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A 77-year-old man was admitted because of lumbago in 1989. Erythrocyte sedimentation rate was 75 mm/hour, hemoglobin 8.0 g/dl, white cell counts 2,400/mm³ without plasma cells, platelet counts 5.0×10⁴/mm³. Bence Jones proteinuria was demonstrated. Roentgenogram of skeleton revealed diffuse osteoporosis with oppression fractures of the thoratic and lumbar vertebrae. Immunoelectrophoresis revealed monoclonal Bence Jones (κ) M bow. Bone marrow smears showed 15.0% large and immature plasma cells. A diagnosis of multiple myeloma (Bence Jones κ) was made. During the next 28 days, leucocyte counts increased to 8,900/mm³ and plasma cell counts to 24.5%(2,181/mm³, respectively. A diagnosis of plasma cell leukemia was made. Plasma cells were proved in pleural effusions. Serum β₂ microglobulin increased to 18.4 μg/ml. In spite of administration of alkeran and prednisolone, he died of pneumonia one month after the onset of plasma cell leukemia.

A 77-year-old man was admitted because of lumbago in 1989. Erythrocyte sedimentation rate was 75 mm/hour, hemoglobin 8.0 g/dl, white cell counts 2,400/mm³ without plasma cells, platelet counts 5.0×10⁴/mm³. Bence Jones proteinuria was demonstrated. Roentgenogram of skeleton revealed diffuse osteoporosis with oppression fractures of the thoratic and lumbar vertebrae. Immunoelectrophoresis revealed monoclonal Bence Jones (κ) M bow. Bone marrow smears showed 15.0% large and immature plasma cells. A diagnosis of multiple myeloma (Bence Jones κ) was made. During the next 28 days, leucocyte counts increased to 8,900/mm³ and plasma cell counts to 24.5%(2,181/mm³, respectively. A diagnosis of plasma cell leukemia was made. Plasma cells were proved in pleural effusions. Serum β₂ microglobulin increased to 18.4 μg/ml. In spite of administration of alkeran and prednisolone, he died of pneumonia one month after the onset of plasma cell leukemia.