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Iron deficiency anemias - Practical hematology of children's age

Table of contents
Practical hematology of children's age
Embryonal hemopoiesis
Morfofunktsionalny characteristic of cells of marrow and peripheral blood
Marrow parenchyma cells
Peripheral blood of children of different age
The system of a hemostasis is normal
Etiology and pathogeny of leukoses
Acute leukoses
Acute leukoses - a preleukosis
Possibilities of a predictive assessment of a course of an acute lymphoblastoid leukosis at children
General principles of treatment of an acute leukosis
Chemotherapeutic drugs
Treatment of an acute lymphoblastoid leukosis
Treatment of myeloid forms of an acute leukosis
Infectious complications and symptomatic therapy of an acute leukosis
Consolidation and maintenance therapy of an acute leukosis
Remission and recurrence of an acute leukosis
Inborn leukosis
Macrofollicular lymphoma
Angioimmunoblastny lymphadenopathy
Leukemoid tests
Infectious lymphocytosis
Infectious mononucleosis
Leukemoid tests of different types
Dysfunctions of granulocytes
Histiocytoses - an eosinophilic granuloma
Malignant histiocytosis
Family erythrophagocytal histiocytosis
Accumulation diseases
Nimann's illness — Peak
Hemorrhagic vasculitis (Shenleyn's illness — Genokh)
Mayokki's purpura
Ataxy teleangiectasia
Entsefalotrigeminalny angiomatosis
Kortiko-meningealny diffusion angiomatosis
Cerebroretinal angiomatosis
Hypertrophic gemangiektaziya
Multiple and huge hemangiomas
Elastic fibrodisplaziya
Hereditary coagulopathies
Hemophilia And
Clinic of hemophilia
Treatment of hemophilia
Cristmas disease (Kristmas's illness)
Hereditary deficit of factors of XI, XII, XIII and I
Hereditary deficit of factors of VII, X, V and II
Deficit K-vitaminozavisimykh of factors of coagulation
Syndrome of the disseminated intravascular coagulation
Clinic and diagnosis of the IDCS
Treatment of the IDCS
Idiopathic Werlhof's disease
Clinic and diagnosis of an idiopathic Werlhof's disease
Treatment of an idiopathic Werlhof's disease
Isoimmune Werlhof's disease
Transimmune Werlhof's disease of newborns
Trombogemolitichesky Werlhof's disease (syndrome Moshkovich)
Hereditary Werlhof's diseases
The anemias connected with blood loss
Chronic posthemorrhagic anemia
Iron deficiency anemias
Clinic and diagnosis of an iron deficiency anemia
Treatment of iron deficiency anemias
Sideroakhrestichesky, sideroblastny anemias
Megaloblastny anemias
Foliyevodefitsitny anemia
Hereditary forms of megaloblastny anemias
Hereditary dizeritropoetichesky anemias
The anemias connected with oppression of proliferation of cells of marrow
Hereditary hypoplastic anemias
Hemolitic anemias
Hemolitic anemias - an ovalocytosis, a hereditary stomatocytosis
Acanthocytosis, piknotsitoz
The hereditary hemolitic anemias connected with disturbance of activity of enzymes of erythrocytes
The hereditary hemolitic anemias connected with disturbance of structure or synthesis of hemoglobin
The acquired immune hemolitic anemias
Isoimmune hemolitic anemias
Treatment of a hemolitic illness of newborns
Autoimmune hemolitic anemias
List of references

