Non-neoplastic hyperplasias of one or more bone marrow cell lineages are often related to changes occurring outside the marrow and must be correlated with peripheral blood findings, other appropriate laboratory data, and, above all, clinical information. Patients recovering from toxic insults, including chemotherapy and radiation therapy, may demonstrate a transient bone marrow hyperplasia. In a similar fashion, destruction of particular hematopoietic elements outside the marrow, as in some autoimmune diseases, often results in hyperplasia of the corresponding cell lineage in the marrow. Because the bone marrow changes may represent a reaction to events elsewhere in the body, the bone marrow specimen alone is often not diagnostic of the patient's underlying disease process.
Erythroid hyperplasias represent a response to peripheral red blood cell loss or destruction or are related to ineffective erythropoiesis, as seen in some chronic anemias. The causes of erythroid hyperplasias are best addressed in combination with the evaluation of red blood cell features in the peripheral blood (Walters & Abelson, 1996; Peterson & Cornacchia, 1999) (Fig. 5.1). In general, ancillary laboratory testing is needed to precisely characterize the cause of the erythroid hyperplasia. Dyserythropoiesis, particularly mild irregularities of the nuclear contours of erythroid precursors, is common in cases of florid erythroid hyperplasia and should not be over-interpreted as evidence of myelodysplasia.
Erythroid hyperplasias associated with normocytic anemia
Hemorrhage, hemolytic anemia, intrinsic bone marrow disease (including aplastic anemia and malignant neoplasms), and anemia of chronic disease are the most common causes of erythroid hyperplasia associated with normocytic anemia in patients with no history of a toxic insult, chemotherapy, or hemoglobinopathy.