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Iron metabolism

The iron, atomic weight 55.8, is present in the human body in the amount of 4-5 grams, three quarters of which used for the formation of hemoglobin, essential metal-protein for the transport of the oxygen to the tissues.

Is introduced into the body with foods, both animal and vegetable, and vitamin C favors the absorption.

The iron, even to being an essential component of hemoglobin, is the constituent of many metal-enzymes and among these are:
- the catalase that protects us from hydrogen peroxide (H202);
- The aldeidossidase, necessary for the aerobic oxidation of carbohydrates;
- Cytochromes needed for the transfer of electrons in the respiratory chain.

The normal serum iron fluctuates between 0.6 and 1.5 mg / ml of serum, but is susceptible to physiological variations in relation to a variety of conditions: age, gender, pregnancy, muscular work, etc. The daily requirement of iron is around 18-20 mg.

Iron metabolism
The iron is ingested with the feeding, especially with compounds of heme and organic salts; it is subjected to the action of hydrochloric acid in the stomach (pH 1.5) where such compounds are cleaved to form ferric ions. Ferric ions react with the reducing agents and with the gastroferrina. Only the iron bound with gastroferrin can meet absorption which has especially in the duodenum and in the proximal portion of the fast.
Most of this iron is deposited as ferritin primarily in the liver (but also detectable in plasma) or is used by the mitochondria for the enzymatic synthesis. The remainder is transferred to the plasma where it binds tightly, in the ferric state, to the beta 1 globulin transferrin.
The iron leaves the plasma especially entering in the erythroid series, from which there is considerable feedback in the plasma, especially through the reticuloendothelial cells. In erythroid cells developing in the bone marrow, ferrous ions combine themselves with the protoporphyrin to form the heme.
The iron is deleted or lost through the normal turnover of hemoglobin in the urine, sweat, with flaking, with feces as unabsorbed and how much comes from small and unapparent continuous bleeding of the gastrointestinal tract, with menstruation.

An acute martial toxicity is the second reason of poisoning in children and is often due to excessive administration of supplements containing iron by relatives.

Iron overload causes:
- Hemosiderosis, characterized by a generalized tissue increase of iron without alterations of fibrotic type
- Hemochromatosis, in which the liver, spleen and pancreas are determined fibrous alterations.

Iron is essential for life (used for the transport of oxygen in the blood, to keep it lodged in the muscles, for the cellular respiratory activity, for cell replication and to build the structure of tissues and organs). Across the iron, if in excess, it is toxic and can be deadly. Any living being, from bacteria to human has so developed systems more or less refined to capture the iron from the outside world and use it, and the other side to transport it and keep deposited in a non-toxic form.
In addition to iron, the main protagonist actors in iron metabolism are the intestine, liver, red blood cells and hemoglobin, macrophages (the so-called scavenger cells of the body), transferrin, ferritin, transferrin receptor.
To these have been added more recently other protagonist actors such as HFE (the protein that causes hemochromatosis classic, if flawed), ceruloplasmin, the T1DM (the protein that regulates iron absorption), the hephaestin and the IREG1 (proteins that regulate the passage of the iron from the intestinal mucosa to the blood) and finally the transferrin receptor 2.

Intestine: in particular the first section, called the duodenum and jejunum, is the main seat of iron absorption. This is a complex mechanism that sees the intervention of numerous proteins that regulate the absorption of dietary iron (T1DM) and the passage of the iron from the intestinal mucosa to the blood (hephaestin and IREG1).
Liver: is the main seat of iron storage with the reticulo-endothelial system. Iron, transferrin-bound, reaches the liver after being absorbed by the intestines. From the liver the iron can be re-transferred again to transferrin in case of need. Due to its primary function of iron storage, the liver is the organ most involved in the diseases from iron overload.

Red blood cells: contain hemoglobin through which carry oxygen to all tissues. Every second the bone marrow produces over 2 million red blood cells. It is therefore necessary that to the bone marrow arrives regularly an adequate amounts of iron to produce hemoglobin. Red blood cells live about 120 days and once aged are destroyed by macrophages.

Hemoglobin: is the protein contained in red blood cells, that carries oxygen from the lungs to all the tissues allowing life. Hemoglobin is composed of a protein portion, the globin, and of a part which contains iron, the heme. Without iron hemoglobin cannot be built and this is the reason why, when there is no iron, anemia develops.

