Home About us Contact
|
Home About us Contact | ||
|
|
||
GVHD Prophylaxis (gvhd + prophylaxis)
Selected AbstractsSuccessful non-T-cell-depleted HLA-haploidentical 3-loci mismatched bone marrow transplantationEUROPEAN JOURNAL OF HAEMATOLOGY, Issue 6 2005Shigeki Yagyu Abstract:, A 17-year-old boy with therapy-related acute myelocytic leukemia (FAB classification-M0) successfully received allogeneic non-T-cell depleted (non-TCD) bone marrow transplantation (BMT) from his 3-loci HLA-mismatch mother, although pre-BMT detection of feto-maternal microchimerism was negative. The BMT was performed with reduced intensity conditioning (total body irradiation; 4 Gy, fludarabine; 20 mg/m2 × 6, and melphalan; 70 mg/m2 × 2) and short-course methotrexate and tacrolimus for GVHD prophylaxis. Complete donor chimera was obtained on day 19, associated with Grade 3 acute GVHD (skin: Stage 1, liver: Stage 0, gut: Stage 3) that was well controlled with immunosuppressive therapies. At day 200 of transplantation, he was in complete remission with no signs of chronic GVHD. Our case suggests that non-TCD HLA-haploidentical 3-loci mismatched BMT can be safely performed from mother to offspring even when feto-maternal microchimerism is barely detectable with the current detection procedure. [source] HLA-haploidentical nonmyeloablative stem cell transplantation: induction to tolerance without passing through mixed chimaerismINTERNATIONAL JOURNAL OF LABORATORY HEMATOLOGY, Issue 2 2005K. IKEGAME Summary There are few reports of unmanipulated HLA-haploidentical nonmyeloablative stem cell transplantation (NST) using only pharmacological acute graft- vs. -host disease (GVHD) prophylaxis. We present here a successful case of unmanipulated HLA-haploidentical NST for mediastinal large B cell lymphoma that was resistant to autologous peripheral blood stem cell transplantation (PBSCT). The conditioning regimen consisted of fludarabine, busulfan and rabbit anti-T-lymphocyte globulin (ATG) in addition to rituximab. GVHD prophylaxis was performed using tacrolimus and methylprednisolone 1 mg/kg. The patient had rapid engraftment, with 100% donor chimaerism in the lineages of both T cells and granulocytes on day +12, but developed no GVHD clinically. The patient is still in complete remission past day +1020, with no sign of chronic GVHD without receiving immunosuppressive agents. HLA-haploidentical NST may be performed without utilizing mixed chimaerism. [source] CD41+ and CD42+ hematopoietic progenitor cells may predict platelet engraftment after allogeneic peripheral blood stem cell transplantationJOURNAL OF CLINICAL APHERESIS, Issue 2 2001T. Demirer Abstract The objective of this study was to quantify subpopulations of CD34+ cells such as CD41+ and CD42+ cells that might represent megakaryocyte (MK) precursors in peripheral blood stem cell (PBSC) collections of normal, recombinant human granulocyte-colony stimulating factor (rhG-CSF) primed donors and to determine whether there is a statistical association between the dose infused megakaryocytic precursors and the time course of the platelet recovery following an allogeneic PBSC transplantation. Twenty-six patients with various hematologic malignancies transplanted from their HLA identical siblings between July 1997 and December 1999 were used. All patients except one with severe aplastic anemia who had cyclophosphamide (CY) alone received busulfan-CY as preparative regimen and cyclosporine-methotrexate for GVHD prophylaxis. Normal healthy donors were given rhG-CSF 10 ,g/kg/day subcutaneously twice daily and PBSCs were collected on days 5 and 6. The median number of infused CD34+, CD41+ and CD42+ cells were 6.61 × 106/kg (range 1.47,21.41), 54.85 × 104/kg (5.38,204.19), and 49.86 × 104/kg (6.82,430.10), respectively. Median days of ANC 0.5 × 109/L and platelet 20 × 109/L were 11.5 (range 9,15) and 13 (8,33), respectively. In this study, the number of CD41+ and CD42+ cells infused much better correlated than the number of CD34+ cells infused with the time to platelet recovery of 20 × 109/L in 26 patients receiving an allogeneic match sibling PBSC transplantation (r = ,0.727 and P < 0.001 for CD41+ cells, r = ,0.806 and P < 0.001 for CD42+ cells, r = ,0.336 and P > 0.05 for CD34+ cells). There was an inverse correlation between the number of infused CD41+ and CD42+ cells and duration of platelet engraftment. Therefore, as the number of CD41+ and CD42+ cells increased, duration of platelet engraftment (time to reach platelet count of , 20 × 109/L) shortened significantly. Based on this data we may conclude that flow cytometric measurement of CD41+ and CD42+ progenitor cells may provide an accurate indication of platelet reconstitutive capacity of the allogeneic PBSC transplant. J. Clin. Apheresis. 