scholarly journals Pure red cell aplasia and hypogammaglobulinemia associated with Tr-cell chronic lymphocytic leukemia

Blood ◽  
1981 ◽  
Vol 57 (6) ◽  
pp. 1025-1031 ◽  
Author(s):  
T Nagasawa ◽  
T Abe ◽  
T Nakagawa
Keyword(s):  
Cell Differentiation ◽  
Chronic Lymphocytic Leukemia ◽  
B Cell ◽  
Colony Formation ◽  
Pure Red Cell Aplasia ◽  
Lymphocytic Leukemia ◽  
Red Cell ◽  
B Cell Differentiation ◽  
Red Cell Aplasia ◽  
Cell Chronic Lymphocytic Leukemia

A 72-yr-old male with Tr-cell chronic lymphocytic leukemia (Tr-CLL) exhibited pure red cell aplasia (PRCA) and hypogammaglobulinemia. During a remission of Tr-CLL, and while receiving cyclophosphamide therapy, he recovered from PRCA and hypogammaglobulinemia. To investigate the pathogenesis of PRCA and hypogammaglobulinemia, we used coculture techniques to study the effect of the malignant Tr cells on erythroid colony formation and B-cell differentiation to immunoglobulin- producing cells. Varying numbers of malignant Tr cells (2 X 10 to 2 X 10(5) cells) were cocultured with 2 X 10(5) normal bone marrow cells. The malignant Tr cells caused a marked reduction of erythroid colony formation in the plasma clot system. This suppression of erythroid colony formation was reversed when the malignant Tr cells were pretreated with antilymphocyte serum and complement. There was no evidence of inhibitory effects in the serum or the supernatant media of the malignant Tr cells stimulated with phytohemagglutinin (PHA). The malignant Tr cells, stored at --80 degrees C before transfusion, were also capable of suppressing autologous erythroid colony formation after recovery from PRCA. In addition, malignant Tr cells were found to have strong suppressor activity against the immunoglobulin biosynthesis by allogeneic B cells. The in vitro suppressions of both erythroid colony formation and B-cell differentiation provide an explanation for the association of PRCA and hypogammaglobulinemia with Tr-CLL.

scholarly journals Pure red cell aplasia and hypogammaglobulinemia associated with Tr-cell chronic lymphocytic leukemia

Blood ◽  
1981 ◽  
Vol 57 (6) ◽  
pp. 1025-1031 ◽  
Author(s):  
T Nagasawa ◽  
T Abe ◽  
T Nakagawa
Keyword(s):  
Cell Differentiation ◽  
Chronic Lymphocytic Leukemia ◽  
B Cell ◽  
Colony Formation ◽  
Pure Red Cell Aplasia ◽  
Lymphocytic Leukemia ◽  
Red Cell ◽  
B Cell Differentiation ◽  
Red Cell Aplasia ◽  
Cell Chronic Lymphocytic Leukemia

Abstract A 72-yr-old male with Tr-cell chronic lymphocytic leukemia (Tr-CLL) exhibited pure red cell aplasia (PRCA) and hypogammaglobulinemia. During a remission of Tr-CLL, and while receiving cyclophosphamide therapy, he recovered from PRCA and hypogammaglobulinemia. To investigate the pathogenesis of PRCA and hypogammaglobulinemia, we used coculture techniques to study the effect of the malignant Tr cells on erythroid colony formation and B-cell differentiation to immunoglobulin- producing cells. Varying numbers of malignant Tr cells (2 X 10 to 2 X 10(5) cells) were cocultured with 2 X 10(5) normal bone marrow cells. The malignant Tr cells caused a marked reduction of erythroid colony formation in the plasma clot system. This suppression of erythroid colony formation was reversed when the malignant Tr cells were pretreated with antilymphocyte serum and complement. There was no evidence of inhibitory effects in the serum or the supernatant media of the malignant Tr cells stimulated with phytohemagglutinin (PHA). The malignant Tr cells, stored at --80 degrees C before transfusion, were also capable of suppressing autologous erythroid colony formation after recovery from PRCA. In addition, malignant Tr cells were found to have strong suppressor activity against the immunoglobulin biosynthesis by allogeneic B cells. The in vitro suppressions of both erythroid colony formation and B-cell differentiation provide an explanation for the association of PRCA and hypogammaglobulinemia with Tr-CLL.

