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Anemia due to iron shortage – sideropenic anemia

Iron deficit is the most common cause of anemia at any age, and in all parts of the world. It is most frequent in women. In their reproductive period, during pregnancy, and in infants.

The metabolism of iron

Iron ( Fe ) is the most represented oligo-element in the human body, and is an integral part of hemoglobim , mioglobin and numerous enzymes. It plays an important part in metabolic processes because it can change its valence (Fe 3+ Fe 2+).

The total amount of Fe in the body is 3-5gr, and 2.5gr is in hemoglobin. In the body, Fe is in an active metabolic pole- functionally (hemoglobin, mioglobin and enzymes); in transport (transferine) and in deposits (feritine and chemosiderine). The deposited Fe and Fe bound to transferine je tri-valent (Fe3+). Fe can pass through the cell membranes only by active transport in the two-valent shape (Fe2+). In hemoglobine there is Fe2+and the ability of carrying oxygen depends mostly on the presence of Fe2+ in the molecule.

The daily need for Fe is1-2mg, depending on age, and is derived by the intake of different food which contains 10-20 mg of Fe, out of which 10% is absorbed in the duodenum and the upper part of jejunum.

In the food we find a mixture of Fe2+ (hem Fe) and Fe3+ (non-hem, Fe from vegetables). The non-hem Fe is usually in the shape of feri-ions, and it must be reducted into fero-ion in order to be absorbed. The gastric juice stabilizes the ion form of Fe and eases its absorption. The compounds that have great reduction potential, like vitamin C, improves the absorption of Fe. Bile eases absorption. Antacides, inhibitors of the protone pump and blockers of H2 histamine, coffee, tea, calcium and vine inhibit the absorption of Fe.

The daily loss of Fe is 1-2mg, and that is because of the cell desquamation of the epithelium of the intestine mucose., the kidney canals, the epiderm and the removal of hair and nails. Small amounts are lost by secretion (sweat, sebum, bile). Women loose, due to menstruation, about 17-35mg a month.

The causes of iron deficit

The homeostasis of Fe is a highly regulated process, so the daily loss of Fe is in balance with the absorption of Fe. When there is a deficit of Fe in the body, the absorption of Fe in the duodenum can be tripled (instead of 1-2mg, 3-6mg are absorbed during 24h). The deficit of Fe occurs when the loss of Fe is greater than the absorptional capacity of the intestine.

The causes of Fe deficit:

  1. insufficient intake of Fe by food (vegetarians, alcoholics);
  2. decreased absorption of Fe in the digestive tract (gastric resection, and resection of the intestines, celiac disease, inflammatory diseases of the intestine etc);
  3. the increased loss of Fe from the body (chronic blood loss);
  4. increased need of Fe (pregnancy, breastfeeding fast growth);
  5. functional deficit of Fe (eritropoetin therapy).

The most common cause of Fe deficit are chronic bleeding, when the deficit evolves gradually, without symptoms for months and years. As 1ml of blood contains 0.5mg of Fe, even small chronic bleedings lead to significant loss of Fe. Chronic bleeding in women are in the reproductive period, severe bleeding such as meno and/or methrorrhagia, and are the most common cause of Fe deficit and sideropenic anemia. During the normal menstrual period, the blood loss is 35-80ml. If more than 80ml 40mg of Fe of blood is lost, deficit of Fe occurs, because the Fe loss can not be compensated by absorption of Fe from food.

Adult men, and women in menopause have Fe deficit due to chronic bleeding from the digestive tract. If the loss of Fe by feces is > 6 mg / day, there is a negative balance of Fe, which, if the bleeding continues, will lead to Fe deficit in the body.

There are three stages in the development of Fe deficit:

  1. STAGE- THE EMPTING OF IRON RESERVES (pre-latent stage of Fe deficit)
    • feritin in the serum is decreased;
    • there are no biochemical and hematologic signs of deficit.
  1. STAGE- DEFICIT OF IRON WITHOUT ANEMIA (latent stage of Fe deficit)
    • serum feritin is lower;
    • serum Fe is lower;
    • decreased saturation of transferin;
    • increased transferin in the serum; – increased concentration of transferin receptors in the serum.
  1. STAGE OF IRON DEFICIT WITH ANEIMIA (there is a clear Fe deficit)
    • the saturation of transferin is less than 16%;
    • clinical and laboratory symptoms of sideropenic anemia.