Macrophage (reticulo-endothelial system): its main function, under the iron metabolism, is to scavenger of aged red blood cells.
The hemoglobin that is released with the destruction of red blood cells is demolished in its two main components, the globin and the heme. From the heme freed the iron that is temporarily stored within macrophages and then released to transferrin, which will transport it back to the bone marrow. Here the iron is used to produce new hemoglobin to incorporate in new red blood cells.

The remainder of the heme is degraded to bilirubin, and transported to the liver who will provide for its elimination through the bile.
Transferrin: it is the protein that carries iron in the organism, from the districts in which the iron is absorbed (intestine) to those that use it (in particular the bone marrow, where red blood cells are produced) or deposit organs (especially the liver). In case of necessity, the iron from the organs of deposit is transferred to transferrin which provides for its transport to the different tissues. Each transferrin molecule can bind up to two atoms of iron. The measurement of transferrin saturation is a very important test to determine iron status of an individual.
In fact, if less than 18% is indicative of a state iron-deficiency and if more than 50% is indicative of an overload of iron. Very low levels of transferrin occur in a rare inherited (congenital hypo-transferrinemia) characterized by severe iron deficiency anemia and iron overload in different tissues.
Ferritin: it is the protein that performs the function of iron storage. The importance of this function is indicated by the fact that ferritin is present in every living form, from microorganisms to man and in all cells. Ferritin is like a shell able to contain up to 4500 iron atoms and can take or yield the iron according to the requirements. Ferritin is also present in the blood in an amount proportional to the iron deposited and is measurable by specific executable routine examining. Low levels of ferritin ( 200 mcg / L in women,> 300 mcg / L in men) indicate the possible existence of an iron overload. For a more specific discussion on hyper-ferritinemie.

What is ferritin?
- Ferritin is a protein found in all living organisms, from plants to humans. It is contained mainly in the cells, where it plays its main function which is to transport iron, release it in case of need or maintained it in a form of deposit.
- It is formed by a complex of smaller elements (subunits) that are joined to form a sort of shell inside of which is stored the iron in a non-toxic form (each molecule of ferritin may contain up to a maximum of 4500 iron atoms).

- A small proportion of ferritin is also present in the blood, in amounts generally proportional to the amount of ferritin present in the tissues, and is measurable (serum ferritin).

What are the factors that regulate the production of ferritin?
- Firstly the iron content in the cells. If the iron increases, also increases the production of ferritin, if it decreases the iron also the ferritin decreases. This is the reason why the dosage of ferritin in the blood is commonly used to identify the states of an overload or iron deficiency.

- Secondly the presence of an inflammatory state (by which we mean more or less severe infections, acute and chronic inflammatory diseases, cancer). In these cases the production of ferritin in tissue increases (and consequently also in the blood) regardless of the content of iron.

What are the conditions in which ferritin increases in the blood?
- In states of iron overload, whatever it is the cause. In these cases the increase of ferritin is often preceded by increase of serum iron (iron circulating in the blood) and, above all, of the percentage of transferrin saturation. In the initial cases of iron overload it is also possible to observe ferritin values still within the normal range in the presence of a high percentage of saturation. There are some exceptions to this rule, i.e states of iron overload characterized by high ferritin values with a percentage of transferrin saturation normal or low. These are conditions in which the iron is locked inside the cells (Aceruloplasminemia hereditary, iron overload associated with metabolic disorders).

- In acute and chronic inflammation, infection or neoplasms. In these cases the increase of serum ferritin is not related to the content of iron in the tissues.

- In states where large parts of tissue die (necrosis). In these cases the ferritin contained in the cells is released into the blood and the value of serum ferritin is elevated, sometimes substantially, but not related to the presence of a real iron overload. This is particularly true in acute and chronic hepatitis in consequence of the fact that in the cells of the liver ferritin concentrations are very high to the primary function that has the liver as an organ of iron storage.

- In some rare conditions in which it is dysregulated synthesis of ferritin to an inherited defect. Also in this case the hyper-ferritinemia is not associated with iron overload. The disease is accompanied by the development of an early cataract (of hyper- ferritinemia syndrome and hereditary cataract).

What tests do in the presence of a hyper ferritinemia?
- Inflammatory indices (ESR, CRP, …). If there are high it is possible that we are facing a condition hyper ferritinemia associated with acute and chronic inflammation, infection or neoplasms. In this case we must proceed with other investigations to identify the various problems.

