Notes by doctor Claudio Italiano
The patient presenting
anemia, in routine, during hospitalization, is usually:
- a young woman with an abundant cycle, which has the form of iron deficiency
anemia, ie with iron scarcity: the diagnosis is simple because it presents a
hemoglobin value around 8 g / dl or less or slightly more, with a volume
globular around 60-70 micron3, VCM (mean corpuscular volume), that is, the size
of red blood cells that are smaller than normal and the attitude of the iron is
altered with low-sideriness and ferritinemia. This is the classic picture. It
may be that the losses also occur from the digestive tube, with occult positive
blood (hemorrhoids, gastritis, diverticulitis, but in this case we generally
speak of elderly patients).
- an elderly person, who may have co-morbidity, e.g. anemia in renal disease,
with chronic renal failure and failure to produce erythropoietin; for example.
the case is an elderly person with aplastic anemia, ie with the poor marrow of
erythropoietic stem cells, with myelodysplasia, an almost similar condition in
the periphery, but not in the medulla where there may be blasts multiplying and
destroying the erythogenic stem cells. Atra frequent cause of anemia is that of
the patient with chronic renal failure and deficiency of the hormone
erythropoietin. To these patients should be added those with acute hemorrhagic
loss, digestive, urinary and gynecological. Finally, the account includes
subjects with Mediterranean anemia or thalassemia trait, healthy carriers.
This is what we see in 60% of cases in normal clinical practice.
• Pregnancy (2nd-3rd quarter)
• Massive splenomegaly
• Increased volemia secondary to congestive heart failure, renal failure with
oliguria, cirrhosis of the liver
• Waldenstrom macroglobulinemia
• Severe food shortages
•Red blood cell anemia
•Myelodysplastic syndromes
•Aplastic anemia
•Pure erythroid aplasia
•Neoplasms infiltrating the bone marrow (myeloftis anemia)
• kidney failure
• endocrine diseases: hypothyroidism
• chronic dyserythropoieric anemia of multiple pathogenesis
• malnutrition
• anemia of chronic diseases
• iron deficiency anemias
• from defective synthesis of the globin chains (thalassemia)
• congenital atransferrinemia
• defective synthesis of the heme tetrapyrrole ring (porphyria, lead poisoning,
congenital sidero-blastic anemia)
• by alteration in DNA synthesis (megaloblastic macrocytic anemias)
• vitamin B12 deficiency
• folate deficiency
• membrane defects (hereditary spherocytosis, ellipsocytosis, acanthocytosis,
hereditary stomatocytosis)
• enzymatic deficiencies (glucose 6-phosphate dehydrogenase-G6PD, pyruvate
kinase-PK, porphyria)
• hemoglobinopathies
• paroxysmal nocturnal hemoglobinuria
• mechanical (hemoglobinuria from march or sportsmen, from cardiac
valvulopathies, microangiopathic)
• chemical-physical (toxic substances, poisons, drugs, burns)
• infections (bacteria, viruses, protozoa)
• mediated by antibodies (autoimmune hemolytic anemias from hot or cold
antibodies, hemolytic disease to the newborn immune system, cross-reacting
anti-drug antibodies with erythrocytes)
• Hypersplenism
• Acute haemorrhage anemia
As regards the physiopathological aspects of anemia, it is believed that this
etiological condition may derive from the intervention of one of the following
factors:
a) modifications of the multipotent or "committed" stem cells in an erythroid
sense
b) changes in the medullary microenvironment in contact with which the
erythropoietic process takes place
e) modifications of the hemoglobin synthesis processes and / or proliferation
and differentiation of the medullary precursors of the erythroid series (from
the pro-erythroblastic to the reticulocyte phase)
d) modifications of the hemocateresis process mainly at the spieno-hepatic level
e) development of alterations of the vessel walls resulting in erythrocyte
hyperduction; Vascular modifications may also occur following invasive surgical
maneuvers such as placement of heart valves or segments of artificial vessels.
In many anemic conditions, several factors intervene, so we talk about anemias
on a multifactorial basis.