Clinical symptoms

Symptoms and signs of sideropenic anemia are the consequence of:

  1. the disease that is the cause of anemia
  2. anemia itself ( symptoms and signs of anemic hypoxy- weakness, fatigue, heart palpitations, difficult breathing in strain, headache, irritability and so on )
  3. disorders in the functions of the tissues and organs due to the reduced activity of enzymes that contain Fe
    • tongue disorders – atrophic glossitis (the tongue is smooth, red, without the filiform papillae, sensitive in contact with food);
    • stomatitis angularis – (splitting of the lip mucose and surrounding skin);
    • disphagia (difficuties when swallowing food);
    • gastric disorders (all stages of gastritis, from superficial to atrophic);
    • coilonichia (concave, or spoon-like hollows of the nails).

Sideropenic anemia is a hypochromic, micro-cyte anemia. The values of Hb and Hct are decreased depending on the deficit of Fe. The quantitative constants of red blood cells ( MCV, MCH and MCHC ) are decreased. The parameter RDW in Fe deficit (distribution of red blood cells) is elevated and shows that the population of red blood cells in the circulation differs in size ( anizocytosis ).

The concentration of Fe in plasma is decreased and is a poor indicator of the whole amount of Fe in the body, because only a small portion of the complete Fe is in the plasma. Many factors influence the values of Fe (sex, age, pregnancy, contraceptives, physical and psychological stress etc). The level of feritin in the serum is most sensitive diagnostic test for deficit of Fe and is in correlation with the amount of Fe stored. The low concentration of is an indicator of Fe deficit, and the concentration of feritine above indicates there is an adequate amount of Fe in reserve, and there is a small possibility of sideropenia. When interpreting the results do not forget that feritin is a positive reactant of the acute phase of an inflammatory answer, so the synthesis of feritin is increase in inflammation.


The therapy of sideropenic anemia is treating the disease that led to the anemia., and compensation of iron.

The goal of treating anemia is the normalization of the concentration of hemoglobin in the blood, and increasing the Fe reserves.

Treatment with iron should start at once, not waiting to establish the cause of Fe deficit. Fe preparations can be administered parenterally or per os ( orally ). The easiest and safest way to compensate Fe is the administration of oral iron preparations that contain Fe2+ and Fe3+. Drugs that contain Fe2+ most frequently used are ferosulphate, ferogluconate and ferofumarate, and those that have Fe3+ are ferihydroxy-polymaltosate and feri-protein-succinate, Adults take daily doses of 200mg of elementary Fe, and in cases anemia has to be treated quickly, the initial dose of the drug can be increased to 300mg of Fe/day.

Iron is best absorbed when taken 1-2 hours before a meal, with vitamin C, while taking Fe with food decreases apsorbtion by 40-50%.

Most patients tolerate well oral therapy, but 10-20% can have symptoms of intolerance.

The most common adverse effects are; nausea, vomiting, heartburn, abdominal pain, diarrhea, constipation ( dark green feces ). These effects can be diminished by taking Fe with food, decreasing the dose of Fe and taking Fe tablets that have a smaller concentration of Fe.

The therapy leads to;

  • increase of the number of reticulocytes 3-5 days after adequate therapy with Fe, and reaches the maximum 8-10th day, and then there is a decrease;
  • increase of the concentration of hemoglobine should be 20g/L, during 3 weeks: simultaneously with the increase of hemoglobine, there is an increase of MCV. Hb is normalized in 2-4 months.

After the anemia is corrected, the treatment is continued until the depots of Fe are filled, 4-6 months, or until the values of feritine in serum are
µg/L 50.

Women in the reproductive period after treatment have check ups in 4-6 months.

Parenteral application of Fe does not accelerate the value of Hb, but the reserves of Fe get filled up more quickly. This kind of treatment has certain risks, especially sensitivity reactions, so this kind of treatment is applied in the following cases:

  • disorders of Fe absorption due to disorders of the gastrointestinal tract;
  • intolerance of oral therapy or the therapy does not have an adequate effect;
  • when uncooperative patients do not take the drug on purpose;
  • post-operative conditions when anemia should be corrected in a short time, and before major surgery;
  • post-operative period when anemia wad not corrected before surgery or caused/worsened by great blood loss after surgery;
  • functional deficit of Fe during application of eritropoetine.

Since Fe administered intravenousely gives defined amount of Fe, it is necessary to calculate the amount of Fe that should be replaced according to the formula:

Deficit Fe (mg) = body mass (kg) x Hb deficit x 0.24 + Fe reserves.

In cases of severe anemia, when Hb < 60g/L, it is mandatory to start red blood cell transfusions and continue with iron preparations.