Erythroid cells are formed from myeloid progenitor cells and from megakaryocyte erythroid pregenitor cells, which are then turned into mature red blood cells.
- results from increased erythropoietin production due to chronic hypoxemia (high altitude stays, chronic lung diseases, cyanotic heart defects) or (rarely) due to erythropoietin-producing tumors (for example renal cell carcinoma)
- or from an increased peripheral erythrocyte loss (for example hemolytic anemias)
Erythroid hyperplasia is usually a compensatory condition. It can develop in case of hemolytic anemia, iron deficiency anemia, thalassemia, hemolytic anemia, angiopathies, thrombotic thrombocytopenic purpura (TTP), polycythemia, pancytopenia secondary to hypersplenism, erythromyelosis and blood loss.
Erythroid hyperplasia is rather a symptom of other diseases than a disease itself.
Anemia symptoms are pale skin color, fatigue, headaches, episodes of fainting, dizziness, shortness of breath, spleen enlargement, etc.
Patients with TTP develop seizures, cognitive deficiency, visual disturbance, and aphasia along with anemia and petechial rash.
Erythroid hyperplasia may be confirmed by bone marrow biopsy. The marrow is normo- or hypercellular with increased normoblastic erythropoiesis, which is organized in clusters. Blood test results may vary depending on the underlying disorder.
Treatment of the cause of the this is required to restore the normal function of the bone marrow. This may include Ferrum-containing medications, vitamins, blood or plasma transfusions.
The marrow is normo- or hypercellular with increased normoblastic erythropoiesis, which is organised in clusters. Erytropoietic precursors mature, often there is a left shift. Other hematopoietic lineages are normal.