16:67,73, 2001. © 2001 Wiley-Liss, Inc. [source] Hepatitic pattern of graft versus host disease in childrenPEDIATRIC BLOOD & CANCER, Issue 5 2007Héctor Melín-Aldana MD Abstract Background Liver involvement by graft-versus-host disease (GVHD) is characterized histologically by bile duct damage, which may be severe. A different pattern, "hepatitic GVHD," has been described in adult patients. This pattern also shows marked lobular hepatitis and hepatocellular damage. We report the development of hepatitic GVHD in six pediatric patients. Procedure Clinical information and histologic features of liver biopsy samples were retrospectively reviewed. Results Patients' ages ranged from 3 to 11 years. Underlying diagnosis, pre-transplant conditioning and GVHD prophylaxis varied. Peripheral blood stem cells were the source of the allograft in four patients, matched sibling in one, and matched-unrelated donor in one. Hepatic GVHD was detected between 149 and 310 days post-transplant. Prior acute GVHD had developed in two patients, and involved the skin and/or gastrointestinal tract. No patients had significant ductopenia. Only one patient had significant lymphocytic infiltration of bile ducts (ductitis). Bile duct epithelial damage and significant portal/periportal inflammation were present in all patients. Lobular necro-inflammation was present in five patients. Five patients improved with immunosuppression and one died with progressive GVHD. Conclusions This series focuses on hepatitic GVHD in pediatric patients. Clinical and histologic patterns are similar to what has been described in adults. Specific etiology and pathogenesis of this entity remain unclear. Pediatr Blood Cancer 2007;49:727,730. © 2006 Wiley-Liss, Inc. [source] Early transplantation of unrelated cord blood in a two-month-old infant with Wiskott,Aldrich syndromePEDIATRIC TRANSPLANTATION, Issue 5 2007Tang-Her Jaing Abstract:, This report exemplified a success of unrelated CBT in a two-month-old boy with Wiskott,Aldrich Syndrome. Umbilical cord blood was chosen as the stem-cell source because of its immediate availability and reduced tendency to cause GVHD. The conditioning regimen was cyclophosphamide, busulfan, and antithymocyte globulin. GVHD prophylaxis consisted of cyclosporin and methylprednisolone. The patient received an HLA 1-locus-mismatched cord blood unit, and the total number of infused nucleated cells was 11.14 × 107/kg. Neutrophil engraftment was achieved on day +11, and a platelet count greater than 50 × 109/L was achieved on day +71. He is currently alive and doing well at nine months post-transplant and free of any bleeding episodes. This case suggests that unrelated donor CBT may be safe and technically feasible, even in early infancy, when an appropriately matched related or unrelated donor is unavailable. [source] Rapamycin and MPA, But Not CsA, Impair Human NK Cell Cytotoxicity Due to Differential Effects on NK Cell PhenotypeAMERICAN JOURNAL OF TRANSPLANTATION, Issue 9 2010D. N. Eissens Cyclosporin A (CsA), rapamycin (Rapa) and mycophenolic acid (MPA) are frequently used for GVHD prophylaxis and treatment after allogeneic stem cell transplantation (SCT). As NK cells have received great interest for immunotherapeutic applications in SCT, we analyzed the effects of these drugs on human cytokine-stimulated NK cells in vitro. Growth-kinetics of CsA-treated cultures were marginally affected, whereas MPA and Rapa severely prevented the outgrowth of CD56bright NK cells. Single-cell analysis of NK cell receptors using 10-color flow cytometry, revealed that CsA-treated NK cells gained a similar expression profile as cytokine-stimulated control NK cells, mostly representing NKG2A+KIR,NCR+ cells. In contrast, MPA and Rapa inhibited the acquisition of NKG2A and NCR expression and NK cells maintained an overall NKG2A,KIR+NCR+/, phenotype. This was reflected in the cytolytic activity, as MPA- and Rapa-treated NK cells, in contrast to CsA-treated NK cells, lost their cytotoxicity against K562 target cells. Upon target encounter, IFN-, production was not only impaired by MPA and Rapa, but also by CsA. Overall, these results demonstrate that CsA, MPA and Rapa each have distinct effects on NK cell phenotype and function, which may have important implications for NK cell function in vivo after transplantation. [source] Encouraging preliminary results in 12 patients with high-risk haematological malignancies by omitting graft-versus-host disease prophylaxis after allogeneic transplantationBRITISH JOURNAL OF HAEMATOLOGY, Issue 2 2000Athanasios B.-T. Immunosuppressive therapy, routinely given after allogeneic transplantation to modulate graft-versus-host disease (GVHD) may have an adverse effect on the graft-versus-tumour (GVT) effect. Twelve patients with high-risk haematological malignancies were given cyclophosphamide, total body irradiation and antithymocyte globulin followed by peripheral blood stem cell grafts from HLA-identical siblings without prophylactic immunosuppression. At the earliest clinical evidence of GVHD, patients were treated with high-dose solumedrol and tacrolimus. Prompt haematological recovery [absolute neutrophil count (ANC) >,1·0 × 109/l] was observed (median time 9 d). All patients developed grade III,IV GVHD (median onset 9 d), involving the skin (11), intestine (five) and liver (three). Of nine evaluable patients, seven developed chronic GVHD [extensive (six), limited (one)]. Six patients died 1,6·5 months after transplantation. Three patients died from treatment-related complications, two from acute GVHD and one from relapsing disease. The remaining six patients are alive 5,26 months after transplantation, five in complete remission and one myeloma patient in very good partial remission. In conclusion, omission of post-transplantation GVHD prophylaxis is feasible, does not lead to graft failure or a high incidence of uncontrollable GVHD and appears to be associated with encouraging clinical responses in a group of patients with high-risk disease features. [source] | |||||||||||||||||||