of iron per day enters milk, which, with insufficient nutrition, is the basis for the occurrence of anemia. Iron deficiency anemia can develop in newborns, especially premature babies (with a low initial iron level), during the period of increased growth in adolescents, more often girls (this is explained, in addition to the addition of menstrual blood loss to the existing small reserves of iron in the body, hormonal influences - the absence, unlike androgens stimulating effect of estrogens on erythropoiesis), as well as in cases of impaired iron absorption (chronic enteritis, extensive intestinal resections, “malabsorption syndrome”) or insufficient intake from food (rarely, mainly in children who remain breastfed or fed goat milk for a long time, during fasting and perversions of diet).
Iron deficiency anemia clinic
With the gradual development of anemia, for example, prolonged blood loss, as a result of the activation of homeostatic mechanisms, complaints may be absent for a long time even with severe anemia, however, tolerance to physical activity in such people is often reduced. Most of the symptoms are similar to those of other types of anemia: increased fatigue, headaches, dizziness. Some of the complaints are related not so much to anemia itself, but to sideropenia and deficiency of iron-containing enzymes. Sideropenic symptoms are muscle weakness. paresthesia, burning sensation in the tongue, dry skin, hair loss, taste perversion (pica chlorotica) - desire to use clay, chalk, glue, etc. Moreover, these manifestations are not always proportional to the severity of anemia.Physical examination reveals glossitis (redness of the tongue with atrophy of the papillae), cracks in the corners of the mouth, and stomatitis. Flattening, thinning and brittleness of the nails are noted, but koilonychia - spoon-shaped nails, previously found in 20% of patients, is now a rarer symptom. Iron deficiency causes damage to the gastrointestinal tract - dysphagia, impaired gastric secretion; Treatment with iron supplements leads to the correction of these disorders.
Laboratory data for iron deficiency anemia
Iron deficiency anemia is characterized by a more significant decrease in the level of hemoglobin in the blood than in the number of red blood cells, SEH and SGE (color index 0.6-0.5) - hypochromia. The reticulocyte count is usually normal or slightly increased (with bleeding). The blood smear reveals hypochromic micro- and normocytes, and the degree of microcytosis and hypochromia depends on the severity of anemia, as well as the severity of anisocytosis and poikilocytosis. In the bone marrow, hyperplasia of erythroid elements is noted with insufficient hemoglobinization. An important sign of iron deficiency anemia is a decrease in serum iron levels. Normally, the concentration of iron in serum using the method of complexing iron with B-phenanthroline is 70-170 mcg per 100 ml, or 13-30 μmol/l; in case of iron deficiency anemia, it can decrease to very low numbers (2-2.5 µmol/l) with a high total iron-binding capacity of the serum (TIBC). TI is measured by the amount of iron that can bind 100 ml or 1 liter of blood serum; normally it is 250-400 mcg per 100 ml, or 45-72 µmol/l. The difference between TIR and serum iron depends on transferrin iron saturation; Normally it is 20-45%, with iron deficiency anemia it is below 16%.To assess iron stores in the body, the concentration of ferritin in the blood serum is determined using RIM. Normally, the ferritin content is 12-325 ng/ml (on average 125 ng/ml in men and 55 ng/ml in women), with iron deficiency anemia it is usually below 10 ng/ml, and with iron overload it can increase a thousand times. patients, the content of free protoporphyrin in erythrocytes is increased due to its non-use for communication with iron (due to iron deficiency). However, this indicator is nonspecific, since an increase in the level of protoporphyrin is also observed in sideroblastic and hemolytic anemia.
There is a certain sequence of changes in laboratory data with developing iron deficiency anemia. First, iron reserves decrease and the level of ferritin in the blood serum decreases, then the life-saving blood value increases, the level of serum iron decreases and the saturation of transferrin with iron decreases, after which the level of hemoglobin decreases. At first, anemia is normocytic and normochromic in nature, but then microcytosis and hypochromia of erythrocytes inevitably develop.
