Is there any evidence that blood transfusion increase the risk of GVHD in patients post hematopoietic stem cell transplantation?
Dear Mojtaba,
I recommend following review: http://www.bloodjournal.org/content/112/8/3036?sso-checked=true
Graft-versus-host disease (GVHD) is a well-known complication of allogeneic bone marrow transplantation. Transfusion associated graft-versus-host disease (TA-GVHD) is much less common and nearly uniformly fatal complication of blood transfusion. The risk factors underlying the development of TA- GVHD are incompletely defined, but it is commonly seen in individuals with congenital or acquired immunodeficiency, transfusions from blood relatives, intrauterine transfusions and HLA-matched platelet transfusions. Diagnosis of TA-GVHD may be difficult at a time due to rarity in occurrence and overlapping clinical features with various infections and drug reactions
link;
Indian J Hematol Blood Transfus. Sep 2010; 26(3): 92–95.
Published online Oct 1, 2010. doi: 10.1007/s12288-010-0028-0
PMCID: PMC3002081
I found a paper from Gutierrez-Aguirre CH Transfusion May 2014, that found increased incidence of acute and chronic GvHD after ABO minor incompatible reduced intensity HCT, followed by ABO compatible, followed by ABO major incompatible, although it did not reach statistical significance. This was a retrospective study on 121 patients treated with reduced intensity conditioning (Bu Flu Cy), and Cyclosporine, miniMethotrexate GVHD prophylaxis, for hematologic malignancies or severe aplastic anemia. Interestingly, the paper reviews in Table V: 'Studies regarding ABO incompatibility with RIC regimens showing important outcome measures'.
Regards
Background=
Transfusion associated GvHD can happen in both immunocompetent or-compromised individuals. It is uncommon, but with >90% mortality.
The proven strategy to prevent it is gamma or X-irradiation of all blood products, and it is indicated pre and post transplant, and usually for life. Additionally, the risk of CMV transmission to CMV negative patient requires the use of CMV seronegative donors and/or leukodepletion.
Irradiation of blood product is also indicated in patient receiving ATG, Campath and even newer purine analogues such as clofarabine, and bendamustine.
Googling this sentence below will display pdf with some review, guidelines or summary slides.= irradiated blood products reduce risks of gvhd after sct.
I don't know how to answer to your question.
Transfusion associated GVHD is a well known risk of transfusion in SCT, however, irradiation is a long established preventive strategy. Universal leukodepletion was implemented by most blood donor centers can even provide some protection, as shown by hemovigilance programs, but we lack data yet to make them equal.
Wether transfusion per se causes or increases the chances to develop GVHD is not proven yet.
The debate about the impact of ABO mismatch on GVHD development is not solved, there are some confusing elements: Is it caused by a greater transfusion need, or by the antigen mismatch itself? Does it actually exist?
I don't think we can answer that firmly. As always, the less you transfuse, the better.
Transfusion-associated GVHD is seen in patients who receive RBC transfusion and they develop skin rash and pancytopenia. In those patients the bone marrow gets hit and it is almost always fatal, and steroids do not work. However, in GVHD after allogeneic HSCT the hematopoiesis in the bone marrow is from the donor; so, it does not get hit by the GVHD process. We use steroids and they are usually effective. Attached you find a retrospective study about the relationship between RBC transfusion and GVHD from the BMT group at Emory University which is quite interesting, it was presented at ASH last December.
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