IRON DEFICIENCY ANEMIA

From Big Medical Encyclopedia

IRON DEFICIENCY ANEMIA (iron + lat. deficit lacks; anemia; synonym: chloranemia, sideropenic anemia, giposideremichesky anemia) — the form of an anemia caused by deficit of iron in an organism.

History of studying. and. as special form of an anemia began with the description of the «pale not urine» of girls named in 17 century by Varandal «chlorosis» on greenish and pale coloring of skin. At the end of the last century along with «an early chlorosis» «the late chlorosis» is allocated. In 1933 Mr. W. Dameshek formulated the concept «essential iron deficiency anemia». Studying by Faber (To. Faber, 1913), M. P. Konchalovsky and M. S. Dultsin (1936) and others of a role of a gastric akhiliya in disturbance of digestion of iron promoted allocation akhlorgidridny, or gastrogenic, anemias. However later it was established that the achlorhydria does not play an essential role in disturbance of absorption of iron and can be not the cause, but a consequence of its deficit. Further studying. and. it is connected with progress of knowledge of exchange of iron in an organism, the mechanism of its disturbances and a role of deficit of iron in development of anemic states (see. Iron ). About degree of anemia judge by the level of hemoglobin and size of serumal iron. and. is the most widespread, making apprx. 80% of all cases of an anemia. Among patients. and. women prevail 30 years are more senior. Definition of serumal iron allowed to establish that frequency. and. (7,3 — 11%) and latent deficit of iron (20 — 22%) at women of the European countries it is almost identical. A research of reserves of iron by desferalovy test (see. Hemosiderosis ) found latent deficit of iron in 33% of women.

== Etiology and pathogeny ==. and. can be caused by a variety of reasons. Repeated blood losses, even not plentiful and hidden, lead to loss of iron, exhaustion of its reserves in an organism and to development of latent deficit of iron, and then hron, posthemorrhagic. and. Often uterine bleedings are the reason of blood losses, went less often. - kish., renal, pulmonary, etc.

The iron deficiency anemia can develop under the influence of exogenous factors. So, the anemia connected with a lack of iron of food is noted at the children who are on uniform milk food, especially at artificial feeding by cow's or goat milk. For development. and. at newborns deficit of iron at mother can matter during pregnancy. In the USSR and other economically developed countries alimentary. and. occurs at adults seldom — at long uniform, preferential milk diet. In developing countries among poor segments of the population alimentary insufficiency can be the cause of anemias much more often. Other exogenous factors (infections, intoxications, helminthic invasions) influence endogenous mechanisms of exchange and utilization of iron that leads to its redistribution and development of relative deficit.

Endogenous insufficiency of iron can be a consequence of the raised consumption of iron in growth periods and maturing of an organism, and also pregnancy, a lactation. Reason. and. at girls in the pubertal period (early, or juvenile, a chlorosis) increase in need of an organism for iron in connection with growth, emergence of menstrual bleedings, the oppressing effect of oestrogenic hormones on synthesis gem can be. and. at adult women it is usually connected with uterine bleedings (dysfunctional or because of a fibromyoma of a uterus). Disturbance of absorption of iron and other substances important for a hemopoiesis happens also after a resection of a stomach or a part of a small bowel.

The iron deficiency anemia can be caused both by each of the listed factors separately, and a simultaneous combination of all or a row from them. Development is possible. and. against the background of hron, inflammatory process, blastomatoses (earlier they combined the concept «symptomatic chloranemias»). In these cases, in addition to deficit of iron which has redistribution character, takes place myelotoxic action of basic process on a hemogenesis.

Pathogeny . and. gem because of a lack of iron of an organism and development of true deficit of iron (with exhaustion of its reserves) or in shortage of iron for an erythrogenesis owing to redistribution consists in disturbance of synthesis.

Geynrikh (N. S. of Heinrich, 1970) distinguishes the following stages of development of deficit of iron: 1) to a pra the latent deficit of iron determined histochemical by lack of hemosiderin in macrophages of reticulohistocytosis system of marrow, and indirectly — on the basis of the increased intestinal absorption of iron; 2) the latent deficit of iron which is characterized by decrease in concentration of serumal iron and increase in the general and especially latent iron-binding ability of serum (OZhSS and LZhSS); 3) iron deficiency (giposideremichesky) anemia with further decrease in content of iron in an organism and disturbance of a gemoglobinization of erythrocytes.

Modern ideas of a pathogeny of deficit of iron and development. and. lean on researches of exchange of iron in normal and patol, conditions. Loss of iron at repeated bleedings or insufficiency of its absorption in connection with reduction of receipt with food, and also disturbance of absorption leads to reduction of reserves of iron, decrease in serumal iron and increase in OZhSS and especially LZhSS with reduction of percent of saturation of a carrier of iron — transferrin (siderophilin). As a result transport of iron in marrow decreases and its inclusion in cells of an erythropoietic row by a mikropinotsitoz from reticular macrophages or direct transfer from transferrin through receptor sites of reticulocytes decreases. At the same time receipt in a cell of the iron necessary for synthesis gem decreases.

