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A two-year old male Welsh Corgi was referred for persistent thrombocytosis and occasional seizure. Hematological findings indicated marked thrombocytosis, eosinophilia, basophilia and moderate anemia. Bone marrow examination revealed marked megakaryocytic hyperplasia with morphologic abnormality. A diagnosis of essential thrombocythemia was made and the treatment was initiated with combination chemotherapy and maintained by prednisolone and busulfan. The dog successfully achieved complete remission on 100 days after initial presentation and has been good in health without chemotherapy since then.

In this report two dogs with essential thrombocythaemia (ET) are described. Both dogs were presented more or less at the same time with a combination of reduced exercise tolerance and pale mucous membranes without any report of blood loss. Moderate-to-severe, Coomb's-negative anaemia and thrombocytosis (> 1249 x 10'/l) were present. In addition, the peripheral blood smear revealed the presence of basophilia and large numbers of abnormally shaped megakaryocytes in the bone marrow of both dogs. Treatment with vincristine (0.7 mg/m2 once intravenously) and hydroxyurea (500 mg/m2 p.o. per day) was started. Because of insufficient response to treatment after 3 weeks, the dosage of hydroxyurea was increased in both dogs to 2000 mg/m2 p.o. per day. The dogs deteriorated further, however, and were euthanized at 6 weeks after the start of treatment. Blood examination revealed pancytopenia in both dogs, most likely due to the myelosuppressive effects of high-dose hydroxyurea. A survey of veterinary literature on ET is presented, including a comparison of ET in humans.

The diagnosis of essential thrombocythemia in a cat was made by fulfilling the five applicable criteria set forth by the Polycythemia Vera Study Group for use in humans. The criteria were 1) a platelet count persistently above 600,000/microL, 2) a normal initial hematocrit that did not rise in response to iron therapy, 3) normal serum iron concentration, 4) absence of collagen fibrosis of the bone marrow, and 5) no cause for reactive thrombocytosis. In addition, normal thrombopoietin concentrations and splenic hypofunction were demonstrated. Melphalan was not effective in decreasing the platelet count and the cat died of sepsis.

Essential thrombocythemia (ET) in an 11-year-old dog was characterized by persistently high platelet counts (range, 4.19 X 10(6)/microliters to 4.95 X 10(6)/microliters, abnormal platelet morphology, marked megakaryocytic hyperplasia in the bone marrow, absence of circulating megakaryoblasts, and history of splenomegaly and gastrointestinal bleeding. Increased numbers of megakaryocytes and megakaryoblasts (15% to 20%) in the bone marrow were confirmed by a positive acetylcholinesterase reaction. Another significant finding was the presence of a basophilia in blood (4,836/microliters) and bone marrow. The marked persistent thrombocytosis, absence of reactive (secondary) thrombocytosis, abnormal platelet morphology, and quantitative and qualitative changes in the megakaryocytic series in the bone marrow suggested the presence of a myeloproliferative disease. Cytochemical and ultrastructural findings aided in the diagnosis of ET. The dog was treated with radiophosphorus. The results was a rapid decline in the numbers of megakaryoblasts and megakaryocytes in the bone marrow and platelets and basophils in the peripheral blood. The dog died unexpectedly of acute necrotizing pancreatitis and diabetes mellitus before a complete remission was achieved.

Thrombocytopenia may be caused by abnormal platelet production, accelerated removal owing to immunologic or nonimmunologic reasons, or sequestration of platelets in the spleen. Bleeding associated with thrombocytopenia usually presents as petechial or ecchymotic hemorrhages or epistaxis. Immunologic and nonimmunologic cases of thrombocytopenia may be diagnosed with routine hematology, bone marrow cytology, and platelet specific tests. Thrombocythemia may also be associated with platelet functional abnormalities, contrasting the normal platelet function noted in reactive thrombocytosis.

Myeloproliferative disorders are uncommon in the dog and may be classified as chronic or acute. Excessive proliferation of mature cells leads to an overproduction of terminally differentiated blood cells (chronic MPD). Inability of cells to mature results in the accumulation of poorly differentiated blast cells in the peripheral blood and bone marrow (acute MPD). Because the lesion appears to be at the level of the hematopoietic stem cell, all cell lines in the bone marrow may be affected. Diagnosis depends upon the accurate identification of neoplastic cells and the absence of other diseases associated with bone marrow hyperplasia. The prognosis for chronic MPD is guarded, whereas for acute MPD it is grave. Accurate identification of these disorders in animals is important. Investigation and greater understanding of the pathophysiologic mechanisms may lead to more lasting therapeutic successes in the future.

In a case of megakaryoblastic leukemia in a dog, definitive diagnosis was made through use of specific cytochemical stains of circulating and bone marrow blast cells. Morphologic and functional abnormalities of platelets were revealed through transmission electron microscopy and in vitro aggregation of platelets after addition of adenosine diphosphate.

Blood platelets and bone marrow megakaryocytes from a dog with essential thrombocythemia were analyzed by transmission electron microscopy and compared with those of control dogs. Platelets varied in size and shape and contained enlarged and dilated open canalicular systems. Megakaryocytes were dysmorphic and had evidence of abnormal maturation, with large numbers of megakaryoblasts containing alpha granules and poorly organized and reduplicated demarcation membranes. The fewer, more mature megakaryocytes lacked normal cytoplasmic organization. Most notable was the absence of well-demarcated "platelet fields," due to the excessive and disorderly array of demarcation membranes.

Dapsone was given for six days to a dog with chronic skin disease. The dog then became weak and anorectic, and it vomited and had purpura caused by severe thrombocytopenic hemorrhagic diathesis. Despite treatment, the dog died a week later. There were clinical and pathologic evidence that the dog's platelets and megakaryocytes had been destroyed during the first few days of dapsone therapy. It was concluded that the syndrome was dapsone-induced and that thrombocytopenia should be considered among the adverse reactions to dapsone in the dog.

The present report describes a myeloproliferative disease, type megakaryocytic leukemia in three cats, 4, 8 and 11 years old. Clinically, the animals showed severe anemia. Neoplastic infiltrates were present in bone marrow, spleen, lymphnodes, liver and kidney. Two animals were FeLV positive.

Between March 1970 and February 1987, radiophosphorus (32P) was used to treat bone marrow disorders in 6 dogs; 4 had polycythemia vera and 2 had essential thrombocythemia. Activities of 32P given initially ranged from 2.4 to 3.3 mCi/m2. Four dogs responded well to 32P treatment, with gradual resolution of high RBC or platelet counts. Two of these dogs died of intercurrent disease unrelated to their bone marrow disorder, before blood counts could be stabilized. Two dogs did not respond to the initial 32P treatment nor to additional treatments with 32P, and had clinical signs and blood counts stabilized by use of phlebotomy or chemotherapeutic agents. We reviewed and analyzed 5 other cases of bone marrow disorders in dogs treated with 32P and included the findings from their records with the records of our 6 dogs in this retrospective analysis. Of the 8 dogs with polycythemia vera treated with 32P, 5 were given a single treatment that controlled clinical signs and blood counts for the remainder of the follow-up period. Of the 3 dogs treated for thrombocytosis with 32P, 2 had blood counts that responded to a single treatment.