Background and Objectives Transfusion-associated graft-versus-host disease (TA-GVHD) is a serious complication of blood component transfusion therapy, caused by donor T lymphocytes. c-Irradiation or pathogen inactivation methods, capable of inactivating proliferating T cells in blood components, should be selected to prevent TA-GVHD. This review summarizes the published evidence to support the use of pathogen-reduced platelets with amotosalen (150 lM) and ultraviolet A light (UVA, 320-400 nm, 3 J/cm 2 ) for preventing TA-GVHD.
Materials and MethodsAvailable literature on the use of pathogen-reduced platelets to prevent TA-GVHD was reviewed.Results Observational studies, animal models, in vitro studies and mechanistic studies of pathogen-reduced platelets with amotosalen and UVA light showed that inactivation of T cells are equal or even superior to c-irradiation.Conclusion Pathogen-reduced platelets with amotosalen and UVA light can be used as a measure to prevent TA-GVHD.Key words: pathogen-reduced platelets, platelet transfusion, TA-GVHD.
IntroductionThe clinical course of allogeneic hematopoietic progenitor cell (HPC) transplantation is complicated by graft-versushost disease (GVHD). This condition results when donor T lymphocytes recognize the human leucocyte antigens (HLA) of the recipient as foreign, generating a characteristic immune response [1]. However, GVHD may also result as a complication of blood component transfusion because of the infusion of viable lymphocytes within cellular blood components [2]. Transfusion-associated graft-versus-host disease (TA-GHVD) is a lethal, although rare, complication of blood component transfusion. Three prerequisites are necessary to develop this complication of blood transfusion: (1) differences in histocompatibility between recipient and donor; (2) presence of immunocompetent T cells in the blood component; and (3) inability of the recipient to reject the immunocompetent cells [2].The clinical picture of TA-GVHD typically appears 8-10 days after transfusion. As seen in GVHD after allogeneic HPC transplantation, a characteristic cutaneous eruption appears, in association with watery diarrhoea, liver function test abnormalities and fever. The development of marrow aplasia with pancytopenia distinguishes TA-GVHD from GVHD occurring after allogeneic HPC transplantation [3]. According to criteria devised by the National Health and Safety Network (NHSN), the diagnosis of TA-GVHD is based on a combination of characteristic clinical findings and a tissue biopsy consistent with GVHD, with imputability established via the demonstration of leucocyte chimerism, specifically donor T lymphocytes in recipient tissue [4].Treatment of TA-GVHD is only rarely effective, and the prognosis of the disease is almost uniformly fatal [5]. Thus prevention of TA-GVHD in patients groups at risk is critical. These groups of patients are identified based on case reports and small case series published in the This is an open access article under the terms of the Creative Commons Attribution-Non...