Context
Pure red-cell aplasia (PRCA) is characterized by anemia, reticulocytopenia, and severe erythroid hypoplasia of the bone marrow associated with normal maturation of myeloid and megakaryocytic cell lines. Its pathogenesis is considered to be heterogeneous with various autoimmune mechanisms (autoantibodies and T cell mediated) and secondary forms (following parvovirus B19 infection) playing a causal role. A notable feature of PRCA is the ability of eythropoietic cells to proliferate in vitro but not in vivo suggesting that there maybe an inhibitor in vivothat blocks erythropoiesis. Most patients respond to immunosuppresive therapy such as cyclosporin. A proportion of PRCA is associated with T cell large granular lymphocytic leukemia, chronic lymphocytic leukemia or thymoma. A combination of large granular lymphocyte (LGL) expansion with PRCA may also occur in association with rheumatoid arthritis or Felty?s syndrome. The role of expansion of large granular lymphocytes (LGLs), some of which may have a natural killer cell or T cell phenotype, in PRCA is not clear. To demonstrate, in a patient with PRCA and expansion of LGLs, that the LGLs are directly involved in the lysis of erythropoietic precursors.