Transfusion‐associated graft‐versus‐host disease: a report of three cases in immunocompetent patients in Lebanon

Kfoury-Baz, Elizabeth M.; Sy, Alami; Re, Nassif; Ag, Kibbi; Ng, Rubiez; Hm, Hannoush

doi:10.1046/j.1537-2995.1996.36396182150.x

Cited by 4 publications

(4 citation statements)

References 3 publications

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“…found no evidence of donor leucocyte survival beyond 6 days in a group of 20 women who received a median of eight units of blood; they used an early generation non‐quantitative PCR assay directed at the DRZ‐1 locus of the Y chromosome [12]. Although occasional cases of transfusion‐associated GvHD (TA‐GVHD) in immunocompetent patients have been reported since 1989 [13], these relatively rare cases seemed to be restricted mostly to populations with unusual degrees of genetic homogeneity [14,15]. Vervoordeldonk et al .…”

Section: Early Evidence Supporting Ta‐mcmentioning

confidence: 99%

Transfusion‐associated microchimerism

et al. 2007

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Blood transfusion is a newly recognized cause of microchimerism, the stable persistence of a minor population of allogeneic cells. Relatively recent advances in polymerase chain reaction technology have spawned new information about the frequency and aetiology of transfusion-associated microchimerism (TA-MC). Although conceptually related to fetal-maternal microchimerism, TA-MC is a distinct and separate entity. Evidence of TA-MC has been strongest among patients with severe traumatic injuries who receive relatively fresh blood products shortly after an episode of massive haemorrhage. The presence of a focal deficit in the cellular immunologic repertoire prior to transfusion that happens to match a blood donor's human leucocyte antigen type also appears to be an important predisposing factor. TA-MC seems to be common (affecting approximately 10% of transfused injured patients), enduring (lasting years to decades) and pronounced (involving up to 5% of circulating leucocytes and multiple immunophenotypic lineages suggestive of haematopoietic engraftment). Further study of this topic may reveal important information regarding potential clinical consequences of TA-MC, as well as basic haematologic and immunologic processes.

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Section: Early Evidence Supporting Ta‐mcmentioning

confidence: 99%

Transfusion‐associated microchimerism

et al. 2007

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“…It is important to note that all 10 cases were immunocompetent patients transfused with whole fresh blood with no irradiation and no WBC reduction, nine of them in outside periphery hospitals and the tenth as an emergency life‐saving procedure at our center. A couple of patients with TA‐GVHD referred to our hospital were previously reported in the literature 5,6 …”

Section: Resultsmentioning

confidence: 99%

Transfusion‐associated GVHD: 10 years’ experience at the American University of Beirut—Medical Center

Aoun¹,

Shamseddine²,

Chehal³

et al. 2003

Transfusion

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“…Although TA‐GVHD was first recognized in immunosuppressed patients, there is a growing awareness of its occurrence in immunocompetent patients (Petz et al , 1993; Orlin & Ellis, 1997). Indeed, a number of reports have described TA‐GVHD in immunocompetent recipients of blood products (Bell, 1993; Van der Mast et al , 1994; Kfoury‐Baz et al , 1996; Ahya et al , 1998; Rososhansky et al , 1999). Many cases of TA‐GVHD in immunocompetent patients appear to occur as a result of transfusion of blood from a donor who is homozygous for an HLA haplotype to a recipient who is heterozygous for the same haplotype (Thaler et al , 1989; Wagner & Flegel, 1995).…”

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confidence: 99%

Irreversible loss of donor blood leucocyte activation may explain a paucity of transfusion‐associated graft‐versus‐host disease from stored blood

et al. 2000

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Summary. Transfusion-associated graft-versus-host disease (TA-GVHD) is usually a fatal outcome of blood transfusion therapy, caused by viable leucocytes contained in the donor blood. Most cases of TA-GVHD occur when less than 4-d-old blood is transfused. We therefore examined the molecular changes that occur during storage that may account for the paucity of TA-GVHD following infusion of older blood. Leucocyte number and viability were essentially unchanged from freshly obtained blood, but the expression of cellsurface lymphocyte activation antigens (CD3, CD4, CD28, CD2, CD45) decreased rapidly within the first 24 h and continued to fall to less than 20% of original levels by d 9 of storage at 48C. The decrease in CD antigen expression directly correlated with a decreasing ability to induce activation of the T-lymphocyte cellular signal transduction pathway. As a result, cells became less responsive in a mixed lymphocyte culture (MLC) by d 3, with abrogation of the MLC responsiveness by d 5. Donor leucocytes stored for 4 d or less at 48C were able to partially re-express CD antigens and reconstitute their signalling pathway when placed at 378C, whereas those stored for more than 4 d were not. These irreversible changes result from a permanent downregulation of donor cell protein synthesis. These findings provide a mechanism to explain the paucity of TA-GVHD following transfusion of blood that is more than 4 d-old. Further study may show that aged blood provides additional assurances for the prevention of TA-GVHD; however, use of aged blood should not replace current protocols using irradiation.

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Transfusion‐associated graft‐versus‐host disease: a report of three cases in immunocompetent patients in Lebanon

Cited by 4 publications

References 3 publications

Transfusion‐associated microchimerism

Transfusion‐associated microchimerism

Transfusion‐associated GVHD: 10 years’ experience at the American University of Beirut—Medical Center

Irreversible loss of donor blood leucocyte activation may explain a paucity of transfusion‐associated graft‐versus‐host disease from stored blood

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