Monitoring systemic donor lymphocyte macrochimerism to aid the diagnosis of graftversus-host disease after liver transplantation

Taylor, Amanda; Gibbs, Paul; Sudhindran, S.; Key, Tim; Goodman, Reyna S.; Morgan, Charles W.; Watson, Christopher J.; Delrivière, Luc; Alexander, Graeme; Jamieson, Neville V.; Bradley, J. Andrew; Taylor, Craig

doi:10.1097/01.tp.0000103721.29729.fe

Cited by 95 publications

(145 citation statements)

References 22 publications

(32 reference statements)

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“…9 The evidence of donor lymphocytes in the blood of the recipient is important for the confirmation of GVHD. 4,5 In the current patient, GVHD initially was not confirmed by the skin biopsies and was masked by CMV disease.…”

Section: Discussionmentioning

confidence: 99%

“…However, GVHD after liver transplant, first described in 1988, 1 is very rare (incidence, 0.1% to 1%), 2,3 and usually occurs within the first 6 weeks after transplant. 4 The most common sites of involvement are the skin and gastrointestinal tract, and GVHD after liver transplant is a progressive and fatal disease with mortality > 85% in adults, 5 mostly secondary to overwhelming sepsis or gastrointestinal bleeding. 4,5 The correct diagnosis and proper treatment of GVHD are challenging and no consensus about the best treatment has been established.…”

Section: Introductionmentioning

confidence: 99%

“…4 The most common sites of involvement are the skin and gastrointestinal tract, and GVHD after liver transplant is a progressive and fatal disease with mortality > 85% in adults, 5 mostly secondary to overwhelming sepsis or gastrointestinal bleeding. 4,5 The correct diagnosis and proper treatment of GVHD are challenging and no consensus about the best treatment has been established. We recently treated a man who had GVHD after liver transplant, who had a response to antibodies against tumor necrosis factor-α (TNF-α).…”

Section: Introductionmentioning

confidence: 99%

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Treatment of Liver Transplant Graft-Versus-Host Disease With Antibodies Against Tumor Necrosis Factor-α

Blank

Li²,

Kratt³

et al. 2012

Exp Clin Transplant

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Acute graft-versus-host disease is uncommon after liver transplant. We recently treated a 60-year-old man with liver transplant for hepatocellular carcinoma. After the primary liver transplant graft did not function, revision liver transplant resulted in excellent function. Subsequently, the patient developed watery diarrhea, systemic inflammatory response syndrome, a skin rash on his limbs and trunk, and palmar erythema. Skin biopsy suggested viral exanthems consistent with cytomegalovirus. Despite treatment for cytomegalovirus, intestinal symptoms worsened. Analysis of peripheral blood with fluorescence-activated cell sorting showed a high proportion of T lymphocytes, with 5% to 10% T cells specific to the second donor, suggestive of graft-versus-host disease. Within 48 hours after beginning therapy with antibodies against tumor necrosis factor-α (infliximab), the skin rash disappeared and endoscopy showed slight improvement of the mucosal regeneration. However, despite antifungal prophylaxis with caspofungin, the patient developed angioinvasive pulmonary aspergillosis and multiple organ failure, and he died. In conclusion, typical clinical symptoms of graftversus-host disease after liver transplant may include skin rash and gastrointestinal symptoms, and diagnosis may be confirmed by histologic examination and testing for blood chimerism. A consensus for the treatment of graft-versus-host disease still is lacking, but tumor necrosis factor-α is an encouraging target for therapy to decrease the symptoms of graft-versus-host disease and enable mucosal regeneration.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Treatment of Liver Transplant Graft-Versus-Host Disease With Antibodies Against Tumor Necrosis Factor-α

Blank

Li²,

Kratt³

et al. 2012

Exp Clin Transplant

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“…The most common manifestation is the antibody-mediated hemolytic anemia that follows ABO-compatible but nonidentical transplantation mediated by donor-derived B cells/ plasma cells primed to host allogeneic red blood cell antigens (7,8,10,11). Other manifestations may include acute graftversus-host disease mediated by donor-derived alloreactive cytotoxic T cells that attack host gut, skin, bone marrow, liver, and lungs (12). Other examples of recipient acquired cellular and/or antibody immunity caused by concomitant transfer of donor lymphocytes following solid organ The HLA-antibody specificities show antigen-specific absorption/modulation against self-HLA (recipient own HLA type) and closely related cross-reactive epitopes (self-CREG), and examples of high-level third party antibodies that are not related to the recipient HLA type.…”

mentioning

confidence: 99%

“…transplantation include idiopathic thrombocytopenia (13), vitiligo (14), and peanut allergy (15). In patients with graftversus-host disease after liver, lung, or intestinal transplantation donor T cell chimerism is well described (12), but is very rare after kidney or heart transplantation. Donor B cell microchimerism has, however, been detected in patients who developed red blood cell alloantibodies following liver and kidney-pancreas transplantation (16).…”

mentioning

confidence: 99%

Transfer of HLA-Specific Allosensitization From a Highly Sensitized Deceased Organ Donor to the Recipients of Each Kidney

Maxfield

Taylor

Kosmoliaptsis

et al. 2015

American Journal of Transplantation

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We report for the first time the adoptive transfer of donor HLA‐specific allosensitization in two recipients following kidney transplantation from a highly sensitized donor. Kidneys from a donation after circulatory death donor were transplanted into two nontransfused, HLA‐specific antibody negative males receiving their first transplant. Antibody screening 7 days after transplant showed high level de novo IgG HLA class I‐ and class II‐specific antibodies in both recipients, with largely overlapping antibody profiles but no antibodies to donor HLA. The unusually rapid appearance of de novo alloantibodies in immunosuppressed nonsensitized recipients and absence of donor HLA‐specific antibody prompted testing of stored donor serum that revealed high antibody levels with specificities very similar to those seen in both recipients, but in addition the presence of strong antibodies to each recipient HLA. Alloantibody levels gradually declined but were still detectable at 3 months. These findings suggest that alloreactive passenger B cells/plasma cells within the kidneys of highly sensitized donors may give rise to rapid development of posttransplant de novo HLA‐specific alloantibodies. While the clinical significance of this phenomenon is uncertain it provides one explanation for the appearance of de novo HLA‐specific antibodies directed against third party but not donor HLA.

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Graft‐Versus‐Host Disease After Liver Transplantation

Wood

Eghtesad

Lindenmeyer

2020

Clinical Liver Disease

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Monitoring systemic donor lymphocyte macrochimerism to aid the diagnosis of graftversus-host disease after liver transplantation

Cited by 95 publications

References 22 publications

Treatment of Liver Transplant Graft-Versus-Host Disease With Antibodies Against Tumor Necrosis Factor-α

Treatment of Liver Transplant Graft-Versus-Host Disease With Antibodies Against Tumor Necrosis Factor-α

Transfer of HLA-Specific Allosensitization From a Highly Sensitized Deceased Organ Donor to the Recipients of Each Kidney

Graft‐Versus‐Host Disease After Liver Transplantation

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