Changes in red blood cell indices
At the stage of latent iron deficiency (LID), hemogram parameters usually remain normal, although an initial decrease in mean corpuscular volume may be noted. As IDA develops, classic hypochromic microcytic anemia forms.
- Hemoglobin (Hb). Unchanged in LID, decreased in IDA. Age-specific normal limits: newborns — 145–240 g/L; children under 6 years — above 110 g/L; patients over 6 years — above 120 g/L.
- Color index (CI). The normal range is 0.86–1.05 (preserved in LID). In IDA, it decreases, indicating hypochromia.
- Mean corpuscular volume (MCV). May be normal or slightly decreased in LID, while microcytosis is always recorded in IDA. Erythrocyte size depends on age: the largest cells are found in newborns (95–116 fL), decreasing by the first month of life (85–115 fL), and after two months the normal value stabilizes at 80–100 fL.
- Erythrocyte saturation. Mean corpuscular hemoglobin (MCH, normal 25–33 pg) and mean corpuscular hemoglobin concentration (MCHC, normal 30–38 g/dL) decrease only in overt IDA.
Biochemical markers of iron metabolism
Unlike the hemogram, biochemical parameters react to trace element deficiency at the earliest stages. They change unidirectionally in both LID and IDA. The logic of the pathological process is simple: reserves are depleted, the body attempts to compensate by increasing transport proteins, and tissues signal starvation.
1. Markers of reserve depletion (decreased)
- Serum iron (normal 10.6–33.6 µmol/L).
- Serum ferritin — the main indicator of tissue reserves (normal >12 mcg/L).
- Transferrin saturation coefficient (normal >17%). Calculated by the formula: (serum iron / TIBC) × 100.
2. Compensation markers (increased)
- Total iron-binding capacity of serum (TIBC, normal 40.6–62.5 µmol/L).
- Latent iron-binding capacity (LIBC, normal <47). Calculated as the difference between TIBC and serum iron.
- Transferrin (normal 2.0–4.0 g/L).
3. Marker of tissue starvation
- Soluble transferrin receptor (sTfR). The normal value is <1.7 mg/L. This indicator demonstrates staging: in LID it is moderately elevated (2–7 mg/L), while in manifest IDA its level exceeds 7 mg/L.
Diagnostic criteria and differential diagnosis
According to UNICEF/WHO guidelines, the diagnosis of IDA is established in the presence of the classical diagnostic triad of laboratory signs:
- A drop in hemoglobin level below the age-specific norm.
- Depletion of tissue reserves (serum ferritin <12 mcg/L).
- Presence of tissue starvation (sTfR >7 mg/L).
What conditions should IDA be differentiated from? IDA must be distinguished from other disorders that also present with hypochromia and microcytosis. The differential diagnosis includes:
- Other types of deficiency anemias.
- Thalassemia (belongs to the group of hereditary hemoglobinopathies).
- Sideroblastic anemias. This is a group of conditions (e.g., lead poisoning or pyridoxine-responsive anemia) where iron is sufficient in the body, but the process of its incorporation into the heme structure is impaired.
Fundamental principles of therapy
Historically established tenets of IDA treatment remain relevant today:
- Pharmacotherapy is mandatory. Replenishing trace element deficiency solely through dietary correction is impossible — specialized medications are always required.
- Priority route of administration. Oral forms (per os) are the first-line drugs.
- Duration of treatment. Therapy must categorically not be discontinued immediately after hemoglobin reaches normal values. The body requires additional time to fully replenish tissue depots.
- Restriction of transfusions. Blood transfusion is not a routine treatment method and should be used exclusively for strict life-saving indications.
The "seesaw" rule of iron metabolism: everything reflecting reserves (ferritin, serum iron, transferrin saturation) drops down. Everything responsible for transport and demand (TIBC, LIBC, transferrin itself, and sTfR) shoots up.
Class and exam questions
Can iron deficiency anemia be cured solely with a diet rich in meat and apples?
No. It is impossible to replenish an already developed iron deficiency solely through diet. The mandatory prescription of medications is required.
How does latent iron deficiency (LID) differ from iron deficiency anemia (IDA)?
In LID, hemoglobin and most erythrocyte indices remain normal, but biochemical markers already change (ferritin drops, TIBC rises). In IDA, hemoglobin decreases and hypochromia with microcytosis appears.
Why doesn't iron help in sideroblastic anemia?
In sideroblastic anemias (e.g., lead poisoning), body iron stores are sufficient or even excessive. The problem lies in the impaired mechanism of iron incorporation into the heme molecule structure.
What else to study on this topic
- Age-related dynamics of erythrocyte indices (MCV, Hb)
- Calculated iron metabolism parameters: LIBC and saturation coefficient
- Differential diagnosis with thalassemia
- Clinical significance of the soluble transferrin receptor (sTfR)
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