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Are HLA antigens a risk factor for acute GVHD in thalassemic patients receiving HLA-identical stem cell
M Mohyeddin Bonab1, K Alimoghaddam, S Vatandoust
1Heamatology, Oncology, and BMT Research Center, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran. mohyeddin@sina.tums.ac.ir
We retrospectively evaluated the association between risk factors and acute graft-versus-host disease (aGVHD) among 182 beta thalassemia patients who received 73 peripheral blood stem cell (PBSC) or 109 bone marrow transplants from HLA-identical siblings between 1991 and 2003. The relationship between the severity of aGVHD was examined for the following factors: HLA antigens, age, sex, ABO mismatch, sex mismatch (between recipient and donor), thalassemia class, graft source, transplant cell dose, CD3+ cell dose, conditioning regimen, GVHD prophylaxis, neutrophil engraftment duration, and blood product transfusions using univariate and multivariate analyses. Overall 61 (34%) patients developed clinical grade III or grade IV aGVHD. Univariate analysis confirmed an increased risk of severe aGVHD, which was associated with HLA-A11, HLA-A26, and PBSCT (P=.04, .03, and .03, respectively). The risk of aGVHD was reduced in the presence of HLA-A3 (P=.03). Multivariate analysis confirmed the increased risk of aGVHD associated with HLA-A11 (P=.04), HLA-A26 (P=.01), and a short-period neutrophil recovery (P=.009). In this study HLA-A11, HLA-A26, PBSCT, and a short neutrophil engraftment period were probable risk factors and HLA-A3 a probable protective factor associated with severe aGVHD. These data may provide useful guidelines to choose strategies for treatment and prevention.
We retrospectively evaluated the association between risk factors and acute graft-versus-host disease (aGVHD) among 182 beta thalassemia patients who received 73 peripheral blood stem cell (PBSC) or 109 bone marrow transplants from HLA-identical siblings between 1991 and 2003. The relationship between the severity of aGVHD was examined for the following factors: HLA antigens, age, sex, ABO mismatch, sex mismatch (between recipient and donor), thalassemia class, graft source, transplant cell dose, CD3+ cell dose, conditioning regimen, GVHD prophylaxis, neutrophil engraftment duration, and blood product transfusions using univariate and multivariate analyses. Overall 61 (34%) patients developed clinical grade III or grade IV aGVHD. Univariate analysis confirmed an increased risk of severe aGVHD, which was associated with HLA-A11, HLA-A26, and PBSCT (P=.04, .03, and .03, respectively). The risk of aGVHD was reduced in the presence of HLA-A3 (P=.03). Multivariate analysis confirmed the increased risk of aGVHD associated with HLA-A11 (P=.04), HLA-A26 (P=.01), and a short-period neutrophil recovery (P=.009). In this study HLA-A11, HLA-A26, PBSCT, and a short neutrophil engraftment period were probable risk factors and HLA-A3 a probable protective factor associated with severe aGVHD. These data may provide useful guidelines to choose strategies for treatment and prevention.
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