- Transaminases. If altered may indicate the existence of a liver suffering from iron overload (in these cases the increase is not particularly sharp), but also the existence of chronic viral hepatitis as a cause of hyper ferritinemia (in this case it is necessary to proceed with the necessary investigations).

And then?
- Analysis of mutations in the HFE gene. It allows to establish the existence of a form of hemochromatosis related to the HFE gene.
- Blood count and reticulocytes. Can either point to a diagnosis of iron overload associated with certain forms of anemia.
- Cholesterol, triglycerides, glycemia, uric acid. Can either point to a diagnosis of iron overload associated with metabolic disorders states. In this case also the increase in the body weight can direct towards this diagnosis.

Transferrin receptor and HFE: transferrin receptor is present on all cells and has the function to bind the transferrin-iron complex, regulating the input of the iron within the cell. This process is in turn regulated by the HFE protein. In HFE hereditary classic hemochromatosis is defective or not working and this determines the entry of larger amounts of iron in the organism.

Transferrin receptor 2: recently discovered, has the functions still unclear. There are identified rare cases of hemochromatosis with characteristics similar to the classical caused by a defect in this gene.
Ceruloplasmin: is the protein that carries copper. However it has a key role in regulating the spillage of the iron from the tissue cells to the blood. The absence of this protein found in rare cases (hereditary Aceruloplasminemia) causes a disease by peculiar iron overload accompanied at low concentrations of iron in the blood and a mild anemia by iron deficiency.


Over the last 15 years, it grew the number of people with high ferritin associated with one or more of the following metabolic alteration: overweight or obesity, hypertension, hypercholesterolemia, hypertriglyceridemia, hyperuricemia, glucose intolerance or diabetes in several combination. This condition differs from the hemochromatosis for various reasons: to the blood tests the percentage of transferrin saturation is generally normal, to the liver ultrasound there was a “fat” liver (or fatty liver), the analysis of HFE gene mutations exclude the diagnosis of hereditary hemochromatosis, the liver biopsy showed an iron overload generally of moderate identity and only sometimes grave. Of this condition, known as iron overload associated with metabolic disorders were, you know neither the cause nor the mechanisms of development. It is assumed that the key factor that unites the various metabolic disorders described above and the iron overload is the increased resistance of cells to insulin. This means that the cells are less sensitive to insulin, a hormone produced by the pancreas and which plays a key role in the metabolism of sugars and fats

This confirms the close association between iron metabolism and metabolic disorders and encourages us to consider the dietary therapy as the first and most correct therapeutic approach in these patients.

Compared to simple serum iron (little significant quantitative determination of iron in the blood), it should be noted the fundamental importance of the diagnostic determination of both the “active iron” that the “iron binding capacity, index of total capacity of transferrin to bind iron or TIBC = Total Iron Binding Capacity (normal value: 48-66 iron μmol / liter, iron or 270/370 μmol / dl) that increases in iron deficiency, while decreases in infections, tumors, the lack of transferrin, etc.
It is important the value of the latent capacity of fixation, LIBC = Latent Iron Binding Capacity, bones of free capacity, not saturated, transferrin iron binding; this latent capacity increases in iron deficiencies, but decreases in cases of decompensated overload of iron, in the hemosiderosis, in abnormalities of hemoglobin synthesis, etc.

The total amount of iron present in sportsmen can be estimated at about 4-5 g / subject.

Absorption and elimination of iron

The iron is supplied with power being content to varying degrees in organ meats (liver, spleen, kidneys), in meats, eggs, in cephalopods (octopuses, squids), brewer’s yeast, vegetables (spinaches, chards) legumes (beans, lentils), chocolate, nuts (almonds, pine nuts, figs, etc.).

Depending on gastric acid, iron is absorbed in various ways thanks to a system of one-way shipping site in the mucosa of the duodenum and small intestin (intestine → blood of the portal vein).

In normal subjects the 5-10% and in iron-deficient subjects 20-30% of ingested iron is assimilated as trivalent iron (Fe 3+) and in form of complexes, although the iron in a divalent form (Fe2 +) is better absorbable, for which the simultaneous ingestion of reducing agents (for example, vitamin C) favors the absorption of the iron itself.

Once past in the bloodstream, the iron binds to transferrin (normal value in the serum: 2-4 g / liter, equal to about 0.1% iron) and transferred as “functional iron” in both the enzymes and in the myoglobin (about 10-16% total iron) that hemoglobin (about 58-68% of the total iron) and, if not immediately necessary, is accumulated as “iron of deposit” in the reticulo-endothelial system, linked in particular to ferritin and hemosiderin (about 18-22% of the total iron).

