Graft‐versus‐host disease in paediatric solid organ transplantation: A review of the literature

Abstract

GvHD is a rare and serious complication of organ transplantation. The literature is sparse following solid organ transplantation. The aim of this report was to review the literature of GvHD in paediatric solid organ transplantation. We searched PubMed for English-language full-text manuscripts between 1990 and 2015 for eligible studies. A total of 28 publications were found pertaining to paediatric GvHD following solid organ transplantation. GvHD had a mean incidence of 11% (range 8.3-13.4%) following SBTx and 1.5% following liver transplantation. Where described, the most common sites for presentation of GvHD were the skin (87%), the native GI tract (43%), the lungs (7%), the eyes (4%), HA (4%), and the kidneys (1%). Diagnosis was confirmed with biopsy (93%) and/or chimerism (41%). Treatments used include steroids (80%), of which 75% showed partial or complete resolution. Mortality was 33.3% (range 0-100%). Novel therapies include ECP and MSC therapy. GvHD is a rare but serious disease with high mortality. Novel therapies may offer hope in the future, but currently there is limited evidence for their efficacy in the context of intestinal or liver transplantation.

Donor mucosal immunocytes perpetuate refractory GVHD after intestinal transplantation without engrafting in recipient bone marrow: Case report and review of the literature

“…Treatment is based on the fact that unlike HSCT, where reconstitution of the bone marrow with donor cells is intended, the chimerism that follows SOT is an unintended consequence. Therefore, GVHD after SOT is treated with steroids to suppress donor T cells and control symptoms, and reduced maintenance immunosuppression to allow the host immune system to limit expansion of donor cells . Our patient was steroid‐responsive with her first GVHD episode, but steroid‐refractory when GVHD recurred, perhaps because immunological repopulation of the allograft had failed, as reflected by the absence of donor immune cells in the allograft mucosa.…”

“…Consistent with these observations, our patient manifested macrochimerism in peripheral blood at all times and did not experience rejection. However, chimerism has been documented in patients with and without GVHD and the level of chimerism does not correlate with symptoms, suggesting a role for other contributors …”

“…Acute GVHD results in cellular apoptosis and direct organ injury by effector T cells, raising the risk of secondary infections and chronic GVHD . The sites often affected by GVHD following SOT include skin and native GI tract, where bacterial translocation is possible . The level of HLA mismatch as risk factor is unclear .…”

“…GVHD is more commonly encountered following HSCT, and its development requires several conditions: the presence of immunologically competent graft cells, the inability of the host to mount an adequate immune response, and the graft's recognition of the host as foreign . In the setting of host tissue damaged by preconditioning regimens, donor T lymphocytes are activated by host antigen‐presenting cells causing cytokine release and donor T cell–mediated cytotoxicity to host tissue . GVHD affects the skin, liver, and gastrointestinal tract, and may mimic drug toxicity or infection, posing a diagnostic challenge .…”

“…Because GVHD is not completely understood in SOT, disease management is difficult and carries significant morbidity and mortality. Therefore, early diagnosis is critical . Here, we describe a young girl with CMV viremia who developed fatal GVHD after isolated intestinal transplantation when recipient immune cells failed to replace donor cells in the allograft.…”