ABSTRACT
A patient with chronic active Epstein-Barr virus (EBV) infection was treated by allogeneic SCT from an HLA-identical sibling donor, using a nonmyeloablative regimen. Even on day 70, mixed chimerism remained together with a quite high viral load. On days 76 and 90, donor lymphocytes were infused after short-term culture with OKT3 plus recombinant IL-2. At 8 days after the last dose, all hematopoietic cells were shown to be donor-type dominant; thereafter, the viral load started to decrease and finally disappeared. Anti-mHA-specific CTLs were generated in vitro, which were shown to be effective in eradicate viral-infected recipient T lymphocytes.
Subject(s)
Epstein-Barr Virus Infections/therapy , Hematopoietic Stem Cell Transplantation/methods , Lymphocyte Transfusion/methods , T-Lymphocytes, Cytotoxic/transplantation , Transplantation Conditioning/methods , Adult , Cells, Cultured , Chronic Disease , Female , Humans , Lymphocyte Activation/immunology , T-Lymphocytes, Cytotoxic/immunology , Transplantation Chimera , Transplantation, Homologous , Treatment Outcome , Viral LoadABSTRACT
A 23-year-old man first visited a local hospital in 1998 because of exertional dyspnea. Peripheral blood examination revealed mild leukocytosis with 82% eosinophils, and he was treated with prednisolone. As the eosinophilia did not improve, he was referred to Tokai University Hospital in March 1999 for further diagnosis and treatment. The patient was diagnosed as having hypereosinophilic syndrome (HES) because of unexplained hypereosinophilia persisting for more than 6 months, resulting in cardiac dysfunction. His disease was progressive in spite of immunosuppressive therapy, interferon-alpha and cytotoxic chemotherapy. Since he had an HLA-identical brother, allogeneic bone marrow transplantation (BMT) was performed in October 1999. After completion of the immunosuppressive therapy on day 79 after BMT, the number of eosinophils gradually increased again. Although we suspected recurrence of the disease, DNA fingerprinting revealed that the peripheral granulocytes were 100% donor type. An increase of interleukin-5 (IL-5) produced by peripheral lymphocytes and a decrease of the Th1/2 ratio suggested that the eosinophilia was related to GVHD. The eosinophilia was eventually controlled by cyclosporin. We conclude that DNA fingerprinting and examination of the IL-5 level and Th1/2 ratio are useful for differentiating between relapse and GVHD in cases of eosinophilia occurring after BMT for HES.
