|| Checking for direct PDF access through Ovid
Over the past three decades, evidence from a variety of sources has suggested that allogeneic blood transfusions can induce clinically significant immunosuppression in recipients. This clinical syndrome is referred to in the transfusion medicine literature as transfusion-associated immunomodulation (TRIM) and has been linked to an improved clinical outcome in the setting of renal transplantation. Possible deleterious TRIM-associated effects include increased prevalence of cancer recurrence and postoperative bacterial infections. The recognition that TRIM can increase morbidity and mortality in allogeneically transfused individuals has become a major concern for those involved in transfusion medicine. Whether TRIM predisposes recipients to increased risk for cancer recurrence and/or bacterial infections is still not proven, however. In contrast to the available clinical data, studies in experimental animal models suggest that TRIM is an immunologically mediated biologic effect associated with the infusion of allogeneic leukocytes, which can be ameliorated by prestorage leukoreduction. Although considerable data have been accumulated in an attempt to unravel the clinically adverse effects of TRIM, the precise mechanism of TRIM has yet to be elucidated. Further studies, both basic and applied, to establish the clinically relevant manifestations of TRIM as well as the mechanism(s) are urgently required.