The ideal conditioning intensity in allogeneic hematopoietic stem cell transplantation (HSCT) is evolving. Previous prospective studies comparing myeloablative versus reduced intensity conditioning regimens in adults with acute myelogenous leukemia (AML) have shown mixed results. In many of these studies, patients were not stratified based on measurable residual disease (MRD).
We evaluated the effect of conditioning intensity on the outcomes of AML patients in complete remission (CR) with flow-cytometric evidence of MRD negativity. Patients aged 20-75 years (n=135) with AML in CR1 or CR2 and flow cytometric evidence of MRD negativity transplanted at our center between the years 2011-2019 were evaluated. We compared overall survival (OS), relapse-free survival (RFS), non-relapsed mortality (NRM), relapse, acute and chronic graft versus host disease (GVHD) in recipients of MAC (n=89) or RIC (n=46).
Although patients receiving RIC were older (62 vs 51 years, P<0.0001), there were no statistically significant differences between the myeloablative conditioning (MAC) and reduced-intensity conditioning (RIC) groups in the Eastern Cooperative Oncology Group (ECOG), European Leukemia Network (ELN) risk criteria and disease status (CR1 or CR2) at the time of transplant. At a median follow-up of 24.6 months, no statistically significant differences in OS (HR, 0.78; 95% CI 0.42-1.42, P=0.411) and RFS (HR, 1.004; 95% CI 0.48-2.09, P=0.99) were identified. The cumulative incidence of NRM (HR, 0.595; 95% CI, 0.24-1.48; P=0.2644) and relapse (HR, 1.007; 95% CI 0.45-2.23, P=0.9872) was not different between the two groups. Grade II-IV and III-IV acute GVHD was higher in MAC vs RIC (39.3% vs 19.9%, P=0.018 and 19.3% vs 2.3%, P<0.001, respectively). Moderate/severe chronic GVHD was also higher in MAC vs RIC (23.6% vs 15.8%, P=0.038).
Conditioning intensity does not appear to affect OS, RFS, NRM, and relapse risk in the MRD-negative AML as measured by flow cytometry. RIC resulted in less severe acute and chronic GVHD.

Copyright © 2021. Published by Elsevier Inc.

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