Concept of the erythron and normal erythrocytes
The erythron system encompasses all cells of the erythroid lineage: from the earliest committed precursors and morphologically identifiable nucleated cells (both proliferating and non-proliferating) to reticulocytes and mature erythrocytes. Differentiation and maturation of these cells take place in the bone marrow. Progenitor cells originate from a pluripotent stem cell, undergoing 5 to 10 divisions.
In healthy individuals, erythrocytes are round and pink with a small central pallor (normochromia). Normally, the cell population is distributed as follows:
- Normocytes (diameter 7.5 µm) make up the vast majority at 68%.
- Microcytes (less than 7.0 µm) account for about 15%.
- Macrocytes (greater than 7.9 µm) account for approximately 17%.
Megalocytes—giant cells with a diameter greater than 11 µm—are classified separately.
Classification of absolute erythrocytoses
Absolute erythrocytoses occur due to reactive enhancement of normal erythropoiesis, which naturally leads to an increased circulating red blood cell mass. According to their pathogenesis, they are divided into four main groups:
- Compensatory (hypoxia-induced): develop against the background of generalized tissue hypoxia. It may present with arterial hypoxemia or as isolated tissue hypoxia (when arterial blood oxygen saturation remains normal). The main source of erythropoietin in this case is the kidneys.
- Dysregulatory renal: provoked by local renal ischemia. The kidneys actively secrete erythropoietin, but this process does not serve useful compensatory functions for the body.
- Dysregulatory paraneoplastic: erythropoietin is secreted directly by the tumor, which also provides no physiological benefit.
- Primary: a group of hereditary conditions in which the developmental mechanism is associated with increased erythropoietin production or reduced sensitivity of renal oxygen receptors to oxygen.
Relative erythrocytoses and cell pathology
Unlike absolute erythrocytoses, relative (hemoconcentration) erythrocytoses are not associated with a true increase in cell mass. They occur when the circulating plasma volume decreases. As a result, formed elements begin to predominate over plasma, although the total mass of circulating erythrocytes remains unchanged.
In various pathological conditions, the morphological characteristics of the erythrocytes themselves may change:
- Poikilocytosis—the presence of cells of varying shapes in the blood.
- Anisocytosis—variation in cell size. The severity is assessed by RDW (red cell distribution width). The mechanisms of size variation differ: microcytosis is associated with impaired hemoglobin synthesis (its concentration drops), macrocytosis results from impaired DNA synthesis, and megalocytosis is accompanied by a significant increase in cell size and increased hemoglobin concentration.
- Anisochromia—disturbance of normal erythrocyte coloration.
- Appearance of intracellular inclusions.
Dynamics of the erythrocyte sedimentation rate (ESR)
Changes in the physicochemical properties of blood directly affect the ESR.
Increased ESR is caused by alkalosis, anemia, hypercholesterolemia, elevated fibrinogen and C-reactive protein levels, as well as dysproteinemia and paraproteinemia. Clinically, accelerated sedimentation is observed in infectious-inflammatory and rheumatic diseases, liver and kidney pathologies, diabetes mellitus, and thyrotoxicosis. ESR also increases sharply in oncological processes (multiple myeloma, Hodgkin lymphoma, non-Hodgkin lymphomas with paraproteinemia).
Decreased ESR is provoked by acidosis, hyperbilirubinemia, elevated bile acid levels, and a hematocrit exceeding 50%. This is typical for erythrocytoses and any clinical conditions accompanied by marked hemoconcentration.
Briefly: answers to topical questions
What are the dimensions of megalocytes and how do they differ from macrocytes?
The diameter of megalocytes exceeds 11 µm. The main differences between megalocytes and macrocytes lie in the degree of size increase and the characteristics of hemoglobin saturation.
| Characteristic | Macrocytes | Megalocytes |
|---|---|---|
| Size | Enlarged | Marked increase in size ($\varnothing$ > 11 µm) |
| Pathogenesis | Result of impaired DNA synthesis | Impaired DNA synthesis and delayed cell division |
| Hemoglobin | No specific data | Increased hemoglobin concentration, cells are hyperchromic with no central pallor |
To easily remember the difference between absolute and relative erythrocytosis, imagine soup. Absolute is when more solids (cells) are added to the pot. Relative is when the broth (plasma) boils down, while the amount of solids remains the same.
Class and exam questions
How does absolute erythrocytosis differ from relative erythrocytosis?
In absolute erythrocytosis, the mass of circulating red blood cells genuinely increases due to reactive enhancement of erythropoiesis. In relative erythrocytosis, the cell mass is unchanged, but plasma volume decreases, leading to hemoconcentration.
Which organs produce erythropoietin during hypoxia?
The main source of erythropoietin in generalized tissue hypoxia, as well as in local renal ischemia, is the kidneys themselves.
Why do macrocytosis and microcytosis alter cell size?
Microcytosis arises from impaired hemoglobin synthesis, which reduces its concentration in the erythrocyte. Macrocytosis, on the other hand, is a direct result of impaired DNA synthesis in precursor cells.
Why does ESR decrease in erythrocytosis?
Due to the increased red blood cell count and elevated hematocrit (above 50%), the blood becomes thicker. This physically impedes the rapid sedimentation of cells to the bottom of the tube.
What else to study on this topic
- Mechanisms of development of isolated tissue hypoxia with normal blood oxygen saturation
- Paraneoplastic erythrocytoses: mechanisms of ectopic erythropoietin secretion by tumors
- Genetic mutations in renal oxygen receptors in primary erythrocytoses
- Intracellular inclusions in erythrocytes: types and clinical significance
- The role of interleukins (IL-4, IL-5, IL-6) in the humoral regulation of hematopoiesis
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