We describe a case of CMV ventriculoencephalitis in a severely immunocompromised bone marrow transplant recipient who was receiving combination therapy with ganciclovir and foscarnet for treatment of viremia and retinitis. Analysis of sequential viral isolates recovered from the patient's cerebrospinal fluid suggested that disease developed because of the presence of viral resistance and, possibly, low tissue penetration of antiviral agents.
Summary. We have employed a new cytoreductive regimen to transplant two patients with Fanconi anaemia (FA), using T cell-depleted two HLA-allele disparate related peripheral blood stem cell transplants (PBSCTs). Patient 1, a 5-year-old male with FA and aplastic anaemia, initially received an HLA two-antigen mismatched unrelated cord blood transplant and failed to engraft. He received fludarabine (Flu) and cyclophosphamide (Cy), followed by a CD34 1 E-rosette, T cell-depleted, granulocyte colony-stimulating factor (G-CSF)-mobilized PBSCT from his HLA B-DRB1 mismatched father. He received anti-thymocyte globulin (ATG), steroids, FK506 and G-CSF after transplant for rejection and graft-versus-host disease (GVHD) prophylaxis. The patient is now 23 months after SCT with no evidence of GVHD and with full haematopoietic and immune reconstitution. Patient 2, a 10-year-old boy with FA and myelodysplastic syndrome, received single-dose total body irradiation (SDTBI), Flu and Cy followed by a CD341 E 2 , Tcell-depleted, G-CSF-mobilized PBSCT from his HLA B-DRB1 mismatched sister. He also received ATG, steroids, FK506 and G-CSF after transplant. The patient is now 12 months after SCT in complete remission with no evidence of GVHD. Absolute neutrophil counts (ANC) of . 1 Â 10 9 /l were achieved on day 11 and day 10 post transplant respectively. Both patients are fully engrafted. In summary, we report two successful T-cell-depleted stem cell transplants from mismatched related donors for the treatment of Fanconi anaemia, using a fludarabine-based cytoreduction. Both patients experienced minimal toxicity, rapid engraftment and no GVHD.
We have employed a new cytoreductive regimen to transplant two patients with Fanconi anaemia (FA), using T cell-depleted two HLA-allele disparate related peripheral blood stem cell transplants (PBSCTs). Patient 1, a 5-year-old male with FA and aplastic anaemia, initially received an HLA two-antigen mismatched unrelated cord blood transplant and failed to engraft. He received fludarabine (Flu) and cyclophosphamide (Cy), followed by a CD34(+) E-rosette(-) (CD34(+)E(-)), T cell-depleted, granulocyte colony-stimulating factor (G-CSF)-mobilized PBSCT from his HLA B-DRB1 mismatched father. He received anti-thymocyte globulin (ATG), steroids, FK506 and G-CSF after transplant for rejection and graft-versus-host disease (GVHD) prophylaxis. The patient is now 23 months after SCT with no evidence of GVHD and with full haematopoietic and immune reconstitution. Patient 2, a 10-year-old boy with FA and myelodysplastic syndrome, received single-dose total body irradiation (SDTBI), Flu and Cy followed by a CD34(+)E(-), T-cell-depleted, G-CSF-mobilized PBSCT from his HLA B-DRB1 mismatched sister. He also received ATG, steroids, FK506 and G-CSF after transplant. The patient is now 12 months after SCT in complete remission with no evidence of GVHD. Absolute neutrophil counts (ANC) of > 1 x 10(9)/l were achieved on day 11 and day 10 post transplant respectively. Both patients are fully engrafted. In summary, we report two successful T-cell-depleted stem cell transplants from mismatched related donors for the treatment of Fanconi anaemia, using a fludarabine-based cytoreduction. Both patients experienced minimal toxicity, rapid engraftment and no GVHD.
61rial and resources will be shared with the learner. A comprehensive, multidisciplinary plan of care should include strategies for overcoming cultural diversity issues.The long term survival rates for children with metastatic neuroblastoma are poor, even with high-dose chemotherapy and autologous bone marrow transplantation. The poor prognosis associated with this disease has led to a search for new treatment modalities that will improve both morbidity and mortality. One such treatment option is the use of metaiodobenzylguanidine (MIBG) with a subsequent autologous bone marrow rescue. MIBG is a guanethidine derivative with a structure analogous to norepinephrine that permits selective concentration in the sympathetic nervous system. Because of this specificity, MIBG is now being studied in the detection and treatment of neuroblastoma.MIBG is administered intravenously. Due to the radioactivity of this agent, patients should ideally be placed in a lead-lined room during the infusion and remain there until cleared by radiation safety (often 3 to 4 days).The use of MIBG in the adult patient has been well documented. The treatment of the pediatric patient with this highly radioactive material remains a challenge. Small children must be placed in a lead-lined room with minimal adult supervision and nursing care. These children require antiemetics, hydration and sedation. The Pediatric Stem Cell Program at Duke is one center that is studying the use of MIBG with autologous bone marrow rescue in children. The purpose of this poster is to: 1. Define the mechanism, rationale and current status of MIBG therapy in neuroblastoma patients. 2. Identify the unique challenges that pediatric patients face while receiving MIBG in a lead-lined room.3. Describe nursing strategies to care for these patients for the duration of the therapy. The use of MIBG with autologous bone marrow rescue has the potential to improve long term survival rates of children with metastatic neuroblastoma. The care of these children requires a well-defined plan of care. This poster will illustrate how to safely provide care to the child receiving MIBG therapy.
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