Complete blood counts done systematically or before a clinical picture suggestive of anemia stated on a hemoglobin level below 13 g / dL in men, 12 g / dL in women and children over 10 years; 11 g / dL in children under 1 year, and 10.5 g / dL in pregnant women during the third quarter.

Orientation diagnosis:

The finding of anemia diagnosed in the low figure of hemoglobin justifies the analysis of biological criteria characteristic of the red line:

– The rate of reticulocytes which affirms the central or peripheral character of anemia;

– Mean corpuscular volume (MCV), which allows the separation of microcytic anemia (MCV <84 m3), the macrocytic anemia (MCV> 98 m3), of normocytic (84 m3 <MCV <98 m3). The mean corpuscular hemoglobin concentration (MCHC) differentiates hypochromia (MCHC <32%) of the normochromie (MCHC O 32%). Thus the analysis of these different constants will separate: anemia or hypochromic microcytic; normocytic anemia / Macrocytic aregenerative;normocytic anemia / regenerative macrocytic.

Microcytic anemia:

The existence of microcytosis translated abnormal synthesis hémoblogine and in the vast majority of cases is a reflection of iron utilization anomaly. Thus the determination of iron will differentiate: microcytic anemia with low iron (260 mg / 100 mL in females and 270 mg / 100 mL in humans), normal iron microcytic anemia.

A- microcytic anemias hyposidérémiques:

They correspond to two situations: the anemia of inflammation, where the iron is stored in macrophages under the action of interleukins inflammation IL6, TNF; anemia by iron deficiency.

1- inflammatory anemias:

Their diagnosis is based on: the clinical context of inflammatory disease (collagen disease, infection); the biological context of inflammatory disease: increased erythrocyte sedimentation rate, increased fibrinogen, of a 2-globulins, the presence of thrombocytosis; the determination of low iron with a capacity of transferrin saturation (CTS) Low (o 50 mmol / L); the determination of normal or elevated ferritin. Anemia is the witness of the inflammatory disease, it does not require any specific treatment. She rarely nécessie transfusions.

2- iron deficiency anemia:

• Biologically: it combines a low dose of iron with a capacity of transferrin saturation increased (> 60 mmol / L) and low ferritin: dosage of ferritin is reliable and reproducible. It is an accurate reflection of the amount of iron in the body.If association of inflammation and iron deficiency, the ferritin always increases can mark the iron deficiency.

• Clinically: we must find a cause for iron deficiency. This etiological research depends on the patient’s age (Table): For women premenopausal, look primarily gynecological cause; in men or postmenopausal women, we must first seek out a digestive cause tumor or non-tumor; will be sought if negative investigations rarer causes and contributing factors.

– Rarer causes: chronic haemolysis hémosidérinurie chronic, parasitic disease (hookworm), malabsorption (celiac disease, dirt absorption), pulmonary haemosiderosis, recurrent epistaxis (Osler Rendu disease), psychiatric illness (anemia Fergeol).

– Facilitating factors: bleeding disorders (von Willebrand disease), repeated blood donations.

3- In infants:

Iron deficiency is common and is almost always due to a dietary deficiency. Twins and iron deficiency in the mother are predisposing factors.

B- microcytic anemias normosidérémiques:

The normality of serum iron should be checked twice before we can say normalcy iron. We must mention two diseases: thalassemia and refractory anemias.

1- Thalassemia:

Not so much the picture of b-thalassemia major or disease but has Colley or minor or heterozygous b-thalassemia.

• The b-thalassemia reaches the subject the Mediterranean and Southeast Asia; realizes the isolated microcytosis table or pseudo-polycythemia microcytic; diagnosis is based on hemoglobin electrophoresis objectifying increased hemoglobin A2 O 3.5%.

• The a-thalassemia reaches the black subjects and topics of Southeast Asia; achieves a secluded microcytosis table or pseudo-polycythemia microcytic; electrophoresis of hemoglobin is normal.

2- Refractory anemia:

This is most often refractory anemia sometimes acquired constitutional. Diagnosis is based on the sternal puncture that objective characteristic abnormalities of erythroblasts.