Anti-CD20 monoclonal antibody rituximab for the treatment of B-cell chronic lymphocytic leukemia-associated pure red cell aplasia

2004 ◽  
Vol 5 (6) ◽  
pp. 546-547 ◽  
Author(s):  
Despina Pantelidou ◽  
Costas Tsatalas ◽  
Dimitris Margaritis ◽  
Vasiliki Kaloutsi ◽  
Emmanuel Spanoudakis ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Chronic Lymphocytic Leukemia ◽  
B Cell ◽  
Pure Red Cell Aplasia ◽  
Lymphocytic Leukemia ◽  
Red Cell ◽  
Red Cell Aplasia ◽  
Anti Cd20 ◽  
Cell Chronic Lymphocytic Leukemia

scholarly journals Difficulties of anemia diagnosis in patients with B-cell chronic lymphocytic leukemia

2021 ◽  
Vol 16 (2) ◽  
pp. 40-47
Author(s):  
I. S. Piskunova ◽  
T. N. Moiseeva ◽  
L. S. Al-Radi ◽  
L. V. Plastinina ◽  
S. R. Goryacheva
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
B Cell ◽  
Hemolytic Anemia ◽  
Autoimmune Hemolytic Anemia ◽  
Immune Thrombocytopenia ◽  
Lymphocytic Leukemia ◽  
Red Cell ◽  
Red Cell Aplasia ◽  
Cell Chronic Lymphocytic Leukemia

Cytopenia commonly occurs in case of chronic lymphocytic leukemia. It can either precede the diagnosis of chronic lymphocytic leukemia or appear at any time during the disease. Autoimmune hemolytic anemia, immune thrombocytopenia, and partial red cell aplasia are most often found among cytopenias in chronic lymphocytic leukemia. At the same time, the development of cytopenia may be associated with the displacement of normal hematopoiesis cells by tumor lymphocytes. It is very important to accurately diagnose and identify the cause of cytopenia in chronic lymphocytic leukemia, since the prognosis and therapy differ significantly.

scholarly journals The B cell IgM Fc receptor: further evidence for the B cell origin of "null" chronic lymphocytic leukemia

Blood ◽  
1984 ◽  
Vol 64 (2) ◽  
pp. 375-379
Author(s):  
RA Rudders ◽  
PA Poldre
Keyword(s):  
Cell Differentiation ◽  
Chronic Lymphocytic Leukemia ◽  
B Cell ◽  
Surface Membrane ◽  
Fc Receptor ◽  
Lymphocytic Leukemia ◽  
B Cell Differentiation ◽  
Facs Analysis ◽  
Membrane Expression ◽  
Surface Immunoglobulin

Fifty-three cases of chronic lymphocytic leukemia (CLL) were studied for the presence of the B cell IgM Fc receptor (Fc microR) using an aggregated IgM reagent. Restricted surface immunoglobulin, using conventional immunofluorescent techniques and FACS analysis, was detected in 43 cases (81%). The cells in the remaining ten cases (19%) expressed negligible surface immunoglobulin (slg-) and did not form E rosettes (E-), but this “null” subset clearly expressed the B cell Fc microR. The coincident membrane expression of the B1 antigen and the la- like antigen, as well as serial studies showing surface membrane light chain acquisition (in one patient), provided additional evidence for the B cell origin of this slg-E- subset. This subgroup of CLL appears to correspond phenotypically to a normal counterpart at a stage of B cell differentiation between the pre-B cell and the slgM+ early B cell. The B cell Fc microR appears to be a consistent and potentially useful marker for sl gE (“null”) CLL.

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