Further Outpatient Care
Regular follow-up with monitoring of immunosuppressive therapy is needed, as well as vigilance for developing chronic GVHD.
Further Inpatient Care
Further inpatient care of graft versus host disease (GVHD) depends on initial response.
Maintenance immunosuppression with close monitoring is required.
Opportunistic infections may become severe and require intravenous (IV) antibiotics and supportive care.
Deterrence/Prevention
Effective prevention against GVHD includes the following:
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Use of histocompatible donor and recipients
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Use of immunosuppressive agents after bone marrow infusion (Most bone marrow transplant [BMT] teams currently use cyclosporine plus a brief course of methotrexate as the standard GVHD prophylaxis regimen. Adding steroids has been proven beneficial in some trials. Other drugs used alone or in combination include tacrolimus, antithymocyte globulin [ATG], and sirolimus.)
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In vitro manipulation of the donor graft, such as marrow T-cell depletion
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Possibly housing the patient in a pathogen-poor protected environment
The best prophylaxis against chronic GVHD is prevention of acute GVHD because de novo chronic GVHD is less common compared with incidence in patients with acute GVHD.
Prognosis
Severe acute GVHD is the important cause of treatment failure after BMT. Survival rates vary from 90% in stage I, 60% in stage II or III, to almost 0% in stage IV. Death is often caused by infections, hemorrhage, and hepatic failure.
Severe chronic GVHD is associated with a higher mortality rate, mostly because of infection complications. Survivors are often severely disabled. The survival rate after onset of chronic GVHD is approximately 42%. Factors that predict death are progressive presentation (ie, acute GVHD followed by chronic GVHD), lichenoid skin changes on biopsy, and elevated serum bilirubin. A patient with one or more of these factors has a projected 6-year survival rate of 60%.
Mild chronic GVHD as with mild acute GVHD is associated with improved outcome in patients with leukemia because of graft-versus-leukemia (GVL) effect.
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Pathophysiological pathways and mechanisms of acute GVHD.
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This boy developed stage III skin involvement with acute graft versus host disease (GVHD) in spite of receiving prophylaxis with cyclosporin A. The donor was an human leukocyte antigen (HLA)-matched sister; however, the sex disparity increased the risk for acute GVHD. Image courtesy of Mustafa S. Suterwala, MD.
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This photo depicts the same boy who has progressed to grade IV graft versus host disease (GVHD). Both cyclosporin A and methylprednisolone had been administered in high dose intravenously. He later died with chronic pulmonary disease caused by chronic GVHD. Image courtesy of Mustafa S. Suterwala, MD.
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Autologous graft versus host disease (GVHD) involving the skin of a patient's arm shortly after showing signs of engraftment after an autologous peripheral blood stem cell transplant for ovarian cancer. Image courtesy of Romeo A. Mandanas, MD, FACP.
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Acute graft versus host disease (GVHD) involving desquamating skin lesions in a patient following allogeneic bone marrow transplantation for myelodysplasia. Image courtesy of Romeo A. Mandanas, MD, FACP.
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Oral mucosal changes in a patient with chronic graft versus host disease (GVHD). Note the skin discoloration (vitiligo), which can result from GVHD. Image courtesy of Romeo A. Mandanas, MD, FACP.
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Acute graft versus host disease (GVHD). Hematoxylin-stained and eosin-stained tissue shows dyskeratosis of individual keratinocytes and patchy vacuolization of the basement membrane. A moderate superficial dermal and perivascular lymphocytic infiltrate is also seen in this case. Image courtesy of Melanie K. Kuechler, MD.
