
Erythrocyte hyperchromia: causes, symptoms and treatment
Carrying out a morphological examination of erythrocytes under a microscope, the hematologist notes not only their physical parameters, but also the shade of color. If the color of the blood cells is saturated, it overlaps the middle enlightenment typical for normal blood cells, a condition such as hyperchromia is recorded. Its statement is a sign that a person has fully developed hyperchromic anemia, or it is in the stage of formation.
When enlarged erythrocytes are found, a diagnosis of "macrocytic or megaloblastic anemia" is made. To confirm it, additional survey methods will be required.

Content:
- Hyperchromia - hyperchromic anemia
- What happens in the bone marrow?
- Causes and symptoms of anemia
- How to treat?
Hyperchromia - hyperchromic anemia
A change in the color of erythrocytes due to their excessive saturation with hemoglobin fixes the color index (CP).
Normochromia - CP: 0.85-1.05, hyperchromia - CP above 1.1. The erythrocyte indices MCH, MCHS, determined by the hematology analyzer, will also not remain unchanged.
Hyperchromia is the leading sign of macrocytic (megaloblastic) hyperchromic anemias:
- Macrocytosis (hyperchromic macrocytic anemia);
- Avitaminosis b12;
-
Folic acid deficiency, or vitamin B 9.
In these conditions, erythrocytes are represented by megaloblasts and megalocytes with a diameter of over 10 microns, while the norm is 7-8 microns.
The picture below shows red blood cells in the blood:

Parameters of hematological analysis typical for patients with hyperchromic macrocytic anemia:
- Hyperchromasia (hyperchromia) - saturation of erythrocytes with chromoprotein (Hb) until the central enlightenment is erased;
- The appearance of macrocytes and megalocytes among blood cells;
- Fixation of schizocytosis (fragments of blood cells), anisocytosis, poikilocytosis (changes in the shape of erythrocytes);
- Fixation of erythrocytes that have not lost nuclear substances;
- Decrease in the number of young forms of erythrocytes (reticulocytes) and impairment of their differentiation;
- Shift of the leukocyte formula to the left: the appearance of young blood cells and myelocytes, the absence of basophils, a decrease in the number of leukocytes;
- Changes in the platelet formula (the acquisition of giant platelets against the background of a decrease in their number).
All changes are provoked by the megaloblastic type of hematopoiesis in the bone marrow. It is a common symptom of genetically determined or acquired anemias associated with DNA abnormalities.
What happens in the bone marrow?

With the megaloblastic type of hematopoiesis, hyperchromic macrocytic anemia occurs.
Hematopoiesis processes as exemplified by B12 deficiency:
- The presence in the bone marrow of high cellularity, ineffective erythropoiesis and megaloblastic hematopoiesis.
- Violation of cell division, preparing to become full-fledged erythrocytes, their transformation into megaloblasts, maturation of the nucleus and cytoplasm at different times.
-
The variability of the maturation of megaloblasts, the maturation of cells at different times, the appearance of such a trait as "blue" bone marrow, when erythrocytes are represented by promyeloblasts or basophils.
- The saturation of the cytoplasm of megaloblasts is earlier than normal (hemoglobinization of the cytoplasm) against the background of an intact delicate nucleus.
- The formation in the nuclei of degenerative processes such as mitosis and the decay of the cell nucleus, as a result of which they become ugly and defective, die early, barely "born".
- The formation of megalocytes and macrocytes are signs of hyperchromic macrocytic anemia.
- The negative effect of cell division on the formation of erythrocytes (ineffective erythropoiesis), although the synthesis of red pigment remains normal.
- Violations of DNA synthesis in white blood cells: changes in the size of myelocytes, young, promyelocytes and rods, mature segmented leukocytes.
Changes similar to those occurring with a B 12 deficiency also occur with a B 6 deficiency.
Causes and symptoms of anemia

Anemia is not an independent disease, but a clinical syndrome indicating a lack of oxygen in the body. The consequence of anemia is heart ischemia and heart failure.
Causes of anemic syndrome and hyperchromia:
-
Avitaminosis B 12: deficiency of cyanocobalamin in food, impaired absorption due to helminthiasis, pancreatic pathologies, toxic poisoning, gastrointestinal diseases, hereditary predisposition.
- Folic acid deficiency anemia: vegetarianism, alcoholism, pregnancy;
- Hyperchromia with megaloblastic anemia: suppression of DNA and RNA synthesis due to impaired enzyme activity.
-
Hyperchromia and macrocytosis: severe liver pathologies leading to impaired synthesis of vitamins, especially vitamins B 12, B 6, synthesizing purine and pyrimidine bases.
- Myelodysplastic syndrome, certain types of hemolytic anemias.
- Hyperchromia can appear against the background of active smoking, since the body experiences chronic hypoxia.
Private and specific symptoms of megaloblastic hyperchromic anemia:
- General: weakness, pallor, tachycardia, headache.
- Specific: burning tongue, shaky and unsteady gait.
The triad of symptoms of B 12 - anemia includes pathologies of the blood, gastrointestinal tract, nervous system, while with a deficiency of folic acid, the nervous system does not suffer. Combined pathology is more often diagnosed - a combination of B 12 and folate deficiency anemia.
How to treat?

There is no specific therapy for hyperchromia, the doctor treats B 12 folate deficiency anemia or these conditions separately. The main direction of treatment is prescribing vitamin B 9 preparations to the patient. It is important to clarify the diagnosis, since excessive use of folic acid will harm the body, exacerbating the symptoms of the disease. It is more expedient to prescribe cyanocobalamin instead of a vitamin.
The principles of therapy for vitamin deficiency B 12:
- Replenishment of the cyanocobalamin deficiency;
-
Active and constant replenishment of vitamin B 12 reserves;
- Prevention of the development of anemia in order to avoid the development of pathology.
Fortification of the diet through the consumption of appropriate products becomes a mandatory measure.

The author of the article: Shutov Maxim Evgenievich | Hematologist
Education: In 2013 he graduated from the Kursk State Medical University and received a diploma "General Medicine". After 2 years, completed residency in the specialty "Oncology". In 2016 completed postgraduate studies at the National Medical and Surgical Center named after N. I. Pirogov.