Cases reported "Graft vs Host Disease"

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1/10. Transplantation of autologous and allogeneic bone marrow with liver from a cadaveric donor for primary liver cancer.

    BACKGROUND: In histocompatibility mismatched experimental animals, a combination of T-cell-depleted autologous and allogeneic marrow may induce mixed chimerism and tolerance. patients with large primary liver tumors have a poor outcome. We investigated whether it were possible to induce mixed chimerism and obtain an antitumor effect in a patient with a large primary liver cancer after combined liver and bone marrow transplantation (BMT). methods: A 46-year-old female with a primary non resectable liver cancer received a liver transplant from a cadaveric donor. Subsequently, she was conditioned with 4x2 Gy of total lymphoid irradiation, 120 mg/kg cyclophosphamide, and 7.5 Gy total body irradiation. Twelve days after liver transplantation, she received T-cell-depleted autologous:cadaveric 5/6 antigen HLA-mismatched marrow in a proportion of CD34 cells of 0.5:3.0x10(6)/kg. chimerism status was determined with polymerase chain reaction amplification of variable number tandem repeats from dna obtained from CD3 , CD19 , and CD45 magnetic-bead-separated cells. RESULTS: The early posttransplant period was uneventful; liver function was normal and the hematopoietic engraftment of donor and recipient origin was prompt. Alpha-fetoprotein levels dropped from 440 to 35 microg/l. One month after marrow transplantation, donor T-cells decreased markedly. Monoclonal antibody OKT-3 and 10(5)/kg donor T-cells were given. One month later, the patient developed diarrhea and abdominal pain. A colonoscopy showed moderate gastrointestinal acute graft-versus-host disease and a cryptosporidium infection. Three months after BMT, she became a complete donor chimera. chimera cells showed little, if any, reactivity in mixed lymphocyte cultures to recipient and donor cells, but reacted to third party. Five months after BMT, she developed progressive aspergillus fumigatus pneumonia and died. No tumor was found at the autopsy. CONCLUSION: We obtained mixed donor-recipient hematopoietic chimerism without severe acute graft-versus-host-disease, after combined T-cell depleted autologous and allogeneic BMT and a transplantation of a liver from an HLA-mismatched cadaveric donor. Additional donor T-cells enhanced donor bone marrow engraftment, but rejected the autograft. On the basis of this first attempt, further clinical studies are warranted.
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2/10. Graft vs autoimmunity following allogeneic non-myeloablative blood stem cell transplantation in a patient with chronic myelogenous leukemia and severe systemic psoriasis and psoriatic polyarthritis.

    OBJECTIVE: No specific therapy exists for autoimmune diseases caused by self-reactive lymphocytes. As shown in experimental animals, which led to pilot clinical studies, elimination of self-reactive lymphocytes can be accomplished with high-dose chemoradiotherapy, followed by autologous stem cell transplantation, by re-establishment of unresponsiveness to self antigens of newly generated lymphocytes, due to a mechanism of central clonal deletion. We hypothesized that self-reactive lymphocytes causing autoimmune disease may be successfully eliminated by highly immunosuppressive yet not necessarily myeloablative conditioning in conjunction with allogeneic blood stem cell transplantation, since immunocompetent alloreactive lymphocytes of donor origin can effectively eliminate residual host-type hematopoietic cells, self-reactive lymphocytes included, by a mechanism that resembles graft-vs-leukemia (GVL) effects. The present report is an attempt to confirm the existence of graft-vs-autoimmunity (GVA) effects in parallel with amplification of the alloreactive potential of donor lymphocytes following allogeneic non-myeloablative stem cell transplantation (NST). methods: We identified a patient with severe psoriatic arthritis who also had philadelphia (bcr/abl) positive chronic myelogenous leukemia and therefore was fully eligible for NST. Both diseases responded initially to non-myeloablative conditioning involving fludarabine 30 mg/m2 x 6, anti-T-lymphocyte globulin 10 mg/kg X 4, and busulfan 4 mg/kg x 2. RESULTS: The initial NST procedure was uneventful and resulted in elimination of all signs of autoimmunity (psoriasis and arthritis). recurrence of polyarthritis and exacerbation of psoriasis were observed in parallel with a significant increase in the proportion of male (host) dna, and 5% of the mitoses were bcr/abl positive, indicating an increase in the clone of CML. Both bcr/abl-positive cells identified by RT-PCR and psoriatic arthritis were successfully eliminated following discontinuation of anti-GVHD prophylaxis with cyclosporine A (CSA), which resulted in activation of the alloreactive potential of donor T cells, accompanied by graft-vs-host disease (GVHD), suggesting the existence of GVA effects. RT-PCR for bcr/abl remains consistently negative for nearly 3 years, and all dna remains donor type. CONCLUSIONS: The response of autoimmune disease manifestations to GVA effects in parallel with elimination of all host-derived hematopoietic cells supports our working hypothesis that autoimmune diseases caused by self-reactive lymphocytes may be effectively treated by elimination of alloreactive self-reactive lymphocytes following induction of host-vs-graft tolerance, in analogy with replacement of malignant or genetically abnormal host cells following DLI. It is therefore suggested that intentional GVA effects may be inducible by DLI following a conventional or preferably safer non-myeloablative regimen in recipients with life-threatening autoimmune diseases resistant to conventional modalities. Adoptive immunotherapy of autoimmunity may thus involve a two-step procedure: first, inducing host-vs-graft and graft-vs-host transplantation tolerance through a transient stage of mixed chimerism; second, inducing controlled GVA effects, initially by discontinuation of CSA and then, if indicated, by late outpatient DLI to eradicate residual hematopoietic cells of host origin.
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3/10. Infiltrating T cells during liver graft-versus-host disease show a restricted T-cell repertoire.

