Expression of CD 10 by human T cells that undergo apoptosis both in vitro and in vivo

CD20 and 2 months after thalidomide, he had Hb concentration of 8.6 g/dL, WBC count of 3.6 3 109/L, PLT count of 650 3 109/L, and IgM count of 1180 mg/dL. Two months later, he presented to our department with an Hb concetration of 8.1 g/dL, WBC count of 2.4 3 109/L (neutrophils 60%, lymphocytes 31%, monocytes 9%), and PLT count of 1000 3 109/L. Bone marrow smear and trephine biopsy revealed an hyperplastic marrow with marked dysplasia of the erythrocyte progenitors, highly increased number of markedly dysplastic megakaryocytes, left shifted myeloid series with 20% blasts, and 30% lymphocytic infiltration by small B-lymphoid cells and lymphoplasmacytes (cIgk). Immunophenotype of the bone marrow, by flow cytometry, confirmed the presence of an immature blast, cell population that was CD131, CD341, and CD381, and a lymphocytic component that was CD201 and CD52 with k light-chain restriction; karyotype was normal. The patient is currently being given hydroxyurea with a PLT count reduction to 740 3 109/L after 2 weeks’ administration. It seems that the administration of thalidomide and the antiCD20 monoclonal antibody was ineffective in controlling the IgM-MGUS problem that subsequently evolved into Waldenstrom macroglobulinemia; on the other hand, it caused a myeloproliferative reaction leading to a myeloproliferative disorder not precisely classifiable, which, however, is currently the major hematologic problem of this patient. This case is another example of myeloproliferative reaction with marked thrombocytosis after thalidomide administration as reported by Tefferi and Eliott.1 These observations indicate that, until thalidomide’s mode of action and its complications are better known, this drug should be used with great caution.