Very important is the transport of iron in the red cells in the ripening stage by the passage of the iron itself by the transferrin to specific receptors on the erythrocyte membrane. Once bound to these receptors, the iron is not easily detachable from the membrane of red blood cells and passes in the erythrocytes where, through the intervention of ferritin, participates in the synthesis of hemoglobin.
Ferritin is also found in the serum (30-120 ng / ml in males from 30 to 260 ng / ml in females) with trend to the decreased in iron deficiency anemia and to the increased in hemochromatosis, in liver diseases, tumors, etc. Because ferritin is in partial equilibrium with that tissue, you can perform the diagnostic determination of the relationship “ferritin / soluble transferrin receptor” that tends to increase in the case of an endogenous or exogenous stimulation of red blood cells formation.

The iron that is released daily by the destruction of red blood cells is almost completely recovered and reincorporated into hemoglobin.

The average loss of iron in males adult is around 0.5-1 mg / day (equal to approximately 9-18 μmol iron / day) that in athletes undergoing significant training and performances can be increased up to 1.5-2 mg / day ( equal to about 27-36 μmol iron / day) given a certain greater iron loss for profuse sweating, for the cell exfoliation of the skin and for the repeated pressure on the plantar microcirculation due to the intense contact and impact of the foot on the playground. Given that in normal conditions the absorption of iron is about 5-10% of that supplied with the feeding, it could be estimated that the food needs of iron of a football player is about 5-15 mg / day which may be normally stocked by the typical Mediterranean diet. In addition it should be noted that, if in the player will also establish the tendency to increase the iron losses, the percentage of iron absorption tends to increase for which, in presence of proper nutrition, it establishes a regulative for itself mechanism of compensation.

Iron metabolism is succinctly expressed in the following diagram:


Diagnostic Bases of iron deficiency and iron deficiency anemia

It should be emphasized that, in general, iron deficiency or anemia are more a symptom than a disease, whereby it becomes essential to the recognition of the causes to correct with specific interventions and not with uncritical administration of preparations based on iron.
On the other hand, the normal production of red blood cells requires the presence of an adequate and constant availability not only iron, but also of various vitamins (among which, cyanocobalamin, and folic acids) and some oligos elements (such as the copper, zinc, cobalt).

For diagnostic purposes are very important longitudinal variations of the clinical hematology parameters that occur in the same subject, both in the medium-long times (some months), which in a short time (a few weeks). In an athlete can, that is, to verify a pathological and / or pharmacological event which leads to a considerable variation of its hematological values which, however, may remain within those that are considered to be rather wide “normal limits” that generally characterize the population.
This applies well, for example, to changes in the value of red blood cells, reticulocytes, hemoglobin and hematocrit (which represents the overall percentage of the volume of red blood cells and is expressed as a percentage). In the population that do not systematically implements a motor activity the hematocrit value, for example, fluctuates approximately between 37 and 49% in males and 36 and 46% in females, although these values there is a complete agreement in the medical field. In individuals who practice systematically effective motor practice, especially if it includes resistance exercises, such values are on average lower (approximately 36-44% in males).
In an athlete, for example, you can establish a pathological situation and / or pharmacological which leads to a considerable variation of its hematocrit values: these can remain within the aforementioned broad limits of the standard. However, a change of more than 3 or 4 percentage points compared to the customary values of the subject requires both an accurate confirmation of laboratory investigations as a careful clinical monitoring because it represents an alarm bell about the onset of the pathological or pharmacological event of above.
So, what is important for diagnosis is the change over time in the clinical-laboratory values relating to the individual athlete in question.
The training, especially if it includes resistance exercises, tends to significantly decrease hematocrit.
Finally it should be emphasized the importance of establishing integrated also in the number of reticulocytes and hemoglobin concentration. In fact, when referring to the pathological changes of the red crasis values are expressed both in hemoglobin concentration (thus underlining the deficiency of the vehicle of oxygen) that with the value of hematocrit (underlining the increased viscosity and risk thrombosis, thrombo-embolic, etc.).
Even in the case of blood doping, implemented in an effort to improve the performances, we should consider both the transport of oxygen (the increase of which can be advantageous) and blood viscosity (whose increase is dangerous). However the increase of the maximal aerobic power per gram of increase of hemoglobin remains unchanged until hemoglobin concentration of about 20 g / dl, while the increase in hematocrit (with elevation accentuated and dangerous of the viscosity) affects the transport of oxygen to hematocrit values greater than 50%.

