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Peripheral blood stem cell harvest (PBSCH) is an essential procedure for autologous stem cell transplantation (ASCT) in patients with multiple myeloma (MM). Safe engraftment was reported to require infusion of more than 2.0 × 106 CD34+ cells/kg of the recipient’s weight.1 Plerixafor is a selective inhibitor of C-X-C chemokine receptor type 4 (CXCR4), which blocks the interaction of CXCR4 with its ligand C-X-C motif chemokine 12 (CXCL12). As this interaction is needed to retain CD34+ cells in the bone marrow, plerixafor facilitates the rapid mobilization of CD34+ cells.2 In patients with non-Hodgkin’s lymphoma (NHL) and MM, plerixafor and granulocyte-colony stimulating factor (G-CSF) were reported to be well tolerated, resulting in a significantly higher number of patients from whom the optimal target number of CD34+ cells was able to be collcted for transplantation than with G-CSF alone.3,4 Plerixafor is expected to facilitate the collection of CD34+ cells to perform ASCT even in patients without sufficient CD34+ cells. However, limited information is available regarding adverse events following ASCT using plerixafor for mobilized stem cells. Here, we present the case of a patient with refractory MM who developed secondary graft failure following ASCT with plerixafor for mobilized stem cells. In 2014, a 63-year-old Japanese female developed left hip pain and was diagnosed with a sacral tumor. She was then referred to our hospital. Her medical history consisted of tonsil surgery at the age of 15 years and total resection of a uterine myoma at the age of 34 years. Her initial laboratory findings are shown in Table 1. Electrophoretic analysis of proteins revealed IgA lambda-type M-protein. Of note, Bence Jones protein was negative, and the free light-chain ratio was within the normal range. Bone marrow examination revealed that the hypocellular bone marrow consisted of 44% atypical plasma cells. Chromosomal analysis of bone marrow specimens using G-band staining was normal. However, bone marrow biopsy specimens demonstrated that the trabeculae were melting or thinning, and there was monotonous proliferation of small circular cells with eccentric nuclei and a perinuclear pale zone. These cells were positive for kappa and IgA, and negative for lambda, IgM, and IgG. In February 2014, radiation therapy was performed for the sacral tumor, and bortezomib plus dexamethasone (BD) therapy comprising subcutaneous injection of bortezomib (1.3 mg/m2) and dexamethasone (20 mg/body weight) on days 1, 8, 15, and 22 was initiated for 5 weeks. After 4 courses of BD therapy, although the M-protein levels decreased, new subcutaneous nodules appeared on the forehead and outside the right orbit. In July 2014, PBSCH with 2 days of cyclophosphamide (CY; 2000 mg/m2) as the conditioning regimen and PBSCH with G-CSF alone were performed; however, the total collection yield from these 2 PBSCH cycles was only 1.1 × 106 CD34+ cells/kg of PBSCs. Following CY administration, the sacral tumor disappeared, the number of plasma cells in the bone marrow decreased to 0.4%, and the M-protein disappeared, as confirmed by protein electrophoresis. In April 2015, lenalidomide therapy of 25 mg per day on days 1–21 every 4 weeks was initiated because an extramedullary mass developed on the anterior chest and forehead. However, the lenalidomide dosage was decreased to 10 mg per day on days 1–21 every 4 weeks because of severe cytopenia. The extramedullary mass disappeared soon after the initiation of lenalidomide therapy, which lasted for 15 courses. In July 2016, although the Therapy-related Myelodysplastic Syndrome after Autologous Stem Cell Transplantation Using Plerixafor for Mobilized Stem Cells in a Patient with Multiple Myeloma

journal of clinical and experimental hematopathology

Therapy-related Myelodysplastic Syndrome after Autologous Stem Cell Transplantation Using Plerixafor for Mobilized Stem Cells in a Patient with Multiple Myeloma