    Data from animal models have shown that hepatic graft-versus-host disease (GVHD) may be mediated by donor T cells interacting with liver adhesion molecules, other minor histocompatibility antigens, or both. We hypothesized that T-cell infiltrates within a liver biopsy during clinical GVHD would show a restricted T-cell response because the T cells would be responding to a limited number of antigens. We studied the peripheral T-cell repertoire and the liver-infiltrating T-cell repertoire of a patient who developed skin GVHD and subsequent liver GVHD after a matched sibling bone marrow transplantation for acute myeloid leukemia. Spectratype analysis of peripheral blood at the time of liver GVHD revealed that the patient had reconstituted a complex peripheral T-cell repertoire as evidenced by the presence of complementarity-determining region 3 (CDR3) length heterogeneity in most of the T-cell families. The repertoire complexity was skewed in variable gene beta (VB) 5.3, VB4, VB7, VB8, and VB15. Spectratype analysis on the liver biopsy sample revealed a limited infiltrate with an oligoclonal expansion in VBs 4, 7, and 8. We evaluated the T-cell infiltrate in more detail by sequencing the relevant expansions noted by spectratype and developing probes for the predominant CDR3 sequences. These clonotype probes were hybridized to peripheral blood and liver samples from the patient, a T-cell line developed from the patient's peripheral blood at the time of the initial skin GVHD, the donor's blood and marrow, and control samples. The results showed that the T-cell infiltrate during liver GVHD is mediated by a limited number of T cells, and that those cells are mostly different from the ones expanded from the peripheral blood during an acute skin GVHD reaction. These data support the concept that liver GVHD is a response to tissue-specific minor histocompatibility antigens.
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4/10. Will mixed chimerism cure autoimmune diseases after a nonmyeloablative stem cell transplant?

    BACKGROUND: Mixed chimerism after allogeneic bone marrow transplantation has been shown to cure a number of genetic disorders in both the clinical and experimental settings. Although encouraging results have been reported from animal experiments, the role of mixed chimerism in eliminating autoimmune disorders is not clear. methods: A 50-year-old man with extensive psoriasis received an allogeneic transplant from his brother after nonmyeloablative conditioning with fludarabine, melphalan, and Campath-1H for relapsed non-Hodgkin's lymphoma. The chimerism status and the immunological recovery after the transplant were serially monitored. RESULTS: Twenty-one months after the transplant, the patient continues to be in complete remission from psoriasis and lymphoma with stable mixed chimerism (30% to 40% donor cells), despite significant recovery of T-cell subsets and antigen-specific response. CONCLUSIONS: If mixed chimerism can be achieved safely with novel low-intensity conditioning regimens and results in sustained remission of autoimmune diseases, allogeneic transplantation may become a realistic therapy in the management of some patients with autoimmune disease.
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5/10. Early onset of acute immune-mediated lung injury in a child undergoing allogeneic peripheral blood transplantation.