Given that the real risk for the athlete is the increase of abnormal viscosity, in this case the diagnostic attention refers to the hematocrit rather than hemoglobin.

The variation in the time of a single hematology parameter cannot be considered sufficient to make the diagnosis of iron deficiency and / or iron deficiency anemia.
For example, low levels of ferritin (an indication of a decrease in reserves of iron in tissue) associated with the normality of other hematological parameters can be the first signal the onset of an iron deficiency. In this case, the values of the hemoglobin concentration, mean hemoglobin concentration and hemoglobin content medium will present a progressive reduction. If iron deficiency persists, the blood picture will be then characterized by both the presence of erythrocytes small (microcytosis), poor hemoglobin (hypochromia), with abnormal shapes (poikilocytosis) and variable size (anisocytosis), both by increase of transferrin and decrease in ferritin.

The low values of ferritin instead do not justify the diagnosis of iron deficiency or iron deficiency anemia if the hematocrit remains normal or tends to increase and, at the same time, the concentration of hemoglobin, the red blood cell count, the avaregehemoglobin concentration and the average hemoglobin content are normal or tend to increase while, at the same time, are absent phenomena microcytosis, anisocytosis, poikilocytosis, etc.
In such a case, the persistence day low ferritin values must be readily and very thoroughly investigated since it can be due to (1) causes primitives, such as some pathological forms of polycythemia (for example, by lung disorders, renal hypoxia, tumors renal production); or (2) secondary causes, such as forms induced by increased endogenous production of erythropoietin ( for example, from renal tumors), or forms induced by the administration, in short times, of erythropoiesis-stimulating drugs (for example, erythropoietin, somatotropin, anabolic steroids, etc.). On the contrary, in case of prolonged administration of iron and of these substances for long times, you can be noted the normality or the increase of ferritin values.

Pathophysiological basis of treatment with iron

Iron deficiency leads, initially, to a decrease of the organic deposits and originates a variety of disorders, ill-defined and subjective, such as asthenia, anorexia, dizziness, palpitations etc., in the absence of hematological alterations, apart from a certain decrease in the ferritin.
If persists iron deficiency, hematological alterations are reflected in the framework of iron deficiency anemia (also known as iron deficiency anemia) is characterized by the presence of small erythrocytes (microcytosis), poor hemoglobin (hypochromia), with forms abnormal (poikilocytosis) and variable size (anisocytosis), both from increase of transferrin and ferritin decreased. In this pathological form, the administration of pharmacological iron is the therapeutic treatment of choice.

In the case of altered utilization of the iron absorbed at intestinal level it can be finished the sideroacrestica anemia, characterized by the appearance in the bone marrow of annular sideroblasts, ie of erythroblasts containing granules ferritin free or thickened and included in vacuoles (siderosomi) in the shape of ring around to the nucleus.
This type of anemia is mostly supported by a deficiency of vitamin B6 and, in this case, it does not respond to pharmacologic administration of iron that is improper treatment.

Many athletes are subjected to repeated treatments and not so much with systemic corticosteroids (for example, dexamethasone, betamethasone, cortisone, corticosterone) because, more frequently, with anti-inflammatory drugs, or FANS (for example, diclofenac, ketoprofen, tolmetin, indomethacin) which reduce the inflammatory process osteo-articular mio- inhibiting the synthesis of prostaglandins which, however, have physiologically significant gastro-protective effect.
Repeated treatments with corticosteroids (for example, with the Bentelan) and, above all, with NSAIDs ( for example, with Voltaren) involve a high risk of onset of gastrointestinal lesions, whose easy sub-chronicity or chronicity can induce repeated micro-bleeding that realize themselves with anemic paintings.
In this case it is essential to a thorough examination of the digestive tract (radiological observations, occult blood in the stool, functional assessments, etc.), while it is absolutely wrong “blind” treatment with iron, since it cannot be in line with the diagnostic picture and produce the side effects associated with the administration of oral iron preparations, given their well-known harmful gastrointestinal effects that overlap with those analogs mentioned induced by anti-inflammatory (treatment detrimental).

Drug delivery iron

The iron is the therapy of choice of sideropenic anemia in which the salts are preferably used instead of ferrous ferric ones because the former are more easily absorbed. In the treatment of iron-deficiency anemia it is essential to establish the optimal dosage for each subject because, in conditions of stimulation of the synthesis of red blood cells, the hemoglobin may be formed, for example, at the rate of 3 g / day / liter of blood.

