Maximilian Christopeit1, Oliver Kuss, Jürgen Finke, Ulrike Bacher, Dietrich Wilhelm Beelen, Martin Bornhäuser, Rainer Schwerdtfeger, Wolfgang Andreas Bethge, Nadezda Basara, Martin Gramatzki, Johanna Tischer, Hans-Jochem Kolb, Lutz Uharek, Ralf G Meyer, Donald Bunjes, Christof Scheid, Hans Martin, Dietger Niederwieser, Nicolaus Kröger, Hartmut Bertz, Hubert Schrezenmeier, Christoph Schmid. 1. Maximilian Christopeit and Oliver Kuss, University of Halle, Halle (Saale); Jürgen Finke and Hartmut Bertz, University Hospital Freiburg, Freiburg; Ulrike Bacher and Nicolaus Kröger, Bone Marrow Transplantation Centre, University Hospital Hamburg-Eppendorf, Hamburg; Ulrike Bacher, Munich Leukaemia Laboratory; Johanna Tischer, Ludwig Maximilian University Hospital; Hans-Jochem Kolb, Technical University Hospital, Munich; Christoph Schmid, Augsburg Medical Hospital, Ludwig Maximilian University of Munich, Augsburg; Dietrich Wilhelm Beelen, University Hospital Essen, Essen; Martin Bornhäuser, University Hospital Dresden, Dresden; Rainer Schwerdtfeger, Deutsche Klinik für Diagnostik, Wiesbaden; Wolfgang Andreas Bethge, University Hospital Tübingen, Tübingen; Nadezda Basara and Dietger Niederwieser, University Hospital Leipzig, Leipzig; Martin Gramatzki, University Hospital Kiel, Kiel; Lutz Uharek, Charité-Campus B. Franklin, University Hospital Berlin, Berlin; Ralf G. Meyer, University Medical Center Mainz, Mainz; Donald Bunjes, University Hospital Ulm; Hubert Schrezenmeier, Deutsches Register für Stammzelltransplantation and Institute of Clinical Transfusion Medicine and Immunogenetics Ulm, German Red Cross Blood Transfusion Service Baden-Württemberg-Hessen and University of Ulm, Ulm; Christof Scheid, University Hospital Cologne, Cologne; and Hans Martin, University Hospital Frankfurt, Frankfurt, Germany.
Abstract
PURPOSE: To evaluate the role of a second allogeneic hematopoietic stem-cell transplantation (HSCT2) given for relapsed acute leukemia (AL) after related or unrelated first hematopoietic stem-cell transplantation (HSCT1) and to analyze the role of donor change for HSCT2 in both settings. PATIENTS AND METHODS: We performed a retrospective registry study on 179 HSCT2s given for relapse after HSCT1 from matched related donors (n = 75) or unrelated donors (n = 104), using identical or alternative donors for HSCT2. Separate analyses were performed according to donor at HSCT1. RESULTS: Independent of donor, 74% of patients achieved complete remission after HSCT2, and half of these patients experienced relapse again. Overall survival (OS) at 2 years was 25% ± 4% (39% ± 7% after related HSCT2; 19% ± 4% after unrelated HSCT2). Long-term survivors were observed even after two unrelated HSCT2s. Multivariate analysis for OS from HSCT2 confirmed established risk factors (remission duration after HSCT1: hazard ratio [HR], 2.37; 95% CI, 1.61 to 3.46; P < .001; stage at HSCT2: HR, 0.53; 95% CI, 0.34 to 0.83; P = .006). Outcome of HSCT2 was better after related HSCT1 than after unrelated HSCT1 (2-year OS: 37% ± 6% v 16% ± 4%, respectively; HR, 0.68; 95% CI, 0.47 to 0.98; P = .042, multivariate Cox regression). After both related and unrelated HSCT1, selecting a new donor for HSCT2 did not result in a relevant improvement in OS compared with HSCT2 from the original donor; however, donor change was not detrimental either. CONCLUSION: After relapse from allogeneic HSCT1, HSCT2 can induce 2-year OS in approximately 25% of patients. Unrelated HSCT2 is feasible after related and unrelated HSCT1. Donor change for HSCT2 is a valid option. However, a clear advantage in terms of OS could not be demonstrated.
PURPOSE: To evaluate the role of a second allogeneic hematopoietic stem-cell transplantation (HSCT2) given for relapsed acute leukemia (AL) after related or unrelated first hematopoietic stem-cell transplantation (HSCT1) and to analyze the role of donor change for HSCT2 in both settings. PATIENTS AND METHODS: We performed a retrospective registry study on 179 HSCT2s given for relapse after HSCT1 from matched related donors (n = 75) or unrelated donors (n = 104), using identical or alternative donors for HSCT2. Separate analyses were performed according to donor at HSCT1. RESULTS: Independent of donor, 74% of patients achieved complete remission after HSCT2, and half of these patients experienced relapse again. Overall survival (OS) at 2 years was 25% ± 4% (39% ± 7% after related HSCT2; 19% ± 4% after unrelated HSCT2). Long-term survivors were observed even after two unrelated HSCT2s. Multivariate analysis for OS from HSCT2 confirmed established risk factors (remission duration after HSCT1: hazard ratio [HR], 2.37; 95% CI, 1.61 to 3.46; P < .001; stage at HSCT2: HR, 0.53; 95% CI, 0.34 to 0.83; P = .006). Outcome of HSCT2 was better after related HSCT1 than after unrelated HSCT1 (2-year OS: 37% ± 6% v 16% ± 4%, respectively; HR, 0.68; 95% CI, 0.47 to 0.98; P = .042, multivariate Cox regression). After both related and unrelated HSCT1, selecting a new donor for HSCT2 did not result in a relevant improvement in OS compared with HSCT2 from the original donor; however, donor change was not detrimental either. CONCLUSION: After relapse from allogeneic HSCT1, HSCT2 can induce 2-year OS in approximately 25% of patients. Unrelated HSCT2 is feasible after related and unrelated HSCT1. Donor change for HSCT2 is a valid option. However, a clear advantage in terms of OS could not be demonstrated.
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