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We have obtained consent from the patient for publication of this case report. The patient was a 73-year-old male. A routine medical checkup in 2008 revealed anemia and he was referred to our department. The laboratory findings at that time were as follows: hemoglobin (Hb), 8.8 g/dL; serum β2-microglobulin, 3.6 mg/mL; serum immunoglobulin M (IgM), 3880 mg/dL. Serum immunoelectrophoresis revealed a positive result for IgM-κ, and bone marrow examination showed an increase in small lymphocytes. The cell surface marker profile was as follows: IgM+, κ+, CD5+, CD10-, CD19+, CD20+, CD22+, CD23-, CD25+), FMC7+ and CD138-. Computed tomographic examination revealed no lymphadenopathy or hepatosplenomegaly. We diagnosed the patient with Waldenstrom Macroglobulinemia (WM). The patient was not tested for the myeloid differentiation factor 88 (MYD88) L256P mutation. The clinical course is shown in the figure. In 2009, the patient became transfusion-dependent, but had no systemic symptoms. In 2010, he developed systemic symptoms, and received treatment with R-COP (rituximab: 375 mg/m2, cyclophosphamide: 750 mg/ m2, vincristine: 1.5 mg/m2 and prednisolone: 100 mg for 5 days). This therapy proved ineffective, and the patient received bendamustine (120 mg/m2/day for 2 consecutive days) in 2011. With this treatment, the patient demonstrated partial response (PR).

journal of clinical and experimental hematopathology

A case of Waldenstrom Macroglobulinemia in which intermittent one-day administration cycles of bendamustine were effective for alleviation of nausea and maintenance of remission