iron deficiency anemia



L & rsquo; ferrlprive anemia is a hypochromic anemia, microcytic iron-deficiency secondary to iron deficiency.


Frequency: Iron deficiency is by far the most common cause of & rsquo; anemias billion worldwide.) In developing countries where it is secondary to malnutrition, it strikes 30% of the overall population. In rich countries, iron deficiency is often the result of gastrointestinal bleeding and genital home Ç. In Algeria, she touches 25% s & rsquo; entire population.

Ageetsexe: Iron deficiency is more common in $ before menopause than in the & rsquo; man. At the & rsquo; child, the 2 sexes are affected equally. It is more common among 6 and 20 months especially in premature infants.

III- Physiology of IRON METABOLISM :

Iron is a noble metal of & rsquo; human organism that contains 4 5g. It is the main component of the & rsquo; hemoglobin (100g d’Hb contient 33% to make, either 340mg. Therefore, IL blood contains 500mg of iron.)

Iron metabolism is done in a vacuum, ie the daily physiological losses, that are weak, are largely compensated in normal subjects.

The distribution of iron is in 2 compartments: D-heme iron found in & rsquo; Hb forming 75% you fer total. D Iron non-heme is iron reserve which forms 25% total iron, which is found in the bone marrow, liver and spleen as well as the recovered iron transport in plasma and which is 1% you fer total.

Iron intake : Iron is found in many foods including legumes (because, lentils, beans), spinach and cabbage, Red meat, the veal, the kidney, liver, Yellow d & rsquo; egg and dates. On the other hand, milk and its derivatives are poor in iron. A balanced diet provides 4 to 12mg of iron and thus largely covers the needs.

Iron needs vary by age, sex and & rsquo; genital activity in Ç. They are estimated to Img humans, and postmenopausal women & rsquo; child, at 3-6 mg in the $ pregnant, at 2 Ç mg in non-menopausal outside pregnancy and 1 mg in infants.

L & rsquo; gastrointestinal iron absorption is at the & rsquo; intestine, it is maximal in the duodenum.

Iron transport in the plasma is effected by a protein called transferrin or transferrin, saturated with & rsquo; normal state in its capacity Vs..

The iron reserves represented 25% you fer total, is 1 to 1.5g. It exists 2 forms of standby, Ferritin and & rsquo; Hemosiderin.

are minimal, estimated 1 mg/jr. They are fecal and urinary.


The breaking of the iron circuit is either by

  • Decreased inputs deficiency d & rsquo; intake or increased requirements with respect to contributions.
  • Increased losses. Iron deficiency evolves 3 increasing severity stages :

– The decrease in reserves of iron which results in an isolated decrease in ferritin and increased synthesis of transferrin.
– The disappearance of iron reserves induced a state & rsquo; erythropoiesis sidéroprive with decreased serum iron and transferrin saturation.
– Finally, l & rsquo; emergence of & rsquo; microcytic hypochromic anemia, consequence of the & rsquo; increased number of mitotic.


anemic syndrome

  1. Asthenia.
  2. Dyspnea effort.
  3. Pale mucocutaneous.

Signes neurologiques dus à l’anoxie cérébrale avec

  1. Dizziness.
  2. 2. headaches.
  3. trend lipothymic.

heart signs with

  1. functional systolic murmur apical.
  2. blue conjunctiva.

Signs of iron deficiency made of appendages disorders, skin and mucous membranes with 1 -striated and brittle nails, then flattened and a maximum deformed cup, c & rsquo; is coelonichie. 2-Dry hair, brittle and easily falling. 3-dry lips Fissured labial commissures, c & rsquo; is angular cheilitis. 4-Glossitis with papillary atrophy +/- clear. 5-Atrophy of the gastric mucosa at endoscopy. 6-Atrophy of pharyngoesophageal mucosa with & rsquo; origin of dysphagia, c & rsquo; is Plummer syndrome Vincent.

l & rsquo Note; no splenomegaly except for the & rsquo; where children are sometimes noted moderate splenomegaly.


A- Hémogramme:

– anemia (Hg between 6 and 10 g/dl)
– A rate of & rsquo; Htc hardly lowered (t,on du nombre des mitoses.)
– Microcytosis with MCV 80fl inf (up 50FL)
– Hypochromia with MCHC and MCH L inf 27pg (up to 17pg)
– A reticulocyte bit rate or not diminished.
– A normal white blood cell count and platelets but leukocytosis may be noted.

B- Blood smear :

– The presence of pale GR, thin with a discolored center, performing a max annulocytose.
– The presence of target cells with aniso-poikilocytosis.

C- Determination of serum iron + lasidérophiline saturation coefficient :

– A lower rate in serum iron 30 pg/dl (Vn between 60 and 140 pg/dl)
– TIBC or a total capacity of saturation of transferrin increased, exceeding 3.6 mg / l (Vn = 3 mg / l)
– A low CS, inf in 16% (Vn between 20 and 60%)

D- Assessment of iron stores :

Made by

  • The dosageradio-immunologiquede ferritin : Which is low (Vn between 60 and 300 pg / dl in the & rsquo; man and between 30 and 150 pg / dl in Ç) Knowing that 1 gr ferritin equals reserve iron LOMG.
  • Coloring Péris: Which allows & rsquo; enjoy the erythroid iron, reflection of its use, and d & rsquo; enjoy the rate sideroblasts (Vn between 20 and 90%, on average 30%) and macrophage iron. In case of iron deficiency, the number of sideroblasts is very low and the macrophage iron is absent.

