We read with great interest the study by Ye and colleagues regarding risk factors and prognosis of transplant‐associated thrombotic microangiopathy (TA‐TMA). Indeed, TA‐TMA represents a devastating and life‐threatening complication occurring… Click to show full abstract
We read with great interest the study by Ye and colleagues regarding risk factors and prognosis of transplant‐associated thrombotic microangiopathy (TA‐TMA). Indeed, TA‐TMA represents a devastating and life‐threatening complication occurring more frequently in allogeneic compared with autologous hematopoietic cell transplantation (HCT). Estimates of its prevalence vary significantly among studies. Although it has been a well‐recognized syndrome for decades, our understanding in terms of epidemiology and, more importantly, treatment options remains unclear. Therefore, we aimed to retrospectively investigate the incidence of TA‐TMA in patients who underwent HCT from unrelated donors and identify prognostic factors and treatment outcomes. We enrolled consecutive patients who underwent HCT from unrelated donors from 2003 to 2015. TA‐TMA diagnosis was based on European Bone Marrow Transplantation criteria: increased (>4%) schistocytes in peripheral blood, thrombocytopenia, increased lactade dehydrogenase, and decreased Hb. Antithymocyte globulin (rabbit) was used as standardized part of the conditioning in almost all patients (total dose of 5‐7.5 mg/kg). Prophylaxis for graft‐versus‐host disease (GVHD) consisted of cyclosporine or tacrolimus plus methotrexate in myeloablative and mycophenolate mofetil plus cyclosporine in reduced intensity conditioning transplants. Upon identification of TA‐TMA, all possible causative factors were fully investigated. The mainstay of treatment strategy was withdrawal of calcineurin inhibitors, plasma infusion, and plasma exchange combined with corticosteroid administration and in refractory cases, humanized anti‐CD20 monoclonal antibody (rituximab). In total, we studied 179 patients, 74 male:105 female, aged 37 ± 14 years, who underwent HCT from matched HLA A/B/C/ DRB1 (8/8, n = 88) and allele‐ or antigen‐mismatched (n = 91) grafts. Grafts were derived from peripheral blood (157), bone marrow (18), and umbilical stem cells (4). Conditioning regimens were myeloablative (139) and reduced intensity (28) and toxicity (12). Median follow‐up was 11.5 (0.1‐147.4) months. TA‐TMAwas diagnosed in 29 (16.2%) patients, 12 male:17 female, aged 34 ± 12 years, 78 (9‐721) days post‐HCT for acute leukemia (21), Hodgkin (3), and non‐Hodgkin (1), lymphoma, myelodysplastic syndrome (2), aplastic anemia (1), and myeloproliferative neoplasm (1). Conditioning regimens were myeloablative in 24 patients (12 based
               
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