Gem is a consequence of shortage of iron for synthesis increase in protoporphyrin in erythrocytes at some forms Zh. and. In the conditions of deficit of iron its reserves will be mobilized for needs of an erythrogenesis that leads to reduction, in particular, of marrowy depot of iron. Disturbance of education gem and gemoglobinization of erythroblasts is a final phase of the insufficiency of an erythrogenesis caused by true or redistribution deficit of iron in an organism.

Pathological anatomy

Patomorfol, changes in bodies and fabrics at. and. depend on the basic disease which caused true deficit of iron or on the infectious, toxic, blastomatous processes leading to redistribution deficit of iron. Directly the following changes are connected with deficit of iron.

Gistol, research of marrow by method trepanobiopsiya (see) finds a normal structure or a moderate hyperplasia with reduction of content of fatty tissue unlike hypo - and aplastic anemias (see. Hypoplastic anemia ). During the coloring on Perlsa granules of hemosiderin are not found that indicates exinanition of reserves of iron. At a long current. and. the hyperplasia of a red sprout is combined with disturbance of maturing of cells of an erythroidal row — basphilic erythroblasts and microgeneration of normoblasts prevail. Disturbances of a gemoglobinization (ferriprivny erythroblasts) and dystrophic changes of an erythrogenesis are a consequence of cellular deficit of iron.

Changes in other bodies are connected with disturbance of enzymatic processes and a long anemic hypoxia. Atrophic processes are characteristic in went. - kish. path, especially atrophic gastritis. Along with atrophic gastritis changes of an oral cavity (a glossitis, a cheilitis, an ulitis, a hyperkeratosis and vacuolation of cells of an epithelium of a mucous membrane of cheeks, damage of teeth owing to disturbance of exchange of enamel), the damages of a mucous membrane of a gullet which are the cornerstone of a sideropenic dysphagy and confirmed with an aspiration biopsy are described.

As a result of decrease in content of iron, reduction of a myoglobin and falling of activity of ferriferous enzymes of tissue respiration at. and. after adaptive functional changes of cardiovascular system true dystrophy of a myocardium can develop.

The long anemic hypoxia leads to fatty infiltration of a liver and other bodies.

Clinical picture

Course of a disease chronic recurrent. Pallor of skin and mucous membranes, puffiness of the person, weakness, physical are characteristic. fatigue and mental slackness, an asthma at the movements, frequent dizzinesses, a sonitus.

Hron, oxygen insufficiency of fabrics in connection with anemia leads to disturbance of a functional condition of a liver, cardiac muscle and other bodies. At objective inspection tachycardia, anemic cordial noise (the systolic noise on a top caused by decrease in viscosity of blood), a nun's murmur on jugular veins, increase in speed of a blood-groove are noted. On an ECG symptoms of a diffusion hypoxia of a myocardium, at polycardiography (see) — decrease in sokratitelny function of a myocardium at is long the existing anemia. Deficit of iron is shown by a food faddism (pica chlorotica) — addiction to chalk in different types, sometimes to coal, a lime, dry grain; the patient likes smells of kerosene, gasoline, exhaust gases; trophic changes of nails are characteristic — longitudinal or cross striation appears, sometimes nails become spoon-shaped (koilonychia); the sideropenic dysphagy develops (Rossolimo's symptom — Bekhterev or Plummer — Vinsona). At an ezofagoskopiya and rentgenol, a research atrophic changes of a mucous membrane of a throat and gullet and spastic narrowing of its initial part are visible. The listed symptoms quite often are found already in a stage of a latent hyposiderosis and precede development of anemia.

Picture of blood it is characterized by hypochromia anemia — decrease in concentration of hemoglobin and a low color indicator (0,6 — 0,5 and below). The number of erythrocytes can be normal, but usually also decreases, though to a lesser extent, than hemoglobin. The hypochromia of erythrocytes, their macrocytosis, anizopoykilotsitoz is morphologically noted (see. Gemogramma ). In the presence of a macrocytosis with a hypochromia of erythrocytes it is possible to assume a combination of deficit of iron and B 12 - vitamin deficiency.

