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Clonality of acquired primary pure red cell aplasia
Author(s) -
Masuda Michihiko,
Saitoh Hiroshi,
Mizoguchi Hideaki
Publication year - 1999
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/(sici)1096-8652(199911)62:3<193::aid-ajh10>3.0.co;2-d
Subject(s) - pure red cell aplasia , peripheral blood mononuclear cell , bone marrow , gene rearrangement , biology , microbiology and biotechnology , t cell receptor , polymerase chain reaction , immunology , pathology , medicine , t cell , gene , immune system , in vitro , biochemistry
Acquired primary pure red cell aplasia (PRCA) has frequently been shown to be associated with T cells that inhibit marrow erythropoiesis. A 41‐year‐old female presented with anemia in December 1985. Bone marrow examination revealed 1.8% erythroid cells. A diagnosis of PRCA was made. She received prednisolone, and her hemoglobin level recovered to 12 g/dl. In February 1995, her hemoglobin level decreased to 5.8 g/dl, and acquired primary PRCA recurred. Surface markers of peripheral blood mononuclear cells demonstrated CD4/8 ratio inversion. The T‐cell receptor (TCR)‐β chain gene showed germ line configuration by Southern blot analysis of the mononuclear cells in peripheral blood. However, stepdown polymerase chain reaction analysis revealed that the TCR‐β gene of peripheral blood mononuclear cells was rearranged. With highly sensitive polymerase chain reaction analysis, clonality of T cells was confirmed. We propose that some acquired primary PRCA patients have a T‐cell clonal disorder, similar to some PRCA patients with large granular lymphocytes leukemia or thymoma. Am. J. Hematol. 62:193–195, 1999. © 1999 Wiley‐Liss, Inc.