Regarding the morphological aspects, the recent introduction of new generation electronic meters has provided the clinical pathologist with new study parameters of the blood cells. The RDV took on particular significance in this context. (Red Distribution Width, width of distribution of the GRs, which corresponds to the Price Jones curve of the pre-automatic epoch which allows to discriminate homogeneous microcytic anemias (eg thalassemia, characterized by reduced MCV and normal RDW) from those inhomogeneous (iron-deficient anemias, marked by reduced or normal MCV and significantly increased RDW.) Even in the context of anemias with altered nuclear maturation (secondary to vitamin B12 or folic acid deficiency, the RDW index was more reliable than 'MCV, in the identification of anemia.The direct measurement of the mean corpuscular hemoglobin concentration (CHCM) has also allowed a substantial re-evaluation of this parameter, considered up to the early eighties of considerable laboratory importance and recently fallen into disuse in clinical practice. This can be explained by the fact that normal automatic meters provide much more reliable values of MCH than all 'MCHC; consequently the old morphological classification that subdivided the anemias into hypochromic, normochromic normocytic and hypercromic macrocytic microcitics, on the basis of the MCHC and MCV values, is, in the light of current knowledge, inaccurate and not very reproducible, and must be integrated with the CHCM and MCH values and RDW where available. However, since CHCM is only available in some laboratories, a modern classification based on morphology must be set taking into account the following indices: MCV, MCH and RDW.
It is processed according to the following parameters: MCV, RDW, and MCH, determined automatically with modern hematology analyzers
Beta thalassemia minor (heterozygous)
Anemia of chronic disease
Iron deficiency anemia
Erythrocyte fragmentation anemia
Haemoglobinopathies
Anemia from acute blood loss
Hereditary spherocytosis
Medullary infiltration anemia
Iron deficiency anemia at an early stage
Idiopathic myelofibrosis
Congenital sideroblastic anemia
Aplastic anemia
Macrocytosis on iatrogenic basis (AZT, hydroxyurea, etc.)
Folate and / or vitamin B12 deficiency anemia
Autoimmune hemolytic anemia
Myelodysplastic syndromes
In clinical practice, however, the anatomo-pathological picture of anemia
depends on the amount of blood loss, the rapidity with which it has established
and its duration, and is also largely influenced by the factors responsible
etiopathogenetic. In general, acute anemia (especially in those post-hemorrhagic)
prevail phenomena related to the severity of the anemia of the skin, mucous
membranes and internal organs, with possible appearance of injury from shock at
the level above the kidney. In chronic anemia, in addition to the depletion
status of the erythrocyte mass, there are morphological changes due to tissue
anoxia. These alterations consist mainly phenomena of steatosis and are most
evident in the myocardium (when the extensive degeneration of muscle fibers can
lead to the framework of the so-called cor tigratum), in the liver (steatosis
with headquarters in centrilobular), in the kidney (when steatosis affects
electrically the epithelial cells of proximal contorted lobules) and in the
central nervous system (nerve cells of the cerebral cortex and basal ganglia),
all organs whose cells are particularly sensitive to anoxia. At morphological
anoxic injury, they are added often phenomena, more or less intense, of
hemosiderosis when the painting depends on extensive destruction of red blood
cells (hemolytic anemia), or as a result of intensive martial therapies, or
repeated blood transfusions. The hemosiderin deposits (already noticeable
macroscopically for color rusty that the organs take in cases of the most
striking emo-siderosis), are located primarily in macrophages (liver, spleen,
lymph nodes, bone marrow and other tissues); in cases of more severe
hemosiderosis, the parenchymal cells of the different organs (liver, pancreas,
myocardium, etc.) are also affected up to siderochromatosis frameworks. The
behavior of the bone marrow depends on its ability to respond to
erythropoietinal stimulation. In the most frequent cases it undergoes
hyperplasia, especially in the red series, with transformation of the fat marrow
into a red-working medulla (regenerative anemias); instead, in cases where the
marrow is unable to react (arigenerative anemias), it may appear fat even at the
level of the spongy bones normally provided with hemopoietic marrow (aplastic
anemias). Finally it should be noted the possible finding of extramedullary
hematopoietic foci, especially in the liver, spleen and lymph nodes, in part
meaning compensatory and most frequently found in the course of
hemoglobinopathies and anemic forms infantile-onset.