The tumor growth-promoting effect of allogeneic blood transfusions.
Over the past decade, many studies have suggested that allogeneic blood transfusions (ABT) may adversely affect a recipient. The ABT-associated deleterious effects include the development of transfusion reactions, graft-versus-host disease, alloimmunization, and immunomodulation. While the ABT-associated immunosuppressive effects might be beneficial for recipients of kidney allografts, in reducing the relapse rate in patients with Crohn's disease, and in ameliorating the rate of abortion in women with recurrent spontaneous abortions; evidence is accumulating that the immunosuppression associated to perioperative ABT might adversely affect overall prognosis in patients with a malignancy undergoing curative cancer surgery. In addition, the ABT-associated immunomodulation has been reported to be associated with an increased risk for postoperative bacterial infections. Data from both inbred and outbred experimental animal models indicate that ABT promote tumor growth. Evidence is available that this ABT-promoting tumor growth effect can be adoptively transferred to naive animals, using splenic immunocytes. Furthermore, data from the experimental animal models indicate that the ABT effect on the growth of tumors is due to the presence of the donor leukocytes in the transfused allogeneic blood, and that this deleterious effect can be ameliorated by the pre-storage leukodepletion of the allogeneic blood. Importantly, recent evidence suggests that post-storage leukodepletion is inefficacious in preventing the ABT-associated tumor growth promotion effect. While results from studies in experimental animals cannot necessarily be extrapolated to the clinical situation, these studies suggest that ABT promote tumor growth and that pre-storage leukodepletion ameliorates this effect.(ABSTRACT TRUNCATED AT 250 WORDS)
Blajchman
M A
MA
Department of Pathology, McMaster University, Hamilton, Ontario, Canada.
Bordin
J O
JO
D000818:Animals; D009374:Neoplasms, Experimental / Q000276:immunology* / Q000473:pathology*; D065227:Transfusion Reaction