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<p>Park and colleagues recently reported, in a single-centre Korean cohort of 391 adult patients with myelodysplastic neoplasms (MDS) receiving fludarabine–busulfan conditioning and antithymocyte globulin (ATG)-based prophylaxis, that matched sibling donor (MSD) recipients experienced a substantially higher 5-year cumulative incidence of relapse (34.3%) than recipients of unrelated (UD; 16.4%) or haploidentical (HID; 16.8%) donors, with reduced acute and chronic graft-versus-host disease (GVHD) in the MSD arm. The authors conclude that under ATG-based prophylaxis, MSD may no longer be the optimal donor choice in MDS. We respectfully argue that this conclusion is constrained by two structural features of the cohort. First, ATG dose is severely confounded with donor type: 61.3% of MSD recipients received 10&#xa0;mg/kg ATG versus 0% of HID recipients, a dose pattern that inverts standard clinical practice and overlaps a range in which independent evidence indicates impaired disease control without offsetting GVHD benefit. Second, the GVHD- non-relapse mortality pattern in the cohort is more consistent with a cumulative immunosuppression-intensity hypothesis than with a primary donor-source effect. We propose that the most clinically actionable inference is to re-examine ATG dosing in MSD transplants for MDS, rather than to displace MSD as a preferred donor.</p>

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Reinterpreting the matched-sibling relapse penalty in ATG-based allogeneic transplantation for myelodysplastic neoplasms: a question of dose, not donor

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  • 发表日期：

    2026年7月29日

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  • Naif I. AlJohani

摘要

Park and colleagues recently reported, in a single-centre Korean cohort of 391 adult patients with myelodysplastic neoplasms (MDS) receiving fludarabine–busulfan conditioning and antithymocyte globulin (ATG)-based prophylaxis, that matched sibling donor (MSD) recipients experienced a substantially higher 5-year cumulative incidence of relapse (34.3%) than recipients of unrelated (UD; 16.4%) or haploidentical (HID; 16.8%) donors, with reduced acute and chronic graft-versus-host disease (GVHD) in the MSD arm. The authors conclude that under ATG-based prophylaxis, MSD may no longer be the optimal donor choice in MDS. We respectfully argue that this conclusion is constrained by two structural features of the cohort. First, ATG dose is severely confounded with donor type: 61.3% of MSD recipients received 10 mg/kg ATG versus 0% of HID recipients, a dose pattern that inverts standard clinical practice and overlaps a range in which independent evidence indicates impaired disease control without offsetting GVHD benefit. Second, the GVHD- non-relapse mortality pattern in the cohort is more consistent with a cumulative immunosuppression-intensity hypothesis than with a primary donor-source effect. We propose that the most clinically actionable inference is to re-examine ATG dosing in MSD transplants for MDS, rather than to displace MSD as a preferred donor.