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GVHD the nuts and bolts
1University of Minnesota, MMC 480, 516 Delaware St., SE, Minneapolis, MN 55455-0480, USA. weisd001@umn.edu
Acute graft-versus-host disease (GVHD) is the most frequent, morbid complication following allogeneic hematopoietic stem cell transplantation (HSCT). Its clinical toxicity, requirement for intensive immunosup-pressive management, and associated infections lead to the greatest risks of nonrelapse mortality in HSCT recipients. In acute GVHD, donor-derived T lymphocyte-mediated alloreactivity is complicated by inflammatory responses, cytokine release, direct tissue injury through target cell apoptosis, and secondary tissue injury. The therapeutic management includes effective GVHD prophylaxis to limit the incidence and severity of acute GVHD, prompt and effective therapy if it develops-modified if possible to protect against chronic GVHD-and intensive supportive care relevant to its association with delayed immune reconstitution. As the major ongoing morbid complication following allografting, chronic GVHD is another barrier to patients' recovery and long-term survival. Recognition of the critical elements in the pathogenesis of GVHD has prompted new approaches to its management and its role in controlling the risks of malignant relapse after allotransplantation. Important elements in the practical management of GVHD will be reviewed.
Acute graft-versus-host disease (GVHD) is the most frequent, morbid complication following allogeneic hematopoietic stem cell transplantation (HSCT). Its clinical toxicity, requirement for intensive immunosup-pressive management, and associated infections lead to the greatest risks of nonrelapse mortality in HSCT recipients. In acute GVHD, donor-derived T lymphocyte-mediated alloreactivity is complicated by inflammatory responses, cytokine release, direct tissue injury through target cell apoptosis, and secondary tissue injury. The therapeutic management includes effective GVHD prophylaxis to limit the incidence and severity of acute GVHD, prompt and effective therapy if it develops-modified if possible to protect against chronic GVHD-and intensive supportive care relevant to its association with delayed immune reconstitution. As the major ongoing morbid complication following allografting, chronic GVHD is another barrier to patients' recovery and long-term survival. Recognition of the critical elements in the pathogenesis of GVHD has prompted new approaches to its management and its role in controlling the risks of malignant relapse after allotransplantation. Important elements in the practical management of GVHD will be reviewed.
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