The diagnosis

the Diagnosis is made on the basis of the described symptoms and results of special researches. 1. Definition of serumal iron, OZhSS and LZhSS with calculation of percent of saturation of transferrin; increase in OZhSS and especially LZhSS with decrease in serumal iron and percent of saturation of transferrin testifies to the iron deficiency nature of anemia or existence of latent deficit of iron without anemia; the atransferrinemiya or a combination of proteinoprivny and iron deficiency genesis of anemia can lead to decrease in OZhSS along with a hyposideremia. 2. Definition of reserves of iron by introduction to an organism of a complexon of desferal (desferrioksamin) which, connecting to negemoglobinovy iron of fabrics, brings him out of depot in a blood channel and is allocated with urine: reduction of uric excretion of iron at desferalovy test speaks about exhaustion of reserves of iron in an organism at. and., finds their decrease at latent deficit of iron, allows to control replenishment of reserves at a ferrotherapy; desferalovy test differentiates true and redistribution deficit of iron — at the last uric excretion of iron is raised, despite a hyposideremia (blocking of iron in reticulohistocytosis system). 3. Definition of marrowy reserves of iron (sideroblasts and siderocytes): intracellular negemoglobinovy iron of marrow can be investigated with the help not only light, but also the submicroscopy allowing to track process of inclusion of iron in erythroidal cells by a mikropinotsitoz and to establish transition of its granules to mitochondrions. 4. Studying of porphyrinic exchange (see. Porphyrines ), which is connected with exchange of iron in synthesis gem: at true. and. increase in porphyrines, especially free protoporphyrins, in erythrocytes is often noted; at infectious anemias owing to disturbance of porphyrinic exchange increase in coproporphyrin and decrease in protoporphyrin prevails

. and. it is necessary to differentiate with zhelezorefrakterny anemia (see), proceeding with a hypochromia of erythrocytes. For specification of nature of disturbance of exchange of iron determine the level of transport iron of serum, carry out desferalovy test, count quantity of siderocytes and sideroblasts of marrow.

Treatment

Treatment shall be directed to elimination of the reasons of anemia (the termination and the prevention to blood loss if necessary — operational removal of their source; treatment of diseases of a stomach and intestines etc.) and on elimination of deficit of iron (ferrotherapy).

For a peroral ferrotherapy a number of drugs is used. Haemostimulinum, Ferroceronum and complex drugs of ferrous sulfate are most effective and well transferable.

Ascorbic to - that, appointed along with iron preparations or being their part, provides the best digestion of iron. Simultaneous injections of vitamin B are useful 6 and reception folic to - you. If lag of growth of number of erythrocytes is observed, then administration of polyneuramin can be recommended 12 at the end of a course of a ferrotherapy.

Parenteral to a ferrotherapy it is shown at intolerance of administration of drugs of iron inside, their inefficiencies, an agastria, at contraindications to peroral therapy (ulcer and inflammatory processes in went. - kish. a path), the heavy anemia demanding bystry stopping (in the preoperative or prenatal period). For intramuscular introduction are recommended ferbitol or an ektofer; for intravenous administration — ferkoven or ferrum Lek. Ampoules of these drugs contain about 100 mg of iron. The number of injections is calculated by the formula given in the special instruction (usually from 15 to 30 injections).

Criterion of efficiency of a ferrotherapy is increase in hemoglobin (on 0,15 — 0,3 g of % a day. Duration of a course of treatment depends on normalization of serumal iron, and in a wedge, conditions the depot of iron on desferalovy test is investigated.

A hematotherapy at. and. it is applied at deep anemia and need of bystry stopping of an anemic hypoxia, and also at hyporegenerative forms, resistant to a ferrotherapy. Transfusions of eritrotsitny weight on 125 — 150 ml 2 times a week in number of 3 — 4 transfusions are preferable. Good nutrition is recommended.

The forecast

the Forecast for life favorable. In the presence of certain premises (repeated bleedings, existence of atrophic gastritis, etc.) there is recurrence. and.

Prevention

Prevention of a recurrence. and. — repeated courses of a ferrotherapy within 1 — 1,5 month 2 times a year or are more often. At the established latent deficit of iron among the inspected group of the population or existence of premises dlitelnopreryvisty preventive courses of a ferrotherapy are recommended for its development (donors, it is long giving blood, women with menorrhagias, an agastria or an organic achlorhydria) (1 four-week and 3 two-week course a year).

Food, protein-rich, is recommended by vitamins, iron and other microelements (fruit). Stay in mountains is useful; long insolation is contraindicated.

Features of an iron deficiency anemia at children

85 — 90%. and. at children (according to pediatric clinics) it is the share of age up to 3 years. Changes of a hemoglobin content and quantity of erythrocytes for the first years of life of the child are defined by the speed of his growth, balance of iron in an organism, changes of an erythrogenesis after the birth and, at last, changes of longevity of erythrocytes. For this period there is a reduction of quantity of erythrocytes of blood and a hemoglobin content twice: the first call early, and the second — late anemia of children of younger age.

