A 74-year-old male complaining of nasal bleeding was admitted to the Kyushu University Hospital on August 25, 1986. On admission his hemoglobin was 7.4 g/d
l, platelet count 0.3×10
4/μ
l, and white blood cell count 3,700/μ
l with 29% blasts. Bone marrow aspirates showed dysplasia of trilineage blood cells with increased blasts (24.4%). Bone marrow chromosome study revealed a karyotype of 48, XY, -2, -7, +19, +21?, +2 mar in all banded cells analyzed. He was diagnosed as having refractory anemia with exess of blasts, and was treated with aclarubicin and low-dose Ara-C. On September 16, the leukemic blasts increased to 54.8% in the bone marrow, suggesting progression to leukemia. He was then transferred to the Kyushu Cancer Center Hospital as an outpatient. On March 31, 1987, he was admitted to our hospital when his white blood cell count increased to 40,500/μ
l with 88% blasts. More than 80% of blasts were positive for platelet specific glycoproteins (Gp Ib, IIb/IIIa) and about 60% of blasts, on electron microscopic study, demonstrated to possess platelet peroxidase in the perinuclear space and endoplasmic reticulum. A diagnosis of acute megakaryoblastic leukemia (AMKL, M7 of FAB) was made. His blasts also reacted with 3Al (84%) and A2B5 (92%) monoclonal antibodies which detect antigens on early T cells and neuroblastoma cells, respectively. Using Southern blot analysis with J
H, Cβ
1 and Cγ probes, his blasts seemed to have the germ-line immunoglobulin and T cell receptor genes. Chromosome analysis of cells from the bone marrow and peripheral blood revealed 50, XY, +8, -9, -18, +19, +21, 1q-, t (2q-; 7p+), +3 mar as the main karyotype. He died of respiratory failure due to pneumonia and pulmonary bleeding on June 4, 1987. Postmortem examination revealed widespread megakaryoblastic infiltration of the bone marrow and other organs but there was no evidence for myelofibrosis.
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