Normocytic anemia or non-regenerative macrocytic:

These are the most common. The lack of regeneration or insufficient regeneration to anemia, is defined by a number of reticulocytes below 150,000 / mm3. This lack of regeneration can be affirmed if the phenomenon that induced anemia develops for more than one week. This is the time required for the cord to produce a sufficient number of reticulocytes. In case of doubt, the number of reticulocytes recontrôlera and they lead a double etiological investigation, that of a normochromic non-regenerative anemia and that of a regenerative normocytic anemia. Apart from this circumstance, the arégénératif character reflects the centrality of anemia. This central involvement may be secondary to extrahématologique or due to spinal pathology pathology.

A- normochromic anemia, macrocytic nonregenerative due to extramedullary disease:

Erythrocytes in tears. Characteristic feature of blade with elongated red blood cells; testifying to the presence of bone marrow fibrosis.
Erythrocytes in tears. Characteristic feature of blade with elongated red blood cells; testifying to the presence of bone marrow fibrosis.

1- anemia due to renal failure:

Due to lack of erythropoietin production. The intensity is proportional to kidney failure as measured by blood levels of creatinine.

2- Anaemia in endocrine deficiencies:

Many endocrine diseases are accompanied by a non-regenerative anemia. Thyroid (hypo- or hyperthyroidism), adrenal insufficiency, hypogonadism, hyperparathyroidism, hypopituitarism.

3- Anemia and Alcoholism:

Alcohol poisoning can through multiple mechanisms cause non-regenerative anemia. Medullary stunning during acute intoxication, macrocytosis due to abnormalities of membrane lipids érythroctaires, hypersplenism syndrome, vitamin deficiency (B12, folate).

4- onset inflammatory syndrome:

Before the onset of microcytosis, inflammatory anemia is normocytic; clinical and biological context can confirm the diagnosis.

Erythrocytes with Plasmodium falciparum, responsible for infectious acute hemolysis.
Erythrocytes with Plasmodium falciparum, responsible for infectious acute hemolysis.

5- Haemodilution:

It should be suspected when anemia occurs in a striking setting: left heart failure, splenomegaly, presence of a peak at protein electrophoresis level b2 or globulins. Apart from these circumstances, an exploration of the cord is required by a sternal puncture at first.

B- normochromic anemia due to a spinal cord pathology:

The puncture and cytological will differentiate several aspects: the absence of bone marrow or red cell aplasia;morphological abnormalities of bone marrow cells either type megaloblastosis or type dysmyelopoiesis. Finally, the puncture is very rich in cells or normal, then requiring bone marrow biopsy.

Schistocytes, indicating hemolytic anemia mechanically.
Schistocytes, indicating hemolytic anemia mechanically.

1- Pure red cell aplasia:

It carries a fairly typical biological table because besides anemia, reticulocyte rate is zero and the red line of the spinal cord is not represented. We distinguish acute Aplasia arising in the aftermath of a parvovirus B19 infection or after drug intake or during the course of chronic lymphocytic leukemia and chronic forms in adults, to be investigated benign thymic, in children, a Diamond-Blackfan syndrome.

2- megaloblastosis:

It achieves a typical medullary cytological appearance indicating a deficiency of folic acid or vitamin B12. It should after dosing of these vitamins and before any treatment (or transfusion) to seek first folate deficiency. It is most often due to a lack of supply or excess use (repeated pregnancies, alcoholism, antifolate drugs); less often, it is due to an absorption deficiency (enteropathy, extensive abdominal surgery). If no cause is found, look for B12 deficiency dominated by pernicious anemia. Its diagnosis is based on: a vitamin dosage and low histamine resistant achlorhydria with lack of intrinsic factor, as demonstrated by its dosage in gastric fluid or a Schilling test with or without intrinsic factor. If there is not a pernicious anemia, it will seek an infection botriocéphale or malabsorption.

3- Myelodysplastic syndromes:

They mainly affect the elderly; normocytic anemia or not the regenerative macrocytic is the most common biological stigma. Their diagnosis is achieved by sternal puncture which further clarifies the prognosis. Indeed, refractory anemia without blasts have a long life span of several years as refractory anemia with excess blasts will quickly evolve to leukemia in a few months.

4- marrow invaded:

The sternal puncture will objectify an invasion by hematopoietic tumor cells (acute leukemia, lymphoma, myeloma) or extrahématopoïétiques (metastasis). Most often, anemia is associated with myelemia or a rather characteristic érythroblastémie.

