Hyperacute GVHD: risk factors, outcomes, and clinical implications

Saliba, Rima M.; Lima, Marcos J.G. de; Giralt, Sergío; Andersson, Börje S.; Khouri, Issa F.; Hosing, Chitra; Ghosh, S.; Neumann, Joyce; Hsu, Yvonne; Jesús, Jorge de; Qazilbash, Muzaffar H.; Champlin, Richard E.; Couriel, Daniel R.

doi:10.1182/blood-2006-07-034348

Cited by 94 publications

(93 citation statements)

References 29 publications

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“…Because ES can resemble acute (or hyperacute 28,29 ) GVHD, the question arises whether ES is an early manifestation of GVHD. Gorak et al 10 described ES following reduced-intensity conditioning (RIC) allotransplants.…”

Section: Engraftment Syndromementioning

confidence: 99%

Engraftment syndrome: double-edged sword of hematopoietic cell transplants

Spitzer

2015

Bone Marrow Transplant

112

128

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Engraftment syndrome (ES) after hematopoietic cell transplantation (HCT) is increasingly diagnosed. Common features include fever, pulmonary vascular leak, rash and organ dysfunction. Different diagnostic criteria likely account for the wide (7-90%) range of reported incidences. ES typically occurs within 4 days of granulocyte recovery although a recently described seemingly similar syndrome occurs 41 week before granulocyte recovery after umbilical cord blood cell transplants. Although the clinical manifestations of ES may be identical to those of acute GVHD, ES also has been well described in patients without acute GVHD. The data are conflicting as to whether ES is associated with a higher nonrelapse mortality and worse survival after HCT. The pathophysiology of ES is unclear, but endothelial injury and activated granulocytes in the setting of proinflammatory cytokines may be important. ES typically is self-limited, but, like acute GVHD, responds to corticosteroids. Because ES and acute GVHD may have overlapping features and response to therapy, these disease processes may often not be distinct events. Moreover, features of ES may overlap with those of drug-and radiation-induced toxicities and infection. Further research to better characterize the clinical spectrum and etiology of ES and to determine its relationship to GVHD is needed.

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Section: Engraftment Syndromementioning

confidence: 99%

Engraftment syndrome: double-edged sword of hematopoietic cell transplants

Spitzer

2015

Bone Marrow Transplant

112

128

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“…This syndrome commonly occurs in heavily pretreated recipients receiving myeloablative conditioning and HLA-mismatched grafts. 67 It is attractive to propose that this syndrome is a manifestation of cytokine dysregulation and akin to the cytokine release syndrome seen after infusion of chimeric antigen receptor T cells in which IL-6 appears to play a central role. 68 Certainly, IL-6 is dysregulated after clinical transplantation, 69 but the nature of the alloantigen presentation driving this syndrome remains unclear at this time.…”

Section: Cytokines and Acute Gvhdmentioning

confidence: 99%

Alloantigen presentation and graft-versus-host disease: fuel for the fire

Koyama

Hill

2016

Blood

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Allogeneic stem cell transplantation (SCT) is a unique procedure, primarily in patients with hematopoietic malignancies, involving chemoradiotherapy followed by the introduction of donor hematopoietic and immune cells into an inflamed and lymphopenic environment. Interruption of the process by which recipient alloantigen is presented to donor T cells to generate graft-versus-host disease (GVHD) represents an attractive therapeutic strategy to prevent morbidity and mortality after SCT and has been increasingly studied in the last 15 years. However, the immune activation resulting in GVHD has no physiological equivalent in nature; alloantigen is ubiquitous, persists indefinitely, and can be presented by multiple cell types at numerous sites, often on incompatible major histocompatibility complex, and occurs in the context of intense inflammation early after SCT. The recognition that alloantigen presentation is also critical to the development of immunological tolerance via both deletional and regulatory mechanisms further adds to this complexity. Finally, GVHD itself appears capable of inhibiting the presentation of microbiological antigens by donor dendritic cells late after SCT that is mandatory for the establishment of effective pathogen-specific immunity. Here, we review our current understanding of alloantigen, its presentation by various antigen-presenting cells, subsequent recognition by donor T cells, and the potential of therapeutic strategies interrupting this disease-initiating process to modify transplant outcome.

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“…However, grade 3-4 severe skin involvement was observed in 71% of hyperacute GVHD. 2 To our knowledge, this is the first case report on hyperacute GVHD with TEN-like severe cutaneous manifestation after BMT for mycosis fungoides. We should note the possibility of hyperacute GVHD in treating mycosis fungoides with allogeneic stem cell transplantation.…”

mentioning

confidence: 72%