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Molecular and flow cytometry characterization during the follow‐up of three simultaneous lymphoproliferative disorders: Hairy cell leukemia, monoclonal B‐cell lymphocytosis, and CD4 ++ /CD8 +/−dim T‐large granular lymphocytosis—A case report
Author(s) -
Garrido P.,
Jiménez P.,
Sánchez C.,
Valero F.,
Balanzategui A.,
Almagro M.,
López P.,
de Pablos J. M.,
Navarro P.,
Cabrera A.,
González M.,
Jurado M.,
RuizCabello F.
Publication year - 2011
Publication title -
cytometry part b: clinical cytometry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.646
H-Index - 61
eISSN - 1552-4957
pISSN - 1552-4949
DOI - 10.1002/cyto.b.20579
Subject(s) - lymphocytosis , hairy cell leukemia , lymphoproliferative disorders , chronic lymphocytic leukemia , hairy cell , leukemia , cd8 , immunology , flow cytometry , immunophenotyping , biology , monoclonal , antigen , microbiology and biotechnology , monoclonal antibody , lymphoma , antibody
The simultaneous diagnosis of hairy cell leukemia and monoclonal B‐cell lymphocytosis with the characteristics of “indolent” chronic lymphocytic leukemia is rare but not unknown. However, an association with a third clonal lymphoproliferative disorder has not previously been described. We report the simultaneous presence of hairy cell leukemia, monoclonal B‐cell lymphocytosis, and alpha beta CD4 ++ /CD8 + T‐cell large granular lymphocytosis in a 63‐year‐old man. After the diagnosis, the three lymphoproliferative disorders (i.e., two of B‐cell lineage and one of T‐cell lineage) were characterized by analysis of multiple sequential bone marrow and peripheral blood samples using flow cytometry and molecular techniques. We discuss these findings in the context of chronic antigen stimulation, immunosuppression, and apoptotic pathway alterations, which might be implicated in the accumulation of these abnormal clones in the same patient. Because the phenotype of the three clones is compatible with fully differentiated B lymphocytes (consistent with a postgerminal origin) and T‐CD4 ++ cells, we favor the possibility of an antigen‐driven mechanism and a dysregulation of homeostatic apoptosis in this patient. © 2010 International International Clinical Cytometry Society