Modulation of CD20 antigen expression after rituximab treatment: A retrospective study in patients with chronic lymphocytic leukemia
2010; Elsevier BV; Volume: 32; Issue: 11 Linguagem: Inglês
10.1016/j.clinthera.2010.10.005
ISSN1879-114X
AutoresFiorella D’Auria, Roberto Guariglia, Oreste Villani, Giovanna Mansueto, Vitina Grieco, Antonia Zonno, Gabriella Bianchino, Luigina Di Giovannantonio, Giulia Vita, Pellegrino Musto,
Tópico(s)Immunodeficiency and Autoimmune Disorders
ResumoBackground: CD20 antigen down-modulation by anti-CD20 rituximab treatment is a well-recognized phenomenon in patients with non-Hodgkin's lymphoma. However, few data are currently available on this topic in other lymphoproliferative disorders, in particular in chronic lymphocytic leukemia (CLL). Objective: The aim of this study was to establish how many patients with CLL show a disappearance of CD20 antigen after salvage treatment with rituximab and its possible clinical significance. Methods: We sequentially analyzed CD20 expression by flow cytometry in patients treated with rituximab in combination with other agents for relapsed/resistant disease. Results: Eleven white patients with CLL (6 females, 5 males; median age, 71.6 years [range, 60–84 years]) were included in the study. Three of the 11 patients were not positive for CD20 due to complete response at baseline. Four of the remaining 8 patients (50%) lacked CD20 antigen on neoplastic cells after monoclonal antibody treatment. Two of them developed Richter's syndrome and died within 4 months. The phenomenon was transient in the other 2 patients, who were alive after a follow-up of 25 and 26 months, respectively, with CD20-positive recurrent disease. Conclusions: In this study, CD20 antigen disappearance in patients with CLL treated with rituximab-containing salvage regimens occurred in 4 of 8 (50%) tested patients, half of whom developed Richter's syndrome. [Note: Since the initial writing and submission, a third patient developed Richter's syndrome.] In 2 patients (50%), CD20 returned at progression.
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