    Animal models have recently clarified the lung injury after allogeneic hematopoietic transplantation. These works have confirmed the role of donor T lymphocytes in immune-mediated inflammatory reactions in the lung. We report here a fatal case of a 3-year-old child who developed acute respiratory failure coinciding with the onset of hyper-acute graft versus host disease (aGVHD) after allogeneic peripheral stem cell transplantation. aGVHD was refractory to treatment and the patient died on day 28. Lung necropsy showed interstitial pneumonia and peribronchial and perivascular infiltration by mononuclear cells, with no viral inclusions. These findings are not specific but have been found by some authors in animal models with acute immune-mediated lung injury related with donor T lymphocytes. Immune-mediated lung injury, as defined by animal models, should be considered in patients with severe signs of systemic aGVHD while excluding other known etiologies of pulmonary disease.
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6/10. Transfer of vitiligo after allogeneic bone marrow transplantation.

    adoptive transfer of donor immunity has been demonstrated in animals after bone marrow transplantation (BMT). In humans, several autoimmune diseases have been similarly transferred. Although BMT may, per se, be associated with a modulation of the recipient's immune system, which could trigger or even cause autoimmune diseases, both animal experiments and experience with humans show the likeliness of adoptive transfer of donor immunity to the recipient. We describe a patient with multiple myeloma in whom generalized vitiligo developed within 3 months after allogeneic BMT from his HLA-matched sister with vitiligo. We believe that a form of adoptive transfer of donor immunity to the recipient might play a role in the development of vitiligo. In spite of this, neither de novo development of vitiligo in a genetically predisposed patient nor autoimmune phenomena associated with graft-versus-host disease can be completely excluded as a contributing factor for development of vitiligo in our patient. To our knowledge, this is the first case report of transfer of vitiligo after BMT from a donor with vitiligo.
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7/10. Treatment of severe acute graft-versus-host disease with third party haploidentical mesenchymal stem cells.

    adult bone-marrow-derived mesenchymal stem cells are immunosuppressive and prolong the rejection of mismatched skin grafts in animals. We transplanted haploidentical mesenchymal stem cells in a patient with severe treatment-resistant grade IV acute graft-versus-host disease of the gut and liver. Clinical response was striking. The patient is now well after 1 year. We postulate that mesenchymal stem cells have a potent immunosuppressive effect in vivo.
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8/10. thalidomide in the treatment of graft-versus-host disease.

    The success of allogeneic bone marrow transplantation has been restricted by the occurrence of graft-versus-host disease (GVHD). Attempts at prevention and treatment of GVHD have resulted in only a limited improvement and the morbidity and mortality rate remains high. thalidomide has been known to have immunosuppressive properties for over 20 years, but it has only recently been used in GVHD. Evidence is now accumulating as to its value both in animal models, and in humans where most benefit has been seen in chronic GVHD. We report our experience using thalidomide in GVHD following allogeneic bone marrow transplantation and review the literature.
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9/10. Membranous nephropathy in a bone marrow transplant recipient.

    A bone marrow transplant recipient is described who had development of nephrotic syndrome in association with chronic graft-versus-host disease (GVHD) and on cyclosporine (CsA) treatment withdrawal. Renal biopsy revealed a membranous glomerulonephritis (MG). The possible relationship between this autoimmune disorder, the immunological features of GVHD in experimental animals, and the influence of CsA is discussed.
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10/10. Lichenoid graft-vs-host disease in an autologous bone marrow transplant recipient.

    BACKGROUND: Graft-vs-host disease (GVHD) represents one of the major complications of allogeneic bone marrow transplantation (BMT) but is less common in autologous BMT. Following autologous BMT, chronic GVHD has been reported in only four patients, all of whom had a self-limited sclerodermoid form. Lichenoid chronic GVHD has not been previously reported in an autologous BMT patient. OBSERVATIONS: Mucosal and cutaneous lichenoid lesions and histologic findings compatible with chronic lichenoid GVHD developed in a patient 35 days after autologous BMT was performed. The onset of clinical lesions at 35 days after BMT is not incongruent with the diagnosis of chronic lichenoid GVHD (rather than a graft-vs-host reaction) and may have been augmented by cyclosporin A in a manner similar to animal model experiments. CONCLUSION: All forms of GVHD can and do occur following autologous BMT.
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