Iron deficiency anemias
There are two forms of deficit of iron — latent deficit of iron, that is the isolated deficit of iron in fabrics without anemia, and an iron deficiency anemia.
Iron deficiency anemias are very widespread pathology as among children's, and adult population. According to various authors, the frequency of iron deficiency anemias at children fluctuates from 10 to 70%. At children's age allocate two periods of which especially high frequency of iron deficiency anemias is characteristic: these are the first two years of life when the iron deficiency anemia is registered in 40% of cases, and the pubertal period in which anemia is observed at 1/3 children (L. M. Kazakova, 1984). Prevalence of deficit of iron among children in general makes 32,4% (Yu. E. Malakhovsky, 1981). At children of the first three years deficit of iron is noted at a half, preschool age — at 1/3 and inspected (G. V. Babash, 1980; Yu. E. Malakhovsky and soavt., 1980).
What role of iron in an organism? Iron is a part of various proteins of an organism, including hemoglobin. Hemoglobin consists of two parts: nonprotein part — gem and proteinaceous part — a globin. Gem is a part not only hemoglobin. In a final form of gems represents strong compound of iron with a porphyrinic ring. It contains in muscles (myoglobin), is a part of tsitokhrom, catalases. In a negemovy form iron contains in a number of enzymes. The main proteins containing negemovy iron are ferritin and transferrin.
The fruit receives iron from mother. Deposition of iron begins already in early durations of gestation, however most intensively it to collect before childbirth in recent months. After the birth the organism receives iron with food. Most of researchers consider that capture of iron can happen on all length of a small bowel, but the main amount of iron is soaked up in duodenal and in upper parts of a small bowel. The regulating mechanism of absorption is the total quantity of iron in an organism. At exhaustion of reserves of iron its absorption in guts kompensatorno increases, and the zone of its active absorption also extends (M. of S. Wheby, 1970). At children of early age at iron deficiency states absorption of iron does not increase, and, on the contrary, decreases. It is connected with the fact that ferriferous enzymes of guts which synthesis in the conditions of deficit is reduced participate in digestion of iron from milk. From total quantity of the food iron coming to an organism in normal conditions 10% are soaked up. And iron is better soaked up from the meat products (9 — 22%) containing gemovy iron and it is much worse — from vegetable (0,4 — 5%) where there is a negemovy iron. Content of iron in women's milk low — 1,5 mg/l. However absorption of iron from breast milk is unique. Besides, breast milk increases absorption of iron from other products accepted along with it.


Fig. 24. Scheme of regulation of absorption of iron
Схема регуляции всасывания железа
The iron absorption mechanism — difficult process and is finally not studied now. The ternary hypothesis of absorption of iron (fig. 24) was offered m of S. Wheby (1966). The component A — iron comes from a gut gleam to a mucous membrane; the component B — iron is transferred from cells of a mucous membrane of a gut to plasma; the component C — iron collects in a mucous membrane and the available stocks influence absorption. In regulation of the mechanism of absorption the ratio of speed of intake of iron in a mucous membrane of a gut and speed of its transfer in plasma is of great importance. The last always less, but more depends on needs of an organism for iron, than iron capture process by a mucous membrane of guts. At an organism overload iron it collects in a mucous membrane of a gut, and the speed of capture is less, than normal. Still more the speed of transfer of iron from a mucous membrane in plasma decreases. Further the epithelial cell saturated with iron is exfoliated and removed with a stake. At deficit of iron in an organism the speed of its transfer from a mucous membrane of a gut in plasma approaches the speed of intake of iron in a mucous membrane. At the same time iron is almost not laid in store. The initial stage of digestion of iron, capture of a gut is carried out by his mucous membrane by active absorption. The big role in it belongs to a cellular border.
Until recently considered that are of great importance for absorption iron valency, recovery of an oxide form (Fe + + +) in a protoxidic form (Fe + +) under the influence of Acidum hydrochloricum and a gastric juice. Now the supporting role is assigned to this process. It is established that crucial importance has not the valency of iron, but its solubility in a duodenum at alkali reaction (T. N. to Bothwell, R. W. Charlton, 1970). The gastric juice and Acidum hydrochloricum participate in iron absorption, provide recovery it, ionization, formation of components, available to absorption, but it belongs only to negemovy iron and is not the main mechanism of regulation of absorption. Process of absorption of gemovy iron is excellent and does not depend on gastric secretion. Gemovy iron is soaked up in the form of porphyrinic structure and only in a mucous membrane of a gut there is its eliminating from gem and formation of the ionized iron (N. A. Huebers, 1986).
The following stage — transition of iron to plasma. According to the concept
P. H. Pinkerton (1969), transfer of iron in plasma is enzymatic reaction. In an epithelial cell special "carrier" which through membranes transfers iron to plasma is formed. Further transfer of iron in marrow follows. It is carried out by transport protein — transferrin. Transferrin also transfers iron from funds and the englobing macrophages where there is a destruction of erythrocytes, to cells of an erythroidal number of marrow and to places of storage of iron. In erythroidal cells of marrow iron takes part in synthesis gem. In the same place from protein of the apoferritin and excess iron which did not be a part of hemoglobin ferritin which leaves afterwards an erythroidal cell and is one of the chief keepers of iron in an organism is synthesized. At death of erythrocytes iron is taken the englobing macrophages where the complex with protein — hemosiderin is formed. Iron of ferritinovy and gemosiderinovy complexes partially is used again for an erythrocytopoiesis, its other part is deposited in reticulohistocytosis system of a liver and spleen. In muscles the most part of iron is in a ferritinovy complex, other iron is a part of hemoglobin. In an organism there are following funds of iron: 1) gemoglobinovy, or erythrocyte, the fund provided by hemoglobin iron (main); 2) the reserve fund is the iron which is a part of ferritin and hemosiderin which are deposited in a liver, a spleen, muscles, marrow. The reserve fund allocates two pools: a) labile which will easily be mobilized for needs of an erythrocytopoiesis; b) stable which is strongly fixed in an organism; 3) the transport fund provided by the iron connected with transferrin; 4) the fabric fund is the iron which is a part of a myoglobin, ferriferous enzymes (cytochrome, a catalase, peroxidase, a succinatedehydrogenase) and not fermental ferriferous biocatalysts (fig. 25).
Losses of iron in normal conditions at adults make about 1 mg, children of early age have 0,1 — 0,15 mg/days. Iron is lost with a stake, urine, then. Pathological losses of iron are caused by blood loss.
The reasons of iron deficiency anemias at children are various. It is possible to allocate several main pathogenetic mechanisms.

