Iron in serum
The total iron content in the human body is approximately 4.2 g. About 75-80% of the total amount of iron is included in Hb, 20-25% of iron are reserve, 5-10% are part of myoglobin, 1% is contained inrespiratory enzymes that catalyze respiration in cells and tissues. Reference values of iron concentration in serum are given in Table.[Tiz U., 1997].Iron performs its biological function, mainly in the composition of other biologically active compounds, mainly enzymes. Iron-containing enzymes perform four main functions:
■ electron transport( cytochromes, iron-speroproteins);
■ oxygen transport and storage( Hb, myoglobin);
■ participation in the formation of active centers of oxidation-reduction enzymes( oxidases, hydroxylases, SOD, etc.);
■ transport and deposition of iron( transferrin, hemosiderin, ferritin).
The homeostasis of iron in the body is provided, first of all, by regulation of its absorption in connection with the limited ability of the organism to isolate this element.
There is a pronounced inverse relationship between the provision of the human body with iron and its absorption in the digestive tract. Absorption of iron depends on:
■ age, body iron availability;
■ Gastrointestinal status;
■ Quantities and chemical forms of incoming iron;
■ quantities and forms of other food components.
Table Reference values for serum iron concentration
Table Reference values for serum iron concentration
For optimal absorption of iron, normal gastric juice secretion is necessary. The intake of hydrochloric acid facilitates the assimilation of iron in the case of achlorhydria. Ascorbic acid, reducing iron and forming with it chelate complexes, increases the availability of this element, as well as other organic acids. Another component of food that improves iron absorption is the "animal protein factor".Improving the absorption of iron simple carbohydrates: lactose, fructose, sorbitol, as well as amino acids such as histidine, lysine, cysteine, which form easily absorbed chelates with iron. Absorption of iron reduces such beverages as coffee and tea, the polyphenolic compounds of which firmly bind this element. Therefore, tea is used to prevent increased iron absorption in patients with thalassemia. A great influence on the absorption of iron has various diseases. It increases with iron deficiency, anemia( hemolytic, aplastic, pernicious), hypovitaminosis B6, and hemochromatosis, which is explained by increased erythropoiesis, depletion of iron stores and hypoxia.
Modern ideas of iron absorption in the intestine allot to a central role for two kinds of transferrin - mucous and plasma. Mucosal apotransferrin is secreted by enterocytes into the lumen of the intestine, where it combines with iron, and then enters the enterocyte. In the latter, he is freed from iron, and then enters a new cycle. Mucosal transferrin is formed not in enterocytes, but in the liver, from which this protein enters the intestine with bile. On the basal side of the enterocyte, mucosal transferrin gives iron to its plasma analogue. In the cytosol of the enterocyte, some iron is included in ferritin, most of it is lost when the mucous membrane cells are clotted every 3-4 days, and only a small part passes into the blood plasma. Before being included in ferritin or transferrin, ferrous iron is converted into a trivalent iron. The most intense absorption of iron occurs in the proximal parts of the small intestine( in the duodenum and lean).Plasma transferrin delivers iron to tissues that have specific receptors. The inclusion of iron in the cell is preceded by the binding of transferrin by specific membrane receptors, in the loss of which, for example in mature erythema
, the cell loses its ability to absorb this element. The amount of iron entering the cell is directly proportional to the number of membrane receptors. The cell releases iron from transferrin. Then the plasma apotransferrin returns to circulation. The increase in the requirement of cells in the gland with their rapid growth or synthesis of Hb leads to the induction of the biosynthesis of transferrin receptors, and on the contrary, with an increase in iron stores in the cell, the number of receptors on its surface decreases. Iron released from the transferrin inside the cell binds to ferritin, which delivers iron to the mitochondria, where it is incorporated into the heme and other compounds.
In the human body there is a constant redistribution of iron. Quantitatively, the metabolic cycle is of greatest importance: plasma, red bone marrow, erythrocytes, plasma. In addition, the cycles are functioning: plasma ^ ferritin, hemosiderin ^ plasma and plasma ^ myoglobin, iron-containing enzymes ^ plasma. All these three cycles are interconnected through the iron of plasma( transferrin), which regulates the distribution of this element in the body. Usually 70% of the plasma iron enters the red bone marrow. Due to the disintegration of Hb, approximately 21-24 mg of iron is released per day, which is many times higher than the intake of iron from the digestive tract( 1-2 mg / day).More than 95% of the iron enters the plasma from the system of mononuclear phagocytes, which absorb by phagocytosis more than 1011 old erythrocytes per day. Iron, which enters the cells of mononuclear phagocytes, either quickly returns to circulation in the form of ferritin, or is stored in reserve. Intermediate iron exchange is primarily associated with the processes of synthesis and decomposition of Hb, in which the system of mononuclear phagocytes plays a central role. In an adult human in the bone marrow, iron transferrin, using specific receptors, is included in the normocytes and reticulocytes, which use it for the synthesis of Hb. Hb, which enters the blood plasma during the decay of erythrocytes, specifically binds to haptoglobin, which prevents its filtration through the kidneys. The iron released after the disintegration of Hb in the mononuclear phagocyte system again binds to transferrin and enters a new cycle of Hb synthesis. In other tissues, transferrin delivers 4 times less iron than red bone marrow. The total content of iron in the composition of Hb is 3000 mg, myoglobin contains 125 mg of iron, in the liver - 700 mg( mainly in the form of ferritin).
