Anemia due to bone marrow failure: diagnosis and treatment.
In the last decade a large increase of our basic understanding concerning erythropoietin and the regulation of erythropoiesis has led to improved methods for the cell culture of human bone marrow cells. These culture methods in turn have been applied to bone marrow failures with a remarkable increase in our knowledge of the pathogenesis of some of these conditions, particularly the aplasias. The pathogenesis of pure red cell aplasia has been elucidated, and 60% of these patients have been shown to respond to cytotoxic, immunosuppressive treatment. Bone marrow transplantation has proved to be very helpful in the treatment of aplastic anemia and has provided impetus for increased knowledge concerning the pathogenesis of the aplasia. Some of these patients may have suppression of marrow hematopoiesis by the marrow T-cells and can be successfully treated with antilymphocyte globulin or high-dose prednisolone. The future looks bright for further clinical advances concerning the bone marrow failures, but more must be learned about the pathogenesis of these anemias if improved methods of treatment are to be developed.
D000368:Aged; D000741:Anemia, Aplastic / Q000097:blood / Q000175:diagnosis* / Q000188:drug therapy; D000756:Anemia, Sideroblastic / Q000097:blood / Q000175:diagnosis; D000818:Animals; D001853:Bone Marrow / Q000032:analysis; D003520:Cyclophosphamide / Q000627:therapeutic use; D004920:Erythropoiesis; D004921:Erythropoietin / Q000032:analysis; D005260:Female; D006801:Humans; D010198:Pancytopenia / Q000097:blood; D011241:Prednisone / Q000627:therapeutic use; D055728:Primary Myelofibrosis / Q000097:blood / Q000175:diagnosis
D004921:Erythropoietin; D003520:Cyclophosphamide; D011241:Prednisone