  1. Insufficient reserves of iron. According to many authors, it plays a large role in development of an iron deficiency anemia in children of early age. The healthy full-term child is born with the general fund of iron, equal 250 mg (70 — 75 mg/kg) and the received way of transplatsetarny transfer from mother. Neonatal reserves of iron satisfy requirement of a haemo cytopoiesis within 3 — 5 months. The mechanism of transplacental transfer is stable and does not depend on concentration of iron at mother, that is existence of an iron deficiency anemia at mother does not exert impact on forming of depot of iron at a fruit (S. Baker, E. De Maeger, 1979). However transplacental transfer of iron to a fruit is broken at heavy toxicoses, blood losses, a hypoxia at mother. Initial level of iron in an organism of a fruit decreases at chronic feto-maternal bleeding and he can be born with an iron deficiency anemia.

Схема обмена железа
Fig. 25. Scheme of an exchange of iron (E. S. Ryss, 1976)

Antenatal insufficiency of iron is connected with development of anemia in children from polycarpous pregnancy and late anemia — at premature. It is established that concentration of iron at the full-term and premature child is identical and makes 70 — 75 mg/kg of body weight. But the absolute general fund of iron at premature children or twins is less. The amount of missing iron in direct ratio to deficit of body weight also makes the same 70 — 75 mg/kg of weight, that is at the child with the body weight of 2 kg the total quantity of iron makes 150 mg, weighing 1,5 kg — 100 — 120 mg. At the full-term newborn the organism contains 200 — 250 mg of iron. For maintenance of normal concentration of hemoglobin and increase in depot of iron by the end of the year to the full-term children the iron arriving with food on condition of the correct feeding suffices. Premature children or children from polycarpous pregnancy differ in more intensive growth rate and in the second half of the year catch up on physical constants of the full-term children. However for achievement of normal concentration of hemoglobin the premature child needs additional absorption of iron (120 — 150 mg) which was half-received during the neonatal period. Even rational feeding cannot satisfy the increased need for iron that inevitably leads to development of an iron deficiency anemia. In development of early anemia premature deficit of iron undoubtedly plays a part (Jl. M. Kazakova, 1979). However the pathogeny of this disease is difficult and diverse. At early anemia premature antenatal deficit of a number of microelements, defects of the enzymatic systems regulating a fruit metabolism, gemological process etc. are noted (G. F. Sultanova, 1978).
A number of authors consider that antenatal insufficiency of iron plays a role in development of iron deficiency states and in children at advanced age (N. I. Ushakova, 1975; I. S. Tiganova and soavt., 1977). However later researches showed that adverse antenatal factors do not increase risk of emergence of iron deficiency states at children 2 years are more senior (G. V. Babash, 1980; Yu. E. Malakhovsky and soavt., 1980).

