Thomas F Michniacki1, Christen L Ebens2, Sung Won Choi3. 1. Department of Pediatrics, Division of Pediatric Hematology/Oncology & Bone Marrow Transplantation, University of Michigan, 1500 E. Medical Center Drive, D4202 Medical Professional Building, Ann Arbor, MI, USA. tmich@med.umich.edu. 2. Department of Pediatrics, Division of Blood and Marrow Transplantation, University of Minnesota, Minneapolis, MN, USA. 3. Department of Pediatrics, Division of Pediatric Hematology/Oncology & Bone Marrow Transplantation, University of Michigan, 1500 E. Medical Center Drive, D4202 Medical Professional Building, Ann Arbor, MI, USA.
Abstract
PURPOSE OF REVIEW: Discuss the pathophysiology, clinical presentation, diagnosis, and treatment of immune-mediated cytopenias (IMC) after hematopoietic cell transplantation (HCT). RECENT FINDINGS: Key risk factors for post-HCT IMC include younger age, non-malignant disease, and umbilical cord blood stem cell source. While anemia predominates, any or all three hematopoietic cell lines can be affected. In rare cases, IMC can cause graft failure or death. IMC is hypothesized to result from immune dysregulation upon reconstitution of donor hematopoietic cells (i.e., dysfunctional regulatory T cells). Aside from blood product transfusions, IMC treatment includes immune-suppressive or ablative agents. First-line therapies, including corticosteroids and intravenous immunoglobulin, are often inadequate, prompting use of additional agents aimed at antibody production/T cell dysfunction or direct antibody removal via plasmapheresis. IMC occurs in up to 20% of high-risk HCT populations. Morbidity and mortality from IMC post-HCT have been reduced by improved recognition and aggressive early interventions.
PURPOSE OF REVIEW: Discuss the pathophysiology, clinical presentation, diagnosis, and treatment of immune-mediated cytopenias (IMC) after hematopoietic cell transplantation (HCT). RECENT FINDINGS: Key risk factors for post-HCT IMC include younger age, non-malignant disease, and umbilical cord blood stem cell source. While anemia predominates, any or all three hematopoietic cell lines can be affected. In rare cases, IMC can cause graft failure or death. IMC is hypothesized to result from immune dysregulation upon reconstitution of donor hematopoietic cells (i.e., dysfunctional regulatory T cells). Aside from blood product transfusions, IMC treatment includes immune-suppressive or ablative agents. First-line therapies, including corticosteroids and intravenous immunoglobulin, are often inadequate, prompting use of additional agents aimed at antibody production/T cell dysfunction or direct antibody removal via plasmapheresis. IMC occurs in up to 20% of high-risk HCT populations. Morbidity and mortality from IMC post-HCT have been reduced by improved recognition and aggressive early interventions.
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