Graft-versus-host disease overview
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Graft-versus-host disease |
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Differentiating Graft-versus-host disease from other Diseases |
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Diagnosis |
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Treatment |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Shyam Patel [2]
Overview
Graft-versus-host disease (GVHD) is a common complication of allogeneic bone marrow transplantation in which functional immune cells in the transplanted marrow recognize the recipient as "foreign" and mount an immunologic attack. It occurs in 4-70% of patients undergoing stem cell transplant.[1] Acute GvHD typically occurs within 100 days of transplant. Chronic GvHD occurs after 100 days from transplant.[2] Nearly 40% of paitents will develop some form of GvHD.[2]
Historical Perspective
Classification
The classification of GvHD is based on bother severity and time of onset. The severity is based upon the stage and grade. The conglomeration of stages of GvHD of each organ affected gives the grade. Each affected organ has a staging system (stages 1-4), depending on the degree of organ dysfunction. The time of onset determines whether GvHD is acute or chronic. Acute GvHD occurs within the first 100 days of stem cell transplant. Chronic GvHD occurs after 100 days from transplant.
Pathophysiology
The pathophysiology of GvHD involves immune activation of donor-derived T cells, which mount a response against host tissue, especially the liver, skin, and GI tract. Antigen-presenting cells (APCs) are key players in the initiation of the process. Immune activation leads to inflammation and organ destruction.
Causes
The cause of GvHD is stem cell transplantation from an allogeneic donor.[2]
Differentiating GvHD from Other Diseases
Other possible etiologies for liver dysfunction in a patient who received stem cell transplant include CMV hepatitis and veno-occlusive disease. It is important to differentiate these etiologies from GvHD, as the treatment implications are different.
Epidemiology and Demographics
GvHD can occur in any population. Certain subsets of donor cells are less likely to result in GvHD, such as umbilical cord blood-derived stem cells, which contain fewer T cells than other sources of stem cells. There are no known racial disparities for GvHD. There are no particular geographic areas that are more prone to GvHD.
Risk Factors
Screening
There is no role for screening (secondary prevention) for GvHD. However, there is a significant role for primary prevention in GvHD. Such primary prevention measures include medications like methotrexate and antibiotics like ciprofloxacin for gut decontamination.
Natural History, Complications, and Prognosis
Natural History
Complications
The complications of GvHD stem from the resultant end-organ damage that occurs from immune activation. Complications include debilitating GI symptoms (including life-threatening diarrhea and abdominal pain), disruption of the GI mucosa and subsequent bacterial translocation and sepsis, liver failure, and skin infections.
Prognosis
The prognosis of GvHD is variable based on the severity of disease. Steroid-refractory GvHD has a much poorer prognosis then steroid-responsive GvHD.
Diagnosis
Diagnostic Criteria
History and Symptoms
Physical Examination
Laboratory Findings
Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Prevention
References
- ↑ Al-Chaqmaqchi H, Sadeghi B, Abedi-Valugerdi M, Al-Hashmi S, Fares M, Kuiper R; et al. (2013). "The role of programmed cell death ligand-1 (PD-L1/CD274) in the development of graft versus host disease". PLoS One. 8 (4): e60367. doi:10.1371/journal.pone.0060367. PMC 3617218. PMID 23593203.
- ↑ 2.0 2.1 2.2 Meyer EH, Hsu AR, Liliental J, Löhr A, Florek M, Zehnder JL; et al. (2013). "A distinct evolution of the T-cell repertoire categorizes treatment refractory gastrointestinal acute graft-versus-host disease". Blood. 121 (24): 4955–62. doi:10.1182/blood-2013-03-489757. PMC 3682344. PMID 23652802.