  1. The increased needs of an organism for iron. As it was already noted, this reason works with an intensive growth at premature and at children from polycarpous pregnancy when even normal intake of iron with food does not provide requirement of quickly growing organism. Increase of need of an organism for iron can be combined with other reasons (chronic blood loss, alimentary deficit). High frequency of anemia is also noted at large babies, rate of increase of weight and which growth on the first year of life considerably exceeds the standard standards.
  2. The increased losses of iron from an organism. At children normal loss of iron makes on the first year of life 0,07 — 0,1 mg, in 1 — 4 years — 0,15 mg, in 5 — 8 years — 0,2 mg, in 9 — 12 years — 0,3 mg; during puberty boys — 0,5 mg, at girls have 1 — 3 mg a day. In pathological conditions iron is lost with blood. In essence chronic posthemorrhagic anemia is an iron deficiency anemia. Blood loss — the most frequent reason of development of iron deficiency states in adults, however at children this reason does not play the leading role. Its greatest importance is shown at girls of advanced age after establishment of periods.
  3. Disturbance of absorption and transport of iron. Disturbance of absorption of iron is caused by pathology of a digestive tract, first of all inflammatory processes — enteritis, a coloenteritis, a gastroenteritis, a duodenitis. Now it is proved that gastric secretion does not influence iron absorption process. At children digestion of iron is reduced at hereditarily the caused syndromes of insufficient absorption (malabsorption). Therefore at a Gee's disease, a mucoviscidosis with intestinal manifestations often accompanying syndrome is the hypochromia iron deficiency anemia. Disturbance of digestion of iron is also noted at the children having exudative diathesis as a result of exfoliating of an epithelium of a mucous membrane of a digestive tract. Among the reasons of development of anemia of disturbance of absorption of iron are noted seldom. The disturbance of transport of iron connected with a hereditary atransferrinemiya or development of antibodies to transferrin is even less often observed.
  4. The disturbance of regulation of an exchange of iron caused by influence of internal causes. It is observed at children of pubertal age that it is connected with a hormonal imbalance.
  5. Insufficient intake of iron with food serves as the most frequent reason of development of anemia in children of the first years of life. It is necessary to emphasize that conditions of a feeding schedule, features of feeding play an extremely important role in forming of iron deficiency anemias at children. Unlike adults at children balance of iron positive as it is necessary not only for completion of physiological losses, but also for needs of the growing organism. The daily need of children on 1 — the 2nd year of life makes 7 — 8 mg of food iron (0,5 — 1 mg/kg of weight a day). In breast milk the content of iron, despite its maximum absorption, low — 1,5 mg/l, in cow's milk and that are less — 0,5 mg/l. And absorption of iron from the cow's milk and mixes prepared on its basis is 2 — 3 times lower, than from breast milk. The first half of the year of life the child compensates exogenous deficit of iron at the expense of the endogenous stocks received from mother. In the second half of the year the food becomes the main supplier of iron and the iron deficiency anemia can develop in this period at unbalanced feeding.