Iron is excreted from the body mainly by mothballing the intestinal mucosa and with bile. Also it is lost with hair, nails, urine and sweat. The total amount of iron so allocated in a healthy man is 0.6-1 mg / day, and in women of reproductive age - more than 1.5 mg. The same amount of iron is absorbed from food( 5-10% of its total content in the diet).Iron from animal food is digested several times better than from plant food. The concentration of iron has a diurnal rhythm, and women have a connection with the menstrual cycle. When pregnancy, the iron content in the body decreases, especially in the second half.
Thus, the concentration of iron in the serum depends on the resorption in the digestive tract, accumulation in the intestine, spleen and red bone marrow, from the synthesis and decomposition of Hb and its loss by the body.
In some pathological conditions and diseases, the content of iron in serum varies. In Table.presents the main signs of iron deficiency and excess in the human body.
Table Major diseases, syndromes, signs of iron deficiency and excess in the human body
Table Major diseases, syndromes, signs of deficiency and excess iron in the human body
Iron deficiency( hypoxidosis, iron deficiency anemia) is one of the most common human diseases. The forms of their clinical manifestations are diverse and range from latent conditions to severe progressive diseases that can lead to typical organ and tissue damage and even to death. At present, it is generally accepted that the diagnosis of iron deficiency states should be made before the development of the complete picture of the disease, that is, before the onset of hypochromic anemia. When the deficiency of iron affects the whole body, and hypochromic anemia - late stage of the disease.
Modern methods for the early diagnosis of hyposiderosis include the determination of serum iron concentration, total iron binding capacity of serum( OCS), transferrin and ferritin in serum. The parameters of iron metabolism for various types of anemia are presented in the table.
Table Iron metabolism rates for various types of anemia
Table Iron metabolism rates for various types of anemia
The excess iron content in the body is called "siderosis" or "hypersiderosis", "hemosiderosis".It can have a local and generalized character. There are exogenous and endogenous siderosis. Exogenous siderosis is often observed in miners participating in the development of red iron ores, electric welders. Siderosis miners can be expressed in massive deposits of iron in the lung tissue. Local siderosis develops when iron fragments enter the tissue. In particular, isolated siderosis of the eyeball with the deposition of iron oxide hydrate in the ciliary body, the epithelium of the anterior chamber, the lens, the retina and the optic nerve.
Endogenous siderosis most often has a hemoglobinic origin and is the result of increased destruction of this pigment of blood in the body.
Hemosiderin is an aggregate of iron hydroxide, combined with proteins, glycosaminoglycans and lipids. Hemosiderin is formed inside cells of mesenchymal and epithelial nature. Focal deposition of hemosiderin, as a rule, is observed at the site of hemorrhage. From hemosiderosis should be distinguished tissue "ferruginism", which occurs when impregnating some structures( for example, elastic fibers) and cells( for example, neurons of the brain) with colloidal iron( in Pick's disease, some hyperkinesia, brown lung induction).A special form of hereditary deposits of hemosiderin, arising from ferritin as a result of the disturbance of cellular metabolism, is hemochromatosis. In this disease, especially large iron deposits are observed in the liver, pancreas, kidneys, in the cells of the mononuclear phagocyte system, the mucous glands of the trachea, in the thyroid gland, the epithelium of the tongue and muscles. The most common primary, or idiopathic, hemochromatosis is a hereditary disease characterized by a disruption in the metabolism of iron-containing pigments, increased absorption in the intestine of iron and its accumulation in tissues and organs with the development of pronounced changes in them.
With an excess of iron in the body, a deficiency of copper and zinc may develop.
Determination of serum iron gives an idea of the amount of transported iron in blood plasma associated with transferrin. Large variations in iron content in the blood serum, the possibility of its increase with necrotic processes in tissues and a decrease in inflammatory processes limit the diagnostic value of this study
.Defining only the content of iron in the blood serum, it is not possible to obtain information about the causes of impaired iron metabolism. To do this, it is necessary to determine the concentration in the blood of transferrin and ferritin.