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T‐cell chronic lymphocytic leukemia with pure red cell aplasia: Laboratory demonstration of persistent leukemia in spite of apparent complete clinical remission
Author(s) -
Hansen Richard M.,
Lerner Neil,
Abrams Ross A.,
Patrick Catherine W.,
Malik Mohammad I.,
Keller Robert
Publication year - 1986
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.2830220112
Subject(s) - pure red cell aplasia , lymphocytosis , medicine , bone marrow , macrocytic anemia , hypoplasia , aplasia , leukemia , peripheral blood mononuclear cell , cyclophosphamide , bone marrow aplasia , pathology , immunology , anemia , biology , chemotherapy , biochemistry , in vitro
A 40‐year‐old woman presented with splenomegaly, macrocytic anemia, and red cell aplasia. Although lymphocytosis was absent in the peripheral blood, large atypical lymphoid aggregates were present in the bone marrow. Splenectomy resulted in partial remission of red cell aplasia, but a gradual increase in the number of peripheral blood lymphocytes followed during the next 36 months. Flow cytometric analysis demonstrated that the majority of these peripheral blood lymphocytes had suppressor, natural killer T‐cell phenotye. No other treatment was given until red cell hypoplasia worsened 42 months after initial presentation. Repeat bone marrow evaluation again demonstrated severe erythroid hypoplasia and large abnormal lymphocytic infiltrates. Cyclophosphamide given for 8 months resulted in complete resolution of the red cell aplasia and complete clinical remission of CLL. However, flow cytometric analysis revealed persistent increase in bone marrow T‐cells, and bone marrow co–culture studies demonstrated residual ability of peripheral blood mononuclear cells to inhibit erythropoiesis in vitro, suggesting that residual, clinically undetectable leukemia persists in spite of complete clinical remission.