Early, physiological, anemia at the full-term newborns comes at the age of 2,5 — 3 months, and at premature — in 1,5 — 2 months and even earlier. Late anemia can come at normal full-term children after the deposited iron completely is utilized, by the end 4 — the 5th month of life later. More often it is observed at quickly growing children, at children who a long time are fed with one dairy products, and also at the children who were born from mothers who had anemia.

At premature and full-term children indicators of red blood are various. In an organism of the premature child the smaller amount of iron at the birth (the full-term child is born with a high level of hemoglobin — to 23 g of %) is noted and it more rapid growth within the first year of life. This results from the fact that iron begins to collect especially quickly in an organism only in the last 3 months of an antenatal life, and prematurity in 1 — 2 month can lead to reduction of reserves of iron by 1,5 — 2 times and more in comparison with norm. The accessory factors strengthening anemia of premature children are the reactivity of marrow lowered in comparison with the full-term children and smaller life expectancy of erythrocytes.

The disease usually comes to light in the presence of heavy anemia. The main symptoms — pallor of integuments and visible mucous membranes, lack of appetite, the slowed-down increase in weight, a hypomyotonia, went. - kish. frustration. Gepatosplenomegaliya takes place only in 10% of cases, and a delay physical. development — at 20% of children. As well as at other anemias, small systolic (anemic) noise during the listening of heart is quite often noted. Symptoms of defeat of epithelial fabrics (fragility of nails and their concave shape, roughness of skin, fragility of hair) and mucous membranes occur at children of advanced age (an atrophy of nipples of language, an erosion in corners of a mouth etc.).

In blood reduction of quantity of erythrocytes, average content of hemoglobin in an erythrocyte, a color indicator (0,4 — 0,6), a hypochromia and a microcythemia is noted. Disturbance of a gemoglobinoobrazovaniye leads to reduction of volume of erythrocytes that in combination with reduction of their quantity leads to considerable reduction of gematokritny number. It is noted anizopoykilotsitoz erythrocytes. As well as at adults, the most characteristic change at. and. reduction of concentration of iron in serum and increase in LZhSS and OZhSS is. In marrow the hyperplasia of an erythrogenesis with dominance of either polychromatophilous, or oxyphilic normoblasts is observed.

The diagnosis is made on the basis a wedge, this and characteristic gematol. indicators.

Treatment. and. at children as well as at adults, it has to be directed to elimination of the reasons of anemia and to elimination of deficit of iron. Much attention should be paid to correction of food. Iron preparations enter inside, intramusculary and intravenously. Use of the drugs containing bivalent protoxidic iron (ironic lactate, Haemostimulinum and others on 0,1 — 0,3 g 3 — 4 times a day), in combination with ascorbic to - that is preferable. Haemostimulinum containing ironic lactate, cuprous sulfate, glucose and dry hematogen has good effect (on 0,1 — 0,5 g 3 times a day). It is reasonable to appoint iron preparations in intervals between meals — 3 — 4 times a day.

The need for transfusions of blood arises seldom; only at very heavy anemias or serious associated diseases, and also in cases of insufficient efficiency of treatment by iron preparations pour eritrotsitny weight.

Premature children in all cases need to administer iron preparations preventively.


Bibliography: Alperin P. M., Mukhametdinova G. M. and Mikhaylova L. I. Reserves of iron at patients with chronic iron deficiency anemias, Probl, gematol, and a modulation, blood, t. 17, No. I, page 34, 1972, bibliogr.; An iron deficiency anemia and some questions of regulation of an erythrogenesis, under the editorship of S. I. Ryabov, L., 1970; Istamanova T. S., Diamonds B. And. and Kanayev S. V. Functional hematology, page 10, 235, L., 1973; Kassirsky I. A. and Alekseev G. A. Clinical hematology, page 50, 149, M., 1970; Lavkovich V., etc. Hematology of children's age, the lane with polsk., Warsaw, 1964; M about with I and - N of an E. H. Anemias of children's age, M., 1969; Pleshkov A. M. About prevention of iron deficiency anemias, Owls. medical, No. 5, page 100, 1970; P y with with E. S. Anemias and digestive tract, page 72, L., 1972; Ryabov S. I. Fundamentals of physiology and pathology of an erythrogenesis, L., 1971, bibliogr.; Ryabov S. I. and Sh about with t to and G. D. Molecular and genetic aspects of an erythrogenesis, page 5, 147, L., 1973; Tarasov O. F. An anemia at children, L., 1960; Shch e r and M. M., etc. Iron deficiency states, L., 1975, bibliogr.; Iron deficiency, pathogenesis, clinical aspects, therapy, ed. by L. Hallberg a. o., L. — N. Y., 1970; W i n t r o b e M. M. and. lake of Clinical hematology, Philadelphia, 1974, bibliogr.

P. M. Alperin; I. V. Koshel (ped.).

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