Etiology: why does deficiency occur?
The development of iron deficiency is caused by an imbalance between its intake and the body's requirements. Several main groups of causes are distinguished:
- Dietary deficiency (alimentary factor).
- Chronic blood loss. Most commonly gastrointestinal, uterine, or urinary tract bleeding.
- Increased expenditure. Characteristic of periods of active growth: in children with high birth weight, in the second half of life, as well as in the prepubertal and pubertal periods.
- Transport disorders. A decrease in the level or activity of the carrier protein, transferrin.
- Hormonal imbalance disrupting trace element metabolism.
In children, specific factors also play a role: antenatal (fetoplacental insufficiency, significant iron deficiency in the pregnant woman) and intranatal (birth trauma bleeding, premature placental abruption, umbilical cord rupture).
Pathogenesis: two pathways of damage
Iron deficiency triggers two parallel pathological cascades in the body:
- Hematological pathway. In the mitochondria of bone marrow erythroid cells, heme synthesis is inhibited. This disrupts its binding to globin and leads to decreased hemoglobin production. The outcome is the development of anemia and tissue oxygen starvation (hypoxia).
- Tissue (metabolic) pathway. The synthesis of other iron-containing compounds suffers: myoglobin, cytochromes, peroxidases, and catalase. Due to a drop in the activity of antioxidant factors, lipid peroxidation is enhanced, which directly damages the cells of parenchymatous organs.
Hematological picture
Hematopoiesis in this pathology remains normoblastic, but undergoes a number of changes.
In the bone marrow, moderate hyperplasia of the erythroid series is observed. A characteristic sign of inhibited erythropoiesis is an increase in the number of basophilic and polychromatophilic erythroblasts against a background of oxyphilic deficiency. The number of sideroblasts (normoblasts with granules of stored iron) drops sharply.
In the peripheral blood, the following are detected:
- Erythropenia (decreased erythrocyte count) and pronounced hypochromia (drop in color index).
- Anisocytosis (predominance of small cells — microcytes) and poikilocytosis (change in shape).
- Appearance of erythrocyte "shadows" (anulocytes) — cells with an extremely low hemoglobin content.
- Reticulocyte levels may be elevated in the early stages, but drop or remain normal in chronic courses.
- Leukopenia (predominantly due to neutropenia) with a normal platelet count.
Biochemical blood analysis registers a drop in serum iron and ferritin, while transferrin levels and total iron-binding capacity (TIBC) increase.
Tissue manifestations (sideropenic syndrome)
Symptoms consist of manifestations of tissue hypoxia and a lack of iron-containing enzymes.
- Muscular system: myasthenia (muscle weakness) develops due to a deficiency of myoglobin and tissue respiration enzymes.
- Skin and appendages: characteristic peeling, cracks in the skin and mucous membranes, hair loss, and a specific nail deformation — koilonychia (increased fragility).
- Gastrointestinal tract: dystrophic changes in the walls of the digestive tract lead to hypertrophic glossitis, gastritis, and enteritis.
Differential diagnosis: iron-refractory anemias
It is important to distinguish true deficiency from iron-refractory (sideroblastic, porphyrin-deficient) anemias. In these conditions, iron is present in the body (sometimes in excess), but due to genetic defects or toxic effects, it is not incorporated into the heme molecule.
Examples of such conditions:
- Vitamin B6 deficiency, which disrupts the incorporation of iron into heme.
- Lead intoxication (saturnism). Lead blocks the sulfhydryl groups of protoporphyrin synthesis enzymes. As a result, the level of aminolevulinic acid in the urine sharply increases, and erythrocytes with basophilic stippling of the cytoplasm appear in the blood.
- Thalassemias — a group of diseases with impaired globin chain synthesis.
The main difference between these forms and classical iron-deficiency anemia is an elevated level of serum iron and ferritin with normal transferrin and TIBC content.
Briefly: answers to topical questions
What stages of iron deficiency are distinguished in pathophysiology?
In pathophysiology, the process of iron store depletion proceeds sequentially and includes four stages.
- Hypoferremic stage — the initial stage with a drop in iron levels at a normal erythrocyte count and morphology.
- Heterogeneous stage — the onset of impaired erythropoiesis with the appearance of erythrocytes of varying diameters (anisocytosis).
- Microcytic stage — progression of deficiency with an overall decrease in mean corpuscular volume (microcytosis).
- Anemic stage — the final stage with a drop in hemoglobin levels, which is the manifestation of iron-deficiency anemia.
What morphological changes of erythrocytes are characteristic of iron-deficiency anemia?
Iron-deficiency anemia (anemia ferripriva) is characterized by specific morphological changes in erythrocytes indicating impaired hemoglobin synthesis. The following signs are distinguished:
- Hypochromia (Hypochromia) — a sharp expansion of the central pallor zone, in which only a narrow peripheral rim remains colored ("ring-shaped" erythrocytes, or "shadows", annulocytes).
- Microcytosis (Microcytosis) — a decrease in the diameter and mean corpuscular volume of erythrocytes.
- Anisocytosis — a change in cell size with a predominance of microcytes.
- Poikilocytosis — a change in cell shape. In severe deficiency, ovalocytes and rod-shaped forms may appear.
To remember the biochemistry of true iron-deficiency anemia, use the seesaw rule: "Iron and ferritin drop down, while transferrin and TIBC soar up, trying to catch the remnants."
Class and exam questions
How does the blood picture in iron deficiency anemia differ from iron-refractory forms?
In true deficiency, serum iron is decreased, whereas in iron-refractory conditions (e.g., lead poisoning), it is elevated because iron cannot be incorporated into heme and accumulates in the plasma.
Why do muscles, skin, and mucous membranes suffer in iron deficiency?
Iron is part of not only hemoglobin, but also muscle myoglobin and tissue enzymes (cytochromes, catalase, peroxidases). Their deficiency causes muscle weakness and epithelial dystrophy.
What are sideroblasts and how does their count change in iron deficiency?
Sideroblasts are bone marrow erythrokaryocytes (normoblasts) containing granules of stored iron. In iron deficiency, their number naturally decreases.
What else to study on this topic
- Pathogenesis of primary iron-refractory anemias (erythroblastic lineage genome defects).
- Mechanisms of lead intoxication development and blockade of porphyrin synthesis enzymes.
- Clinical picture of lead encephalopathy, polyneuritis, and gastrointestinal lesions.
- Thalassemias: classification by globin chains and hematological manifestations.
- The role of vitamin B6 in iron metabolism and the consequences of its deficiency.
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