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Primary Bone Marrow Diseases


Primary bone marrow disease or failure from any cause can lead to nonregenerative anemia and pancytopenia. With diffuse marrow involvement, granulocytes are affected first, followed by platelets and finally RBC.

Aplastic anemia has been reported in dogs, cats, ruminants, horses, and pigs with pancytopenia and a hypoplastic marrow, replaced by fat. Most cases are idiopathic, but known causes include infections (feline leukemia virus, Ehrlichia), drug therapy, toxin ingestion, and total body irradiation (see Table 1: Toxic Causes of AnemiaTables and see Table 2: Infectious Causes of AnemiaTables). Treatment consists of eliminating the underlying cause and providing supportive measures such as broad-spectrum antibiotics, (amoxicillin/clavulanic acid, 20 mg/kg, bid) and transfusions. Recombinant human erythropoietin and granulocyte colony-stimulating factor (5 μg/kg, PO, sid) can be used until the marrow recovers. If the disease is idiopathic or if marrow recovery is unlikely (eg, phenylbutazone toxicity in dogs), bone marrow transplantation is beneficial if a suitable donor is available.

In pure red cell aplasia (PRCA), only the erythroid line is affected. It is characterized by a nonregenerative anemia with severe depletion of red cell precursors in the bone marrow. It has been reported in dogs and cats and may be primary or secondary. Primary cases are most commonly immune mediated and often respond to immunosuppressive therapy. Feline leukemia-positive cats can have PRCA. Recombinant human erythropoietin has been reported to cause PRCA in dogs and horses. Discontinuation of therapy may eventually lead to RBC recovery in some animals.

Primary leukemias are uncommon to rare in domestic species but have been reported in dogs, cats, cattle, goats, sheep, pigs, and horses. Retroviruses are a cause in some cattle, cats, primates, and chickens. Leukemias can develop in myeloid or lymphoid cell lines and are further classified as acute or chronic. Most affected animals have nonregenerative anemia, neutropenia, and thrombocytopenia, with circulating blasts usually present. Acute leukemias, characterized by infiltration of the marrow with blasts, generally respond poorly to chemotherapy. In animals that do respond, remission times are usually short. In acute lymphoblastic leukemia (ALL) in dogs, the response rate to chemotherapy is ~30% with a median survival of 4 mo. Acute myeloblastic leukemias are less common and even less responsive to treatment than ALL. In acute leukemias, the cell lineage is often difficult to identify morphologically, so cytochemical stains or immunologic evaluation of cell surface markers may be necessary for definitive diagnosis. Chronic leukemias, characterized by an overproduction of one hematopoietic cell line, are less likely to cause anemia and more responsive to treatment.

Myelodysplasia (myelodysplastic syndrome, MDS) is considered a preleukemic syndrome characterized by ineffective hematopoiesis, resulting in a nonregenerative anemia or other cytopenias. MDS has been described in dogs, cats, and people. The disease can be primary or secondary and is commonly seen in cats with feline leukemia. Primary syndromes probably arise from mutations in stem cells. Secondary syndromes are caused by other neoplasia or drug therapy. Some cats and dogs respond to treatment with recombinant human erythropoietin and prednisone. Supportive care with transfusions may be helpful. Survival is variable because MDS can progress to leukemia; many animals are euthanized or die of sepsis, bleeding, or anemia.

Myelofibrosis causes bone marrow failure secondary to replacement of normal marrow elements with fibrous tissue. It has been observed in dogs, cats, people, and goats. It can be a primary disorder or secondary to malignancies, immune-mediated hemolytic anemia, whole body irradiation, and congenital anemias (eg, pyruvate kinase deficiency). Diagnosis can be made by bone marrow biopsy. Treatment varies with the underlying cause but usually consists of immunosuppressive therapy.

Last full review/revision July 2011 by Sarah E. Kraiza, DVM, DACVIM (Oncology)

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