From the Guidelines
Reactive bone marrow with erythroid hyperplasia is primarily caused by conditions that increase the demand for red blood cell production, such as chronic blood loss, hemolytic anemias, nutritional deficiencies, chronic inflammatory diseases, and certain medications. The main causes of reactive bone marrow with erythroid hyperplasia can be broken down into several categories:
- Chronic blood loss (e.g., gastrointestinal bleeding, heavy menstrual periods) 1
- Hemolytic anemias (e.g., sickle cell disease, thalassemia) 1
- Nutritional deficiencies (particularly iron, vitamin B12, or folate) 1
- Chronic inflammatory diseases (e.g., inflammatory bowel disease) 1
- Certain medications (e.g., erythropoiesis-stimulating agents) 1 To address this condition, the underlying cause must be identified and treated. For example:
- In cases of chronic blood loss, the source of bleeding should be identified and stopped.
- For hemolytic anemias, appropriate disease-specific treatments should be initiated.
- Nutritional deficiencies should be corrected with supplements (e.g., iron 325 mg orally daily for iron deficiency, vitamin B12 1000 mcg intramuscularly weekly for B12 deficiency) 1.
- Inflammatory diseases may require immunosuppressive therapy 1.
- Medication-induced cases may improve with dose adjustment or discontinuation of the causative agent. The bone marrow responds to increased demand for red blood cells by expanding the erythroid lineage, resulting in erythroid hyperplasia, as noted in a study on anemia of chronic kidney disease 1 and another on inflammatory bowel disease 1. This is a compensatory mechanism to maintain adequate oxygen delivery to tissues. Once the underlying cause is addressed, the bone marrow typically returns to its normal state over time.
From the Research
Causes of Reactive Bone Marrow with Erythroid Hyperplasia
The causes of reactive bone marrow with erythroid hyperplasia can be attributed to various factors, including:
- Hemolytic anemia, which can lead to increased erythropoiesis and bone marrow hyperplasia 2, 3
- Chronic hypoxia, which can trigger erythroid hyperplasia in the bone marrow and increase the quantity of peripheral red blood cells 4
- Autoimmune hemolytic anemia, which can result in ineffective erythropoiesis and marrow erythroid hyperplasia 2
- Bleeding, which can lead to enhanced erythropoiesis in the spleen and reticulocytosis, but may not result in significant changes in bone marrow cellularity or erythroid cell numbers 3
- Infection, such as Plasmodium infection, which can cause hemolytic anemia and alter marrow and bone physiology 3
Underlying Mechanisms
The underlying mechanisms contributing to reactive bone marrow with erythroid hyperplasia include:
- Upregulation of the HIF-2α/EPO pathway, which can be triggered by chronic hypoxia and VHL gene methylation 4
- Increased expression of DNMT3α and DNMT3β, which can contribute to VHL methylation and decreased VHL expression 4
- Impaired erythropoiesis, which can result in ineffective erythropoiesis and marrow erythroid hyperplasia 2
- Altered bone metabolism, which can lead to reduced trabecular bone volume, enhanced trabecular spacing, and lower trabecular numbers 3