Because the concentration of iron in the hemoglobin is of 0.34%, realizing that the anemic player has a blood volume of about 5.5 liters, they are required 56 mg / day of iron to maintain the erythropoietic efficiency. So, in the case of a oral drug treatment with ferrous sulfate, if the subject anemic absorbs 25% of the ferrous sulfate itself, it must be administrated 225 mg / day to maintain the rhythm of hemoglobin synthesis.

It must however take into account that, in time, the synthesis of hemoglobin does not stabilize itself at the cited levels and that the absorption hardly remains above 20% of the dose of iron administered.
After about a week of treatment iron deficiency anemia martial, haematological response is evidenced by an increased number of reticulocytes that is peaking in the second week, then return to normal by the third week. After the first week begins to increase the rate of synthesis of hemoglobin, with a return to normal levels within 4-8 weeks.

The failure of the iron therapy may depend on:
(1) erroneous diagnosis of iron deficiency anemia;
(2) microhaemorrhages cronicizzate consistency than the rate of synthesis of hemoglobin;
(3) reduced rate of intestinal absorption of iron administered;
(4) the coexistence of infection, inflammation, uremia, cancer, etc., Inhibiting the use of iron absorbed;
(5) Failure of the regimen.
As for the rate of absorption of iron preparations for oral use, you can make the following classification: ferrous sulfate ferrous glicinsolfato => glutamate = ferrous ferrous gluconate> = tartrate ferrous citrate, ferrous iron pyrophosphate => = colinisocitrato ferric sulfate, ferric citrate = ferric> versenato ferric.

The preparation most used orally appears to be the ferrous sulphate.
There is also the possibility of treating subjects suffering from iron-deficiency anemia with iron preparations for parenteral use, such as ferrodestrano, iron oxide saccharate, destriferone and complex iron-sorbitol-citric acid. The parenteral treatment (mostly intravenous) must be reserved oculatamente only to cases of intestinal malabsorption or serious alterations of the gastrointestinal tract.

Side and toxic effects induced by treatment with iron
With variable frequency, already during the administration of therapeutic doses of iron, you can verify the onset of more or less accentuated gastrointestinal disorders (nausea, vomiting, diarrhea, abdominal pain, etc.).
These side effects are mainly due especially to the detrimental action of the iron on the morphological and functional status of the gastrointestinal tract.
More rarely, even if in much more serious form , there can be the acute toxicosis by inappropriate and / or excess iron doses that cause hemo-concentration, leukocytosis, metabolic acidosis, liver failure, etc., And alterations in the digestive tract (ulcers , hemorrhagic erosions), liver (hepatocellular necrosis) and kidney (vascular congestion, tubular degeneration).
Clinically in acute iron toxicosis it is observed an early stage characterized by nausea, vomiting, diarrhea and abdominal pain, which they followed psychomotor agitation, pale skin, drowsiness, signs of cardiovascular collapse and blackish diarrhea or frankly hemorrhagic. If they do not appear more serious complications, takes over an improvement of the clinical picture that is not to be considered as definitive since the moment that they can recur signs of cardiovascular collapse, also accompanied by convulsions facts. Finally, after weeks or months of remission of the toxicological, events can arise from intestinal obstruction due to scar stenosis produced by lesions of the stomach and / or intestine.
Iron overload by pharmacological protracted treatment can determine an excess of deposit of the same (hemosiderosis) especially in some organs and systems (for example, gastrointestinal tract, liver, spleen, pancreas) because of the inability of the reticuloendothelial system to respond to the increased intake of exogenous iron.
If you do not avoid the prolonged use of preparations of iron (oral and / or systemic) it can be established the typical paintings of organ function failure concerned.
Typical, for example, the signs of liver failure also highlighted in the laboratory by alterations of GOT, GPT, GDH, LDH, LAP, gammaGT, alkaline phosphatase. For the gastrointestinal tract, also, the harmfulness of prolonged oral administration of iron can lead to serious late development morpho-functional damages compared with the treatment or to his suspension.

The use of preparations of iron, especially if implemented on an ongoing basis, is not without side and toxic effects that can be enhanced by concomitant administration of other drugs (FANS, corticosteroids).
Therefore the iron therapy should be given to a few cases of confirmed presence of an iron deficiency or iron deficiency anemia.

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