E- therapeutic test:

Useful in d & rsquo; & rsquo impossibility; appreciation of circulating iron and iron reserve. It involves administering 4 Cp / JR Fumafer. In case of iron deficiency, reticulocyte crisis is obtained 7th day. Half of Hb deficit is corrected after 21 days and & rsquo; anemia is completely corrected after 2 month.


Faced with microcytic hypochromic anemia, must be eliminated

  • Anemias inflammatory, due to excessive sequestration of iron in macrophages. However, the TIBC is normal or low, ferritin is high and there is an inflammatory syndrome with accelerated VS. The coloring Peris reveals lower rates sideroblasts while iron is normal or elevated macrophage. Finally, the iron test is negative.
  • Heterozygous thalassemia, which produce a moderate anemia microcytic but hypersidérémique. L & rsquo; electrophoresis of & rsquo; Hb A2 is greater in 3.3%
  • The acquired sideroblastic anemia primary or secondary with presence of ringed sideroblasts.


Any deficiency anemia involves careful investigation because the treatment is primarily etiological. This investigation will include a research interview

  • An unfavorable socio-economic context.
  • A faulty diet.
  • Taking certain drugs (Aspirin, antacids, etc.)
  • The genital and obstetric history in women.
  • History of gastrectomy or intestinal resection.
  • The concept of & rsquo; repeated nosebleeds, hematuria or hemodialysis may be a disease of HHT.
  • The concept of & rsquo; gastrointestinal bleeding distillantes (hernia, hemorrhagic gastritis, hemorrhoids, peptic ulcer, digestive cancer, etc.)
  • The notion of geophagia.
  • If & rsquo; negative etiological, we think the Lasthenie Ferjol syndrome is caused blood spoliation.

The causes are as follows


  • Over and over malnutrition.
  • In infants when the exclusive milk diet is continued too long.


  • Over and during pregnancy, prematurity and twin pregnancy.
  • Over and over growth.


  • In case of partial or total gastrectomy.
  • Over and over the affections of hail (celiac disease, Crohn's disease, intestinal fistulas.)
  • If geophagia, also called PICA.
  • If diet rich in phytates, phosphate and tannins.


Besides the clinically evident bleeding, chronic minor bleeding can easily be overlooked in the long term resulting in the & rsquo; depletion.

  • If & rsquo; genital bleeding in the ♀ (breakthrough bleeding or menorrhagia.)
  • If & rsquo; gastrointestinal bleeding (hemorrhoids, hemorrhagic gastritis, ulcers, RCUH,
    intestinal angiodysplasia,
  • If & rsquo; recurrent epistaxis in Rendu-Osler (hereditary telangiectasia
  • If & rsquo; gross hematuria.
  • If & rsquo; intravascular prolonged chronic hemolysis or hemoglobinuria hémosidérinurie (HPN, nephrotic syndrome, microangiopathies thrombotique.)
  • If & rsquo; intra-alveolar hemorrhage diffuse and recurrent (pulmonary hemosiderosis.)
  • If bleeding caused in neuro-psychological context (Lasthenie Ferjol syndrome.)


But :

Correct & rsquo; anemia. -Restore reserves. – Treating & rsquo; etiology.

Means :

A- replacement therapy :

¾ Feredetate de sodium (Ferrostrane *) syrup, Here which contains 33 mg of iron;.

¾ Ferrous Fumarate (Fumafer *) Cp dosed 200 mg containing 66mg of iron.

¾ where chocolate powder 1 cl contains 33 mg of iron;.

¾ injection Iron (Maltofer * or * Jectofer) in Amp dosed to 100ml by deep IM.

Side effects are blackish stool, digestive intolerance (nausea, diarrhea or constipation) allergy with iron

injectable. Go dietary measures with diet based on meat and pulses. ¾ Blood transfusion unnecessary for the good tolerance of & rsquo; iron deficiency anemia.

B- etiological treatment :

It is essential when & rsquo; it is possible because it allows the healing of the & rsquo; anemia.

Indications :

  • curative iron therapy uses iron by mouth to be taken during the meal to promote tolerance.
  1. At a dose of 240 mg/jr (is 4 Cp Fumafer) in the & rsquo; adults and & rsquo; children over 35kg.
  2. When the weight is between 15 and 35Kg, use half the dose.
  3. In infants, the dose is 6 at 10 mg/kg/jr, is used Ferrostrane or chocolate powder.
  • The duration of treatment is 6 month (2 months to correct the & rsquo; anemia 4 months to replenish)
  • The injectable iron is indicated for digestive malabsorption or & rsquo; gastrointestinal intolerance at a dose of 1.5 mg/kg/jr, is 1 Amp/jr, without exceeding 2 g/jr.

Results :

A reticulocyte crisis is obtained 7th day. The deficit is corrected Hb after 21 days and & rsquo; anemia is corrected after 2 month. The trophic disorders disappear after 3 at 6 month.


L & rsquo; Iron deficiency anemia is an extremely common benign condition, most often linked to adverse socio economic level in populations of poor countries, digestive damage and bleeding.

The treatment is easy but long (6 month enmoyenne) His diagnosis encourages careful etiological research and treatment accordingly.

Courses of Dr. Benhalilou – Faculty of Constantine