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Successful mobilization using a combination of plerixafor and G-CSF in pediatric patients who failed previous chemomobilization with G-CSF alone and possible complications of the treatment

DOI: 10.1186/1756-8722-5-14

Keywords: Plerixafor, Hematopoietic Stem Cell Mobilization, Pediatrics, Complications, Interstitial Lung Diseases

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Abstract:

Plerixafor has been introduced for the mobilization of hematopoietic stem cells to peripheral blood, by interfering with the SDF1-CXCR4 interaction. Although it has been FDA-approved in adult patients with non-Hodgkin lymphoma or multiple myeloma [1,2], the pediatric data usage are scarce, particularly in Asian children [3-8].We retrospectively reviewed all 6 patients (3 males, 3 females), who received plerixafor-based mobilization at our center after obtaining the Institutional Review Board approval (H-1108-103-374). They had all previously failed peripheral blood stem cell (PBSC) mobilization by chemotherapy and G-CSF. The patient's characteristics, previous treatments and mobilization chemotherapies are shown. (Table 1) All patients received G-CSF (10 μg/kg) for 4 days, without prior chemotherapy. Then plerixafor (240 μg/kg; Mozobil, Genzyme Inc, Naarden, The Netherlands) and G-CSF (10 μg/kg) were administered subcutaneously, at 10 and 2 hours before each apheresis. CD34+ cells (median, 11.08 × 106/kg; range, 6.34-28.97 × 106/kg) were mobilized successfully in all patients, after 2 to 3 apheresis without immediate complications (for each apheresis: mean, 6.28 × 106/kg: range, 3.17-14.49 × 106/kg). Seven autologous stem cell transplantations were performed, including 1 tandem transplantation, and the results of engraftment were acceptable. (Table 2)Patients #1, #3 and #6 were disease-free at the last follow-up (28, 12 and 3 months after transplantation, respectively), however, patient #4 died on day 3, due to sudden cardiac arrest. Interestingly, two medulloblastoma patients (patients #2 and #5) showed serious lung problems, which include spontaneous pneumomediastinum on day 56 and 11, died on day 102 and 89, respectively. The cause of death of both patients showed to be respiratory failure, of which, the pathogen was not revealed by bronchoalveolar lavage or lung biopsy. The pathologic finding was consistent with a diffuse alveolar damage. In our center, 6 other

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