It is necessary to notice that at some feeding women (to 10%) concentration of iron in milk low (less than 1 mg/l) what is also the factor promoting deficit of iron. Now in connection with broad implementation of the adapted milk mixes the importance of artificial feeding in development of iron deficiency anemias decreases. The main place among the reasons causing insufficient intake of iron belongs irrational feeding of children — unilateral milk and flour food, absence in a diet of meat dishes. And the wrong feeding plays a role in development of deficit of iron not only in children of younger, but also advanced age. It is noted that at school students of one of the reasons of latent deficit of iron vegetarianism is, and among all age groups every fourth child with latent deficit of iron is a vegetarian (G. V. Babash and soavt., 1980; Yu. E. Malakhovsky, 1981).
Researches of cellular kinetics of erythron at iron deficiency anemias showed reduction of an effective erythrocytopoiesis (S. I. Ryabov, G. D. Shostka, 1973). Daily products of erythrocytes decrease, proliferative activity of erythron decreases, the level of an inefficient erythrocytopoiesis increases. At a stage of basphilic erythroblasts the strengthening of proliferation of erythroidal cells which is followed by defect of maturing is noted. The quantity of polychromatophilous erythroblasts decreases (G. I. Kozinets, I. A. Bykova, T. G. Sukiasova, 1982).
The erythron kinetics at iron deficiency anemias is also characterized by reduction of average life expectancy of erythrocytes though hemolysis is expressed very slightly (Ya. D. Sakhibov, 1981). According to L. M. Kazakova (1982), extent of hemolysis in many respects is defined by weight of an iron deficiency anemia. Considerable reduction of average life expectancy of erythrocytes was observed only at deep anemia.
In recent years in pediatric practice deficit of iron is connected with the increased infectious incidence. According to S. M. Chumachenko's data (1977), S. V. Shangutov (1977), V. I. Kalinicheva (1978), V. P. Bisyarina and M. M. Kazakova (1979), J. D. Cook, T. Lynch (1986), one of adverse effects of deficit of iron is the raised susceptibility of children to infectious and inflammatory diseases. The prevalence respiratory infections and gastrointestinal diseases, suffering from an iron deficiency anemia, is 2 — 4 times more, than at healthy. The increased incidence of acute respiratory infections is also noted at children with latent deficit of iron (G. V. Babash and soavt., 1980). According to a number of authors, the fact of the raised susceptibility to infections at iron deficiency states is finally not proved as the available data are based on anamnestic data without background states (Yu. E. Malakhovsky and soavt., 1982).
Disputable is a question of a condition of an immune responsiveness of the children suffering from an iron deficiency anemia. A number of authors note defects of phagocytal system of neutrocytes. (R. To. Chandra and soavt., 1977; J. Prasad, 1979) which are generally caused by disturbance of the bactericidal function of leukocytes connected with decrease of the activity of ferriferous enzyme of a miyeloperoksidaza. The disturbances of a cellular link of immunity at iron deficiency anemias consisting in decrease in maintenance of T lymphocytes are revealed (M. Baggi and soavt., 1980). According to T. 3. Marchenko (1983), at the children of early age suffering from an iron deficiency anemia broke a ratio of separate populations of lymphocytes: the maintenance of Ti of V-lymphocytes is reduced and the quantity of zero cells is at the same time increased. And parallelism between degree of ratio distortion of cell populations of lymphocytes and severity of anemia is established.
However there is also other point of view. According to researches Yu. E. Malakhovsky and coauthors (1983), the immune response at the children suffering from an iron deficiency anemia does not depend on the level of hemoglobin and indicators of an exchange of serumal iron. To correlative communication between degree of deficit and frequency of developing of an acute respiratory viral infection it is not established. At children with anemia the infection arises not more often than at healthy. And the specified authors consider repeated infections as the reason, but not as a result of iron deficiency anemias, considering that infectious processes are the factor promoting development of anemia. In turn, against anemia the frequency of associated diseases and complications increases. Authors see possible communication of anemia with respiratory diseases not in disturbance of an immune responsiveness, and in the insolvency of an epithelium (epiteliopatiya) caused by a hyposiderosis. Disturbance of barrier function of an epithelium of upper respiratory tracts, easing of its protective properties can lead to development of an acute respiratory viral infection.

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