5- poor or normal marrow:

Given this result myelogram, you must provide a bone marrow biopsy. Only, indeed, the biopsy will make the diagnosis of aplastic anemia before a desert marrow myelofibrosis indicating its importance for non metastatic lesion myelogram or finally a picture of myelodysplasia lean marrow.

Normocytic or macrocytic anemia regenerative:

The regenerative nature (reticulocytes O 150 000 / mm3) says the peripheral nature of anemia. We must seek first hemorrhagic syndrome, hyperhemolysis, and if negative of these two causes, we must mention the repair of a failure of erythropoiesis.

A- hemorrhagic syndrome:

It is often obvious at times, as part of a particular context (hemostasis disorders, anti-inflammatory drugs, anticoagulants), sometimes more difficult, if bleeding is not externalized. It is therefore important to seek an evocative context, signs of shock, signs of acute anemia (mucocutaneous pallor, thirst, dizziness, sudden weakness).

B- hyperhemolysis:

If anemia accompanied by hemolysis stigmata, further regeneration, the collapse is noted haptoglobin and increased free bilirubin.

1- hemolysis extracorpusculaires:

The red blood cell is normal, it is destroyed by an agent or a mechanism that is external to it. To make the diagnosis in case of difficulties, the life of a compatible allogeneic red blood cell may be an important contribution. Their diminished life extracorpusculaire confirms the nature of the phenomenon. It should evoke an infectious cause, malaria gram-negative septicemia; a lead poisoning; a snake bite, a mechanical heart valve; thrombotic microangiopathy; considerable physical effort (hemolysis marathon); immunological cause with demonstrated anti-erythrocyte antibodies, Coombs testing. Thus, the clinical setting is evocative. In addition to hemolysis, febrile context will lead to practice a thick and blood cultures. Mechanical anemia will seek schistocytes, whose presence confirms hemolysis mechanism. If hemolysis is suspected, the realization of the Coombs test will confirm its immunological in nature without the latter to specify the autoimmune nature, allo-immune or allergic immune hemolysis.

2- corpuscular Hemolysis:

It is usually part of a family history to look; it may be due to abnormalities;

• Membranes: the most frequent anomalies is the Minkowsky-Chauffard disease or hereditary spherocytosis, characterized by the family nature; the increased autohémolyse corrected by adding sugar makes the diagnosis.Other abnormalities of the membrane (elliptocytosis, acanthocytosis) may give the same table.

• Abnormal hemoglobin: homozygous sickle cell disease and sometimes heterozygous responsible hyperhemolysis.The diagnosis, in addition to the family survey, based on hemoglobin electrophoresis. Hemoglobin C and unstable hemoglobins are the other two causes hemoglobinopathies causing hyperhemolysis.

• enzymatic anomaly: a great many enzyme deficiencies can cause hyperhemolysis. Two summarize the vast majority: glucose 6 phosphate hydrogenase (G6PD) and pyruvate kinase (PK). G6PD deficiency, primarily affect man and realizes hemolysis crises waning of drug intake (malaria, sulfonylurea) or fevers. Their diagnosis is based on family history, body Heintz’s presence on blood smears and dosage of the enzyme away from the hemolytic crisis.PK deficiency is rare also affecting men and women; Diagnosis is made by enzymatic assays and by the test of autohémolyse corrected adhénosine triphoshate.

Cause of iron deficiency in adults:


– Uterine fibroid or polyp

– Vaginal or uterine cancer

– Hormonal imbalances

– Intrauterine contraceptive device


• nontumoral

– Reflux esophagitis

– Oesophageal varices

– Hiatus hernia

– Drug or alcohol gastritis

– Meckel’s diverticulum

– Crohn’s disease / ulcerative colitis

– Colonic angiodysplasia

– Polyp

– Hemorrhoids

• tumor

– Cancer

– Kaposi syndrome

– Ampulome watérien

– Lymphoma

* These are elimination diagnoses

Strong Points to remember:

• Only through careful analysis of the counts that can properly orient the etiologic research to anemia. Any inaccurate interpretation of one of its three values, lead to requests for unnecessary tests.

• Sometimes anemia has many causes and it is through the clinical and biological confrontation, that we can determine all the causes of anemia.

• Monitoring the evolution of the waning of anemia treatment